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Rosemary – Rosmarinus Officinalis
Family: Lamiaceae
1 Part Used-2 Abstracts of Published Research on Rosemary – Rosmarinus Officinalis-3 Oligo-elements-4 Vitamins and Minerals-5 Phytochemical Constituents-6 Plant Stem Cell Therapy Indications-6.1 Neurology & Nervous System-6.2 Cardio Vascular System-6.3 Hematology Oncology-6.4 Immunology-6.5 Infectious Disease-6.6 Pulmonary System-6.7 GI – Digestive – Hepatology-6.8 Musculoskeletal System-6.9 Ob Gyn/Reproductive System-6.10 Uro Genital System-6.11 Endocrine System-6.12 Dermatology-6.13 Opthalmology-6.14 Environmental Medicine
Part Used: Young Shoots
NOTE: These indications are only for use with embryonic plant stem cell tissues. Adult plants do not have the same constituents, actions or applications in most cases.
The Rosmarinus officinalis is a woody, perennial herb that is native to the Mediterranean region. Its Latin name, ros-marinus, meaning “dew of the sea,” is presumed to be linked to the plant’s preference to grow near the sea. The Rosmarinus officinalis has gray, scaly bark and grows about 6 feet tall with a spread of 4 to 5 feet. The pungent fragrance exuded by its needle-like leaves is reminiscent of pine. About an inch long, the leaves are evergreen on top and grayish-white underneath. Clusters of delicate, sea-blue flowers blossom in spring and last throughout the summer in warm, humid environments. Common uses include dye, essential oil, ground cover, hair, hedges, incense, insect repellent.
Drug Interaction:
Doxorubicin In a laboratory study, rosemary extract increased the effectiveness of doxorubicin in treating human breast cancer cells. Meanwhile, those taking doxorubicin should consult with a healthcare practitioner before taking rosemary.
Most evidence for rosemary’s medicinal uses comes from clinical experience rather than from scientific studies. However, recent laboratory studies have shown that rosemary slows the growth of a number of bacteria such as E. coli and S. aureus that are involved in food spoilage, and may actually perform better than some commercially used food preservatives.
Alopecia One traditional use of rosemary has been to try to stimulate hair growth. In one study of 86 people with alopecia areata (a disease of unknown cause characterized by significant hair loss, generally in patches), those who massaged their scalps with rosemary and other essential oils (including lavender, thyme, and cedar wood) every day for 7 months experienced significant hair re-growth compared to those who massaged their scalps without the essential oils. It is not entirely clear from this study whether rosemary (or a combination of rosemary and the other essential oils) was responsible for the beneficial effects.
Cancer Both laboratory and animal studies suggest that rosemary’s antioxidant properties may have activity against colon, breast, stomach, lung, and skin cancer cells. However, much more research in this area, including trials involving people, must be conducted before conclusions can be drawn about the value of rosemary for cancer. Carnosol is a naturally occurring phytopolyphenol found in rosemary. Carnosol functions as an antioxidant and anticarcinogenic. In the present study, we compared the antioxidant activity of carnosol and other compounds extracted from rosemary. Carnosol showed potent antioxidative activity in -diphenyl-ß-picrylhydrazyl (DPPH) free radicals scavenge and DNA protection from Fenton reaction. High concentrations of nitric oxide (NO) are produced by inducible NO synthase (iNOS) in inflammation and multiple stages of carcinogenesis.
Rosemary’s Effect on Insulin Levels
Al-Hader, A.A., Z.A. Hasan, and M.B. Aqel. “Hyperglycemic and Insulin Release Inhibitory Effects of Rosmarinus officinalis,” Journal of Ethnopharmacology. Vol 43 1994: An aqueous extract prepared from leaves of rosemary (Rosmarinus officinalis) is widely used in Jordan as a folk remedy for abdominal colic. It has been suggested that rosemary’s volatile oil causes smooth muscle relaxation by inhibiting the increase in cytosolic free calcium concentrations; in turn, a raised cytosolic free calcium level is known to be a trigger for pancreatic insulin release. With this information in consideration, the present study was conducted, using normal and diabetic rabbits, to determine the potential effects of rosemary oil on insulin release and blood glucose levels. It was found that administration of the oil produced a significant change in plasma glucose and serum insulin levels in the normal rabbits, and a significant hyperglycemic effect in the diabetic rabbits. No effect on the fasting plasma glucose levels in normal rabbits was observed. Based on these results, the authors conclude that the volatile oil of rosemary leaves (young shoots) has significant hyperglycemic and insulin release inhibitory effects.
Other Uses:
Dye; Essential; Ground cover; Hair; Hedge; Incense; Repellent.
Abstracts of Published Research on Rosemary – Rosmarinus Officinalis:
J Food Prot. 2009 Aug;72(8):1744-52
In vitro antimicrobial and antioxidant activity of commercial rosemary extract formulations.Klancnik A, Guzej B, Kolar MH, Abramovic H, Mozina SS.
2. J Food Prot. 2009 May;72(5):1107-11
Inhibitory effect of commercial green tea and rosemary leaf powders on the growth of foodborne pathogens in laboratory media and oriental-style rice cakes. Lee SY, Gwon SY, Kim SJ, Moon BK.
3. Prog Neuropsychopharmacol Biol Psychiatry. 2009 Jun 15;33(4):642-50. Epub 2009 Mar 13.
Antidepressant-like effect of the extract of Rosmarinus officinalis in mice: involvement of the monoaminergic system.Machado DG, Bettio LE, Cunha MP, Capra JC, Dalmarco JB, Pizzolatti MG, Rodrigues AL.
4. Lett Appl Microbiol. 2009 Apr;48(4):440-6. Epub 2009 Feb 2.
The antimicrobial activity of four commercial essential oils in combination with conventional antimicrobials. van Vuuren SF, Suliman S, Viljoen AM.
5. J Med Food. 2008 Dec;11(4):741-6.
Anti-inflammatory and antinociceptive effects of Rosmarinus officinalis L. essential oil in experimental animal models.Takaki I, Bersani-Amado LE, Vendruscolo A, Sartoretto SM, Diniz SP, Bersani-Amado CA, Cuman RK.
6. Harefuah. 2008 Oct;147(10):783-8, 838.
The treatment of respiratory ailments with essential oils of some aromatic medicinal plants. Rakover Y, Ben-Arye E, Goldstein LH.
7. J Nutr. 2008 Nov;138(11):2098-105.
Rosmarinic acid antagonizes activator protein-1-dependent activation of cyclooxygenase-2 expression in human cancer and nonmalignant cell lines. Scheckel KA, Degner SC, Romagnolo DF.
8. Neuroreport. 2008 Aug 27;19(13):1301-4.
Beneficial effects of carnosic acid on dieldrin-induced dopaminergic neuronal cell death. Park JA, Kim S, Lee SY, Kim CS, Kim do K, Kim SJ, Chun HS.
9. Int J Food Sci Nutr. 2008 Nov-Dec;59(7-8):691-8.
Chemical composition and antifungal activity of rosemary (Rosmarinus officinalis L.) oil from Turkey. Ozcan MM, Chalchat JC.
Oligo-elements:
B, Cu, Fe, K, Mg, Mn, Na, P, Se, Si, Zn.
Vitamins and Minerals:
B-1, B-2, B-3, C, Calcium.
Phytochemical Constituents:
1,8-Cineole, 13-O-Acetyloleanolic-Acid, Acetic-Acid, Alpha-Amyrin, Alpha-Humulene, Alpha-Phellandrene, Alpha-Pinene, Alpha-Selinene, Alpha-Terpinene, Alpha-Terpineol, Alpha-Thujone, Apigenin, AR-Curcumene, Ascorbic-Acid, Benzyl-Alcohol, Beta-Amyrin, Beta-Carotene, Beta-Elemene, Beta-Phellandrene, Beta-Pinene, Beta-Sitosterol, Beta-Thujone, Betulin, Betulinic-Acid, Borneol, Bornyl-Acetate, Caffeic-Acid, Camphene, Camphor, Carnosic-Acid, Carnosol, Carvacrol, Carvone, Caryophyllene, Caryophyllene-Oxide, Chlorogenic-Acid, Delta-3-Carene, Delta-Cadinene, Diosmetin, Diosmin, Dipentene, Elemol, Ethanol, Eugenol-Methyl-Ether, Fenchone, Fiber, Gamma-Terpinene, Genkwanin, Geraniol, Glycolic-Acid, Hesperidin, Hispidulin, Hispiduloside, Isoborneol, Isobornyl-Acetate, Isobutyl-Acetate, Isopulegol, Isorosmanol, Labiatic-Acid, Limonene, Luteolin, Luteolin-3′-O-(3-O-Acetyl)-Beta-D-Glucuronide,Luteolin-3′-O-(4-O-Acetyl)-Beta-D Glucuronide, Luteolin-7-Glucoside, Methyl-Eugenol, Myrcene, Myrtenol, Neo-Chlorogenic-Acid, Nepetin, Nepetrin, Octanoic-Acid, Oleanolic-Acid, P-Cymene, Pectin, Piperitenone, Rosmadial, Rsomanol, Rosmaridiphenol, Rosmarinic-Acid, Rosmariquinone, Sabinene, Safrole, Salicylates, Sinensetin, Squalene, Styrene, Tannin, Terpinen-4-OL, Terpinolene, Thymol, Toluene, Trans-Anethole, Trans-Carveol, Trans-Pinocarveol, Ursolic-Acid, Verbenone, Zingiberine
Diterpenes such as picrosalvin (= carnosol), carnosolic acid, rosmariquinone and salicylates.
Miscellaneous; rosmaricine, the triterpenes ursolic acid, oleanolic acid & derivatives.
Carnosol is a naturally occurring phytopolyphenol found in rosemary. Carnosol functions as antioxidant and anticarcinogenic. In the present study, we compared the antioxidant activity of carnosol and other compounds extracted from rosemary. Carnosol showed potent antioxidative activity in, -diphenyl-ß-picrylhydrazyl (DPPH) free radicals scavenge and DNA protection from Fenton reaction. High concentrations of nitric oxide (NO) are produced by inducible NO synthase (iNOS) in inflammation and multiple stages of carcinogenesis.
Studies have shown Rosemary to be as effective as the synthetic preservatives BHA and BHT.
Several laboratory studies suggest that rosemary contains compounds that prevent carcinogenic chemicals from binding to and inducing mutations in DNA.
The compounds epigallocatechin gallate (EGCG) and carnosol are known to be anti-inflammatory and cancer preventive.
Therefore, we studied their effect on the generation of peroxynitrite radicals and nitrite. They inhibited lipopolysaccharide (LPS) and interferon-gamma (IFN gamma) induced nitrite production by mouse peritoneal cells by more than 50% at 2.5-10 microM. Cell viability assays verified that the inhibition was not due to general cellular toxicity.
Rosemary seems to have also anti-cancer properties. Researchers at Rutgers University have demonstrated that rosemary oil can prevent the development of tumors in animals. When applied externally, rosemary oil reduced the risk of skin cancer and when taken internally it reduced the incidence of colon and lung cancer. Plant Stem Cell Therapy Indications: The Greatest Liver Agent!
Neurology & Nervous System:
‘P’ Balances Nervous Equilibrium euphoric action, Improves Memory, Neuro vegetative dystonia. Rosemary may prevent the breakdown of acetylcholine, a chemical that allows neurons within the brain to communicate with each other. Neuroprotective carnosic acid activates a novel signaling pathway that protects brain cells from free radical damage, seen in stroke and other neurodegenerative conditions such as Parkinson’s and Alzheimer’s diseases. Carnosic acid to promote the production of Nerve Growth Factor. Cerebral artery ischemia/reperfusion. Carnosic acid reduces cytokine-induced adhesion molecules expression and monocyte adhesion to endothelial cells. Carnosic acid, may shield the brain from free radicals, lowering the risk of strokes and neurodegenerative diseases like Alzheimer’s and Lou Gehrig’s. For this purpose you will have to use 10 to 20 drops 3 x a day.
Carnosic acid has two therapeutic properties that make it a vital neuroprotective agent:
1. It protects against the narrowing of the left and right middle cerebral arteries – two of the major arteries carrying blood to the brain. Narrowing of these arteries with age is a common and important factor contributing to the development of neurodegenerative diseases.
2. Carnosic acid increases the body’s production of the antioxidant, glutathione. Glutathione is one of the most important antioxidants that help to protect the brain against free radical damage.
Also the antiplatelet activity of carnosic acid is mediated by the inhibition of cytosolic calcium mobilization and that carnosic acid has the potential of being developed as a novel antiplatelet agent.
CA activates the Keap1/Nrf2 transcriptional pathway by binding to specific (Kelch-like ECH-associated protein 1, also known as KEAP1, is a human gene) Keap1 cysteine residues, thus protecting neurons from oxidative stress and excitotoxicity. In cerebrocortical cultures, CA-biotin accumulates in non-neuronal cells at low concentrations and in neurons at higher concentrations. It was presented evidence that both the neuronal and non-neuronal distribution of CA may contribute to its neuroprotective effect. Furthermore, CA translocates into the brain, increases the level of reduced glutathione in vivo, and protects the brain against middle cerebral artery ischemia/reperfusion, suggesting that CA mayrepresent a new type of neuroprotective electrophilic compound.
References: Journal of Neurochemistry, Volume 104, Number 4, February 2008 , pp. 1116-1131(16).
Cardio Vascular System:
‘P’ Reduces Cholesterol LDL and Triglycerides due to the rosmarinic acid and carnosic acid which assists the liver in breaking down lipids. Atherosclerosis, Improves Circulation of the extremities. Reduces the level of urea and uric acid. General detoxification by being an anti oxidant. Balances the Ionic and Mineral equilibrium. Normalizes the Vagus response A study found that depressed patients with VNS improved over time in terms of remission and response and also improved in their ability to function. It protects against the narrowing of the left and right middle cerebral arteries – two of the major arteries carrying blood to the brain. Carnosic acid prevents the migration of human aortic smooth muscle cells by inhibiting the activation and expression of matrix metalloproteinase-9 and NF-kB activation may be due to its antioxidant and antiinflammatory properties. Carnosic acid, a new class of lipid absorption inhibitor lowers triglycerides, its effectiveness in inhibiting LDL (low density lipoprotein). Carnosic Acid is the starting element of a process known as the “Carnosic Acid Cascade” of chemical reactions in the body where free radicals are quenched. Carnosic acid is transformed into carnosol; carnosol into rosmanol; and rosmanol into galdosol. With each of these transformations, free radicals are quenched. Its containment of this multi-step process that makes Rosemary young shoots one of the most potent antioxidants found in nature.
A study showed that carnosic acid effectively inhibited the TNF-a-induced migration of HASMC. The levels of ROS production, MMP-9 activation and expression, and nuclear translocation of NF-kB p50 and p65 were also all reduced by CA pretreatment. The present results led us to conclude that CA inhibits TNF-a-induced nuclear translocation of p50 and p65, thereby suppressing the activation and protein expression of MMP-9, resulting in decreased HASMC migration. Thus, CA may play an important role in the prevention of atherosclerosis.
References: British Journal of Nutrition (2008), 100, 731–738.
Elemol (sesquiterpene) a γ-lactone and not a δ-lactone as previously assumed: Antiacetylcholinesterase, Anticheilitic, Anticoronary, Antidementia, Antidepressant, Antigingivitic, Antiglossitic, Antigout, Antiinfertility, Antimetaplastic, Antimyelotoxic, Antineuropathic, Antiperiodontal, Antiplaque, Antipolyp, Antipsychotic, Antiulcer, Cancer-Preventive, Hematopoietic, Immunostimulant, Uricosuric, Xanthine-Oxidase-Inhibitor. Effect of elemol,, on the tracheal smooth muscle.
Fenchone (monoterpene and a Ketone): Antialzheimeran; Anticholinesterase; Counterirritant; Perfumery; Secretolytic.
Carnosic acid reduces cytokine-induced adhesion molecules expression and monocyte adhesion to endothelial cells.
References: European journal of nutrition 48(2):101-6, 2009 March.
Rosmariquinone (RQ), an ortho-quinone diterpenoid: act as a hydrogen-donating antioxidant.
Hematology Oncology:
‘P’ Increases RBCs, Anticoagulant. Reduced the incidence of skin, colon and lung cancer. Anti-Cancer. Induces Apoptosis in Human Leukemia Cells through Caspase Activation and Poly (ADP-ribose) Polymerase Cleavage.
Immunology:
‘P’ Increases WBC, Allergies associated with liver problems. Eye-related symptoms associated with seasonal allergies. Rosmarinic acid (suggested as a treatment for septic shock, since it suppresses the endotoxin-induced activation of complement). Rosmarinic Acid Induces p56lck-Dependent Apoptosis in Jurkat and Peripheral T Cells via Mitochondrial Pathway Independent from Fas/Fas Ligand Interaction 1.
Rosmarinic acid
has been shown to kill allergy-activated T cells and neutrophils during allergic reactions without affecting the T cells or neutrophils in their resting state. Using traditional antihistamines in allergic reactions, on the other hand, is somewhat analogous to turning off a fire alarm without putting out the fire. Antihistamines do nothing to lower the number of excess immune cells once they are formed. High levels of immune cells in their active form can lead to other dangers, such as free radical damage to normal tissues and to circulating proteins like HDL. They are many different types of Luteolins in Rosemary which inhibits antigen-specific proliferation and interferon-gamma production by murine and human autoimmune T cells. Flavonoids such as luteolin and apigenin are inhibitors of interleukin-4 and interleukin-13 production by activated human basophils.
Infectious Disease:
‘P’ Contains 44 Antibacterial phytochemicals, 26 Antiviral and 12 Antiherpetic phytochemicals. Effective against: H-Pylori, Bacillus cereus, Staphylococcus aureus, Vibrio parahaemolyticus.
Pulmonary System:
‘P’ Respiratory Decompensation. Advanced Tuberculosis. Antiasthmatic; Acute Asthma; Allergic Rhinitis; Chronic Bronchitis. In another study, researchers showed that rosmarinic acid inhibited lung injury from diesel exhaust particles, and outlined the exact steps by which rosmarinic acid brings about the cell death of activated T cells. The study also showed that the accumulation of neutrophils in human lung disease is directly related to the localized elevation of the cytokine IL-8, which supports the theory that IL-8 plays a central role in the pathogenesis of acute lung injury.
GI – Digestive – Hepatology:
‘P’ Intestinal Decompensation, Epithelial action on colon mucosa intestinal smooth muscle relaxant. Crohn’s Disease & Colitis, Diverticulosis, Celiac Disease, Hepatic Function: Hepato Protective 63%. Liver Insufficiency, Biliary Dyskinesia. Cholelithiasis, Liver & Gallbladder major detoxifier, Gallbladder antispasmodic action in Chronic Cholecystitis. Antiacetylcholinesterase, Hepatitis A, B & C. Maintains good liver function in patients on birth control pills and implants. Protects against damage of Excess fat consumption. Carnosol and carnosic acid have been suggested to account for over 90% of the antioxidant properties of rosemary extract. Carnosic acid increases the body’s production of the antioxidant, glutathione. Fenchone components have a secretolytic effect on the respiratory tract. Also help to relieve smooth muscle spasms in the bowel.
Keap1 regulates both cytoplasmic-nuclear shuttling and degradation of Nrf2 in response to electrophiles. Transcription factor Nrf2 regulates the expression of a set of detoxifying and anti-oxidant enzyme genes. Several lines of evidence suggest that electrophiles and reactive oxygen species liberate Nrf2 from its cytoplasmic repressor Keap1 and provoke the accumulation of Nrf2 in the nucleus.
Piperitenone (monoterpene ketone): Antiacetylcholinesterase; Intestinal smooth muscle relaxant.
Musculoskeletal System:
‘P’ Contains 33 Antiinflammatory phytochemicals, 21 Analgesic and 8 COX-2-Inhibitor phytochemicals. α-thujone (pain killing) effect, comparable to codeine.
Ob Gyn/Reproductive System:
‘A’ Frigidity, Dysmenorrhea.
Uro Genital System:
‘A’ Prostate Congestion. Reduces the level of urea and uric acid.
Endocrine System:
‘A’ Adrenal Insufficiency, Gonad Senescence, (Potential for diabetes as from the latest research). Andropause, Impotency, sexual anomaly functional, Dysendocrinia. Anti-TSH action of rosmarinic acids for Hyperthyroidism.
Dermatology:
‘A’ Skin regenerative and wound healing, displays its main activity in the dermis,Rosmarinic Acid is a potent Antioxidant it inhibits the activity of Elastase (an Enzyme that catalyzes the breakdown of Elastin). verbenone phytochemical especially useful for treating chronic skin conditions, dermatitis, eczema and psoriasis. Acne prone skin may respond favorably to the renewing effects of Rosemary verbenone, as well as to its action to fight infection and promote glandular balance and function. Its skin nourishing action makes it ideal for dry and mature skin. Alopecia, Oily Hair, Skin, Scalp conditions, and Dandruff. Antiscar.
Opthalmology:
A Hispiduloside, Nepetrin and Sinensetin (flavonoids): Anticataract. Rosmarinic acid particularly inhibited the eye-related symptomsassociated with seasonal allergies.
Environmental Medicine:
‘A’ as a treatment for septic shock, since it suppresses the endotoxin-induced activation of complement. Rosmarinic acid inhibits lung injury from diesel exhaust particles, and outlined the exact steps by which rosmarinic acid brings about the cell death of activated T cells. The accumulation of neutrophils in human lung disease is directly related to the localized elevation of the cytokine IL-8, which supports the theory that IL-8 plays a central role in the pathogenesis of acute lung injury.
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New mosquito-borne virus spreads in Latin America
SANTO DOMINGO, Dominican Republic — An excruciating mosquito-borne illness that arrived less than a year ago in the Americas is raging across the region, leaping from the Caribbean to the Central and South American mainland, and infecting more than 1 million people. Some cases have already emerged in the United States.–While the disease, called chikungunya, is usually not fatal, the epidemic has overwhelmed hospitals, cut economic productivity and caused its sufferers days of pain and misery. And the count of victims is soaring.–In El Salvador, health officials report nearly 30,000 suspected cases, up from 2,300 at the beginning of August, and hospitals are filled with people with the telltale signs of the illness, including joint pain so severe it can be hard to walk.–“The pain is unbelievable,” said Catalino Castillo, a 39-year-old seeking treatment at a San Salvador hospital. “It’s been 10 days and it won’t let up.”–Venezuelan officials reported at least 1,700 cases as of Friday, and the number is expected to rise. Neighboring Colombia has around 4,800 cases but the health ministry projects there will be nearly 700,000 by early 2015. Brazil has now recorded its first locally transmitted cases, which are distinct from those involving people who contracted the virus while traveling in an infected area.–Hardest hit has been the Dominican Republic, with half the cases reported in the Americas. According to the Pan American Health Organization, chikungunya has spread to at least two dozen countries and territories across the Western Hemisphere since the first case was registered in French St. Martin in late 2013.–There have been a few locally transmitted cases in the U.S., all in Florida, and it has the potential to spread farther, experts say, but Central and South America are particularly vulnerable. The chief factors are the prevalence of the main vector for the virus, the aedes aegypti mosquito, and the lack of immunity in a population that hasn’t been hit with chikungunya in modern medical history, said Scott C. Weaver, director of the Institute for Human Infections and Immunity at the University of Texas Medical Branch.–“There are going to be some very large populations at risk down there, much larger than the Caribbean,” Weaver said.—Chikungunya is a word that comes from the Makonde language of Tanzania in eastern Africa and translates roughly as “that which bends up,” in reference to the severe arthritis-like ache in joints that causes sufferers to contort with pain. It’s usually accompanied by a spiking fever and headache. There have been only 113 deaths linked to the region’s outbreak, according to the most recent data, but chikungunya can be crippling.–Herman Slater, a 60-year-old gardener in Jamaica’s capital of Kingston, said he was laid out for almost two weeks this month with unimaginable joint pain, hammer-pounding headaches and fevers that came in waves.–“I tell you, I was surprised by how painful it was. It was taking me five minutes to get out of bed, and then I could hardly even walk,” Slater said. “My hands were so bad I couldn’t open a bottle, couldn’t comb my hair. Every night I was wet from sweat.”–In acute cases, pain can last for months. Joanna Rivas, who works as a maid in the Dominican capital of Santo Domingo, said she has had joint pain since May, and her 12-year-old daughter’s case is so severe the girl can’t hold her pen at school. Both have been taking the pain reliever acetaminophen, the main treatment for chikungunya, which has no cure or vaccine.–Besides the suffering, chikungunya has caused economic damage with the cost of providing treatment and controlling mosquitoes and by absenteeism from work. A study by the Universidad Eugenio María de Hostos in the Dominican Republic found nearly 13 percent of businesses said they had people miss work because of chikungunya in June.–Authorities throughout the region have been spraying pesticide and encouraging people to remove water containers where mosquitoes can breed. Oxitec, a British company that has tested genetically modified aedys aegypti to combat dengue in Brazil, Cayman Islands and Panama, says it has received a surge of interest since the start of the outbreak.–Chikungunya, which has been known for decades in parts of Africa and Asia, is transmitted when a mosquito bites an infected person and then feeds on someone else. It may have found fertile ground in Latin America and the Caribbean because many people are outside in the daytime, when aedes aegypti bite, or lack adequate screens on their windows.–In an article in the New England Journal of Medicine, Dr. Erin Staples of the U.S. Centers for Disease Control and Prevention said access to air conditioning to keep mosquitoes at bay might also be a factor. During an outbreak of mosquito-borne dengue in 1999 along the Texas-Mexico border, aedes aegypti were three times as abundant on the U.S. side but the number of people infected with dengue was twice as high on the Mexican side.-Conditions vary widely in the region. Haiti, where many people live in flimsy shacks with little protection from mosquitoes, has been hit hard. In Venezuela, air conditioning is widespread but the country has a shortage of insect repellent and pesticide sprayers due to the country’s economic problems.–Staples said past outbreaks have been known to affect around 30 per cent of a population, so there is room for the epidemic to grow, although it’s too early to accurately project how many will get sick or whether chikungunya will become endemic to the region like dengue.–The good news is that people seem to acquire immunity to all major strains.–“We do believe currently that if someone is unfortunate enough to get infected, they should not be infected again,” Staples said.
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Mycotoxin present in many types of food deteriorates neuroregeneration
Date:
September 19, 2014
Source:
Asociación RUVID
The research, carried out in the Faculty of Health Sciences of CEU Cardenal Herrera University, in cooperation with the University of Valencia, was published in the Journal of Applied Toxicology. This is one of the first articles worldwide to research the effect of Ochratoxin A on the subventricular zone of the brain, which in the adult mammalian brain is where neurogenesis primarily occurs.–Researchers at the Institute for Biomedical Sciences at CEU-UCH, in cooperation with colleagues of University of Valencia, showed through in vitro as well as in vivo experiments on lab animals the potential negative effect on neuroregeneration caused by Ochratoxine A, a mycotoxine found in many types of food, especially cereals and their derivatives. The study showed that Ochratoxine A deteriorates the formation of new neurons in the brain, a process called neurogenesis that, in particular, takes place in the subventricular zone, which in the adult brain is the largest of the neurogenic zones.–CEU-UCH professors José Miguel Soria, head of the research group ‘Strategies in Neuroprotection and Neuroreparation’ at the CEU-UCH Faculty of Health Sciences, and María Ángeles García Esparza, a member of the group, monitored the research, which was published in the Journal of Applied Toxicology. The authors further show that Ochratoxin Acan accumulate in the brain, where it causes increased cellular decay in the neurogenic zones, which in turn affects the production of neural stem cells. As neural stem cells regenerate neural populations, a decreased production of these could be a crucial factor in neurodegenerative diseases.–Story Source–The above story is based on materials provided by Asociación RUVID. Note: Materials may be edited for content and length.–Journal Reference-Sara Paradells, Brenda Rocamonde, Cristina Llinares, Vicente Herranz-Pérez, Misericordia Jimenez, Jose Manuel Garcia-Verdugo, Ivan Zipancic, Jose Miguel Soria, Mª Angeles Garcia-Esparza. Neurotoxic effects of ochratoxin-A on the subventricular zone of adult mouse brain. Journal of Applied Toxicology, July 2014 DOI: 10.13140/2.1.1347.1362
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How to make silver citrate
Norton, Steve Thu, 21 Jan 2010 13:45:10 -0800
Richard, Marshall has already provided some excellent information. I do make anduse silver citrate. I think it has a place but I also believe that EISdoes as well. I think that EIS is best in some applications and thatsilver citrate has benefits in others. Remember that what you read onweb sites is biased towards the sellers products and the information maynot be accurate. I do not think that one can state that in general thatEIS or silver citrate is better than the other but maybe in certain usesone is better than the other. Below are some repeats of information Ihave posted below on silver citrate. They may be of help. – Steve N _______________________________________________________ I know of three versions of silver citrate on the market. One is calledSliver 100 and is made by Opti-Silver:http://www.silver100.com/productinfo.pdf It is made using silver oxide as the ionic silver source. The silveroxide is mixed with citric acid and tripotassium citrate to create SC.According to the manufacturer: “While the patent covers a broad range ofsubstances, the company has chosen to use citrate as the complexingagent, and potassium as the counter-ion for maximum stability” While Idon’t make this version, I would guess that you could add tripotassiumcitrate to standard SC if you are interested in potassium as thecounter-ion. A patent related to the product is at: http://www.silver100.com/USPatent.PDF A second silver citrate supplier is Pure Bioscience who sells SC forboth internal use and as a disinfectant under the Biocide and Axenohllabels. They sell the SC in concentrations of up to 2400 ppm. I haveseen other SC sellers that appear to buy the concentrate, dilute it to20 ppm and sell it under their private label. Pure Bioscience refers totheir SC as silver dihydrogen citrate, but it is simply SC made same thesame way as EIS but using a citric acid solution instead of distilledwater. Here is an article regarding their disinfectant spray: http://cr.pennnet.com/display_article/310415/15/ARCHI/none/TOPST/1/MRSA-infection-eradicated-for-14-months-With-SDC-disinfectant-in-Tulsa-County-Jail/<http://cr.pennnet.com/display_article/310415/15/ARCHI/none/TOPST/1/MRSA-infection-eradicated-for-14-months-With-SDC-disinfectant-in-Tulsa-County-Jail/%20 The antibacterial spray is silver citrate at 30 ppm. Not to be outdone,they also have a patent: http://www.freepatentsonline.com/6197814.html _______________________________________________________ You need to use powdered citric acid. I use 1/8 cup for 2 liters water.The citric acid increases the conductivity of the solution so you cannotuse an automated CS generator. Also if the generator uses currentlimiting it will take a long time to get to a high ppm. A manual setupwithout current limiting is best. Also, a battery powered setup may nothave enough current capability. _______________________________________________________ You can only achieve about a 285 ppm concentration of silver citrate inwater. To get higher concentrations, you need to have the silver citratedissolved in a citric acid solution and that is the reason for theadditional citric acid. In my first attempt at silver citrate, I used a10 percent solution because the following patent performed testing withsolutions of 1, 5, and 10 percent: http://www.freepatentsonline.com/6197814.html According to the patent, 400 ppm SC made with 5 and 20 percentsolutions of citric acid are stable during storage but with 1 percent itwas not. I had plenty of citric acid powder so I went with 10 percentfor the first try. Next, I used a 5% solution, by volume, of citric acid dissolved indistilled water for concentrations of up to 600 ppm. Measurement of thecitric acid was not critical since I used more citric acid than isnecessary. Currently, I am using 1/8 cup for 2 liters water, which I think is inthe 2 – 3% range. I do it to keep the tart taste of the SC at anacceptable level while easing the effort to make the SC. The solution isstable over time too. I use a manual setup with no stirring. When Imake the SC, I just cut the top off a gallon distilled water plasticbottle to where I will have 2 liters water in the container and a littleadditional height to prevent spillage. The separation if the electrodesis determined by the container’s width..Given, the conductivity of thesolution, I could use a wider container but there is no need to. My earlier attempts with higher citric acid concentrations showed alittle formation of silver oxide on the negative electrode near the endif the generation. With the current concentration I see oxide formationstarting just around the 200 ppm concentration. So I continue to use the1/8 cup of citric acid to minimize the need to clean the electrode.Also, the higher citric acid concentrations showed little or no currentdrop off during the generation. At the present concentration, I do seesome drop off of electrode current. The current plus the silver oxideformation indicate to me that I might be getting around the max ppm forthe concentration. Remember that the patent indicated that 400 ppm at a1% solution is not stable and that some of the citric acid is consumedin the making of the silver citrate. Just FYI:If you use enough citric acid you can generate silver citrate solutionsto over 23,000 ppm. See Figure 4 in: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2590638/ “Silver citrate is a white substance with a very limited solubility inwater. Under the normal physicochemical conditions, 1 part of silvercitrate is soluble in 3500 parts of water, which corresponds to 285 ppmof Ag(I) ion in the solution [11].” “Formation of silver citrate/citric acid complexed solutions wasinvestigated. Although, silver citrate is minimally soluble in water, itcan successfully be dissolved in citric acid solutions. The maximumconcentration of Ag(I) in solution is estimated at 23 to 25 g/L if theconcentration of citric acid is at least 4 mol/L or higher.” In the report above, the graph in Figure 4 shows how much citric acidyou need vs the ppm of the silver citrate. Please note that the graphdoes not include the citric acid needed to create the silver citrate inthe first place so one will need to use more than is shown. –The Silver List is a moderated forum for discussing Colloidal Silver. Instructions for unsubscribing are posted at: http://silverlist.org To post, address your message to: [email protected] Address Off-Topic messages to: silver-off-topic-l…@eskimo.com The Silver List and Off Topic List archives are currently down… List maintainer: Mike Devour <mdev…@eskimo.com>
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Show of the Month October 10 2014
Turmeric compound boosts regeneration of brain stem cells
Copper Power- Copper in medicine- Incorporation of copper into chitosan scaffolds promotes bone regeneration-
A Brief History of The Health Support Uses of Copper– Ancient Uses of Copper-
19th Century Copper-20th Century Copper– Copper in the 21st Century- Copper sulphate as a fish disease treatment
Disinfectant and method of making
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Turmeric compound boosts regeneration of brain stem cells
Date:
September 25, 2014
Source:
BioMed Central
A bioactive compound found in turmeric promotes stem cell proliferation and differentiation in the brain, reveals new research published today in the open access journal Stem Cell Research & Therapy. The findings suggest aromatic turmerone could be a future drug candidate for treating neurological disorders, such as stroke and Alzheimer’s disease.–The study looked at the effects of aromatic (ar-) turmerone on endogenous neutral stem cells (NSC), which are stem cells found within adult brains. NSC differentiate into neurons, and play an important role in self-repair and recovery of brain function in neurodegenerative diseases. Previous studies of ar-turmerone have shown that the compound can block activation of microglia cells. When activated, these cells cause neuroinflammation, which is associated with different neurological disorders. However, ar-turmerone’s impact on the brain’s capacity to self-repair was unknown.—Researchers from the Institute of Neuroscience and Medicine in Jülich, Germany, studied the effects of ar-turmerone on NSC proliferation and differentiation both in vitro and in vivo. Rat fetal NSC were cultured and grown in six different concentrations of ar-turmerone over a 72 hour period. At certain concentrations, ar-turmerone was shown to increase NSC proliferation by up to 80%, without having any impact on cell death. The cell differentiation process also accelerated in ar-turmerone-treated cells compared to untreated control cells.–To test the effects of ar-turmerone on NSC in vivo, the researchers injected adult rats with ar-turmerone. Using PET imaging and a tracer to detect proliferating cells, they found that the subventricular zone (SVZ) was wider, and the hippocampus expanded, in the brains of rats injected with ar-turmerone than in control animals. The SVZ and hippocampus are the two sites in adult mammalian brains where neurogenesis, the growth of neurons, is known to occur.–Lead author of the study, Adele Rueger, said: “While several substances have been described to promote stem cell proliferation in the brain, fewer drugs additionally promote the differentiation of stem cells into neurons, which constitutes a major goal in regenerative medicine. Our findings on aromatic turmerone take us one step closer to achieving this goal.”—Ar-turmerone is the lesser-studied of two major bioactive compounds found in turmeric. The other compound is curcumin, which is well known for its anti-inflammatory and neuroprotective properties.–Story Source–The above story is based on materials provided by BioMed Central. Journal Reference Joerg Hucklenbroich, Rebecca Klein, Bernd Neumaier, Rudolf Graf, Gereon Fink, Michael Schroeter, Maria Rueger. Aromatic-turmerone induces neural stem cell proliferation in vitro and in vivo. Stem Cell Research & Therapy, 2014; 5 (4): 100 DOI: 10.1186/scrt500
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Copper Power
Copper in medicine- homeostasis, chelation therapy and antitumor drug design.
Wang T1, Guo Z.
Author information
Abstract
As one of the most important essential transition metals, copper is involved in a variety of biological processes such as embryo development, connective tissue formation, temperature control and nerve cell function. It is also related to severe diseases such as Wilson’s and Menkes diseases and some neurological disorders. Novel components of copper homeostasis include copper-transporting P-type ATPases, Menkes and Wilson proteins, and copper chaperones in humans have been identified and characterized at the molecular level. These findings have paved the way towards better understanding of the role of copper deficiency or copper toxicity in physiological and pathological conditions. Therefore, organic compounds that can interfere with copper homeostasis may find therapeutic application in copper-dependent diseases. The antitumor activity of copper complexes was reported several decades ago, and many new complexes have demonstrated great antitumor potential. Copper complexes may have relatively lower side effects than platinum-based drugs, and are suggested to be able to overcome inherited or acquired resistance of cisplatin. In this overview, the most recent advances in copper homeostasis, copper-related chelation therapy and design of copper-based antitumor complexes will be summarized.
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Incorporation of copper into chitosan scaffolds promotes bone regeneration in rat calvarial defects.
D’Mello S1, Elangovan S, Hong L, Ross RD, Sumner DR, Salem AK.
Author informationEK
Abstract
The objective of this study was to investigate the effects of a copper loaded chitosan scaffold on bone regeneration in critical-sized calvarial defects in rats. Chitosan scaffolds and copper-chitosan scaffolds were fabricated and characterized by scanning electron microscopy (SEM). Chitosan and copper-chitosan scaffolds were implanted into 5 mm diameter critical-sized calvarial defects in Fisher 344 male rats. Empty defects (no scaffolds) were included as a control. After 4 weeks, the rats were sacrificed for microcomputed tomography (micro-CT) and histological analysis of new bone tissue development. Microscopy images revealed the uniformly porous structure of chitosan and copper-chitosan scaffolds. Significant bone regeneration was noted in the defects treated with copper-chitosan scaffolds when evaluated using micro-CT and histological analysis, when compared with other groups tested. On analysis of the micro-CT scans, an eleven-fold and a two-fold increase in the new bone volume/total volume (BV/TV) % was found in defects treated with the copper-chitosan scaffolds, when compared to empty defects and chitosan scaffolds, respectively. This study demonstrated the suitability of copper-crosslinked chitosan scaffolds for bone tissue engineering and provides the first evidence that inclusion of copper ions in scaffolds can enhance tissue regeneration. © 2014 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2014
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A Brief History of The Health Support Uses of Copper
Throughout history, healers have understood the value of copper in obtaining and maintaining optimum health. Whether topically applied or ingested, many forms of copper and copper compounds (such as copper carbonate, copper silicate, copper oxide, copper sulfate, copper chloride, etc.) were used throughout history for the treatment of disease. Copper has been used for medicinal purposes as far back as ancient Egypt, Greece and Rome as well as in the ancient Aztec civilization.
Ancient Uses of Copper
An ancient Egyptian medical text, known as the Smith Papyrus (circa 2400 B.C.), mentions using copper as a sterilization agent for drinking water and wounds. Another ancient text, known as the Ebers papyrus (circa 1500 B.C.) mentions the use of copper for headaches, “trembling of the limbs,” burns, and itching. The island of Cyprus provided a readily available supply of copper to Greece and is known to have provided much of the copper needed for the empires of ancient Phoenicia and Rome as well. It has also been documented that Israel’s Timna Valley provided copper for the Pharaohs.
Hippocrates (circa 400 B.C.), known as the father of modern medicine (and for whom the doctor’s Hippocratic oath was named) mentions copper as a treatment for leg ulcers associated from varicose veins. The Greeks also sprinkled a powder of copper oxide and copper sulfate on open wounds and treated wounds with a mixture of honey and red copper oxide.
In the first century A.D., the book De Materia Medica by Dioscorides, describes using verdigris (which they made by exposing metallic copper to vinegar steam to form copper acetate) in combination with copper sulfate as a remedy for bloodshot eyes, inflamed eyes, “fat in the eyes”, and cataracts.
Evidence from the time of Roman physician Aulus Cornelius Celsus (14 to 37 A.D.), tells us that copper and its derivatives were firmly established as important drugs. In his book, De Medicina, Celsus details numerous uses for copper, along with specific instructions for the preparation of the particular form of copper recommended for each disease or condition. Among his specific directions are a copper oxide mixture made with raisin wine, saffron and myrrh for the treatment of venereal disease and a copper mixture made with rose oil for chronic ulcers.
Pliny (23 to 79 A.D.) described a number of remedies involving copper. Black copper oxide with honey was used to kill intestinal worms and purge the stomach. In diluted form, nose drops were used to “clear the head”; eardrops relieved ear discomfort and infection, and taken by mouth it relieved mouth sores and ulcers. Diluted copper mixtures were also used for “eye roughness,” “eye pain and mistiness.”
The ancient Aztec civilization also used copper for medical purposes, including gargling with a copper mixture for sore throats. In ancient India and Persia, copper was used to treat lung diseases. Copper compounds such as malachite and copper oxide were used on boils and other skin conditions. Copper acetate and copper oxide were used for eye infections. Evidence also shows us that nomadic Mongolian tribes used copper sulfate, taken by mouth, to treat venereal ulcers.
19th Century Copper
The first recorded observation of copper’s role in the immune system in modern times was published in 1867 when it was reported that, during the cholera epidemics in Paris of 1832, 1849 and 1852, copper workers were immune to cholera.
In 1885, the French physician, Luton, reported using copper acetate in his practice to treat arthritic patients. For external application he made a salve of hog’s lard and 30% neutral copper acetate. For internal treatment, he used pills containing 10 mg. of copper acetate.
In 1895, in a published review of the pharmacological actions of copper compounds, copper arsenate was reported to treat acute and chronic diarrhea as well as dysentery and cholera. An organic complex of copper developed by Bayer was shown to have curative powers in the treatment of tuberculosis. Copper treatment for tuberculosis continued until the 1940s.
20th Century Copper
As early as 1912, patients in Germany were treated for facial epithelioma with a mixture of copper chloride and lecithin, suggesting that copper compounds might assist anti-cancer activity.
Recent work with mice in the U.S. has shown that treatment of solid tumors with non-toxic doses of various organic complexes of copper markedly decreased tumor growth and metastasis and thus increased survival rate. These copper complexes did not kill cancer cells but caused them to revert to normal cells. Based on work in the treatment of cancers using copper complexes, researchers have found that these same complexes may prevent or retard the development of cancers in mice under conditions where cancers are expected to be induced.
First observed in rats in 1936, numerous studies have drawn attention to the relationship between copper deficiency and heart disease, which effect has now been traced to both a deficiency in copper and an imbalance in the copper-to-zinc ratio in the body.
In 1939, the German physician, Werner Hangarter, noticed that Finnish copper miners were unaffected by arthritis as long as they worked in the mining industry. This observation led Finnish medical researchers plus the Germans, Hangarter and Lübke, to successfully use a mixture of copper chloride and sodium salicylate to treat patients suffering from rheumatic fever, rheumatoid arthritis, neck and back problems, and sciatica.
A Manual of Pharmacology and its Applications to Therapeutics and Toxicology, published by W. B. Saunders Company in 1957 recommends the use of 0.5 gram of copper sulfate, dissolved in a glass of water, in a single dose, or three doses of 0.25 gram fifteen minutes apart, to induce vomiting. Interestingly, Pliny (23 – 79 A.D.) also mentions using copper for just this purpose.
Copper aspirinate has been shown not only to be more effective in the treatment of rheumatoid arthritis than aspirin alone, but it has been shown to prevent or even cure the ulceration of the stomach often associated with aspirin therapy. More than 140 copper complexes of non-steroidal anti-inflammatory agents (aspirin and ibuprofen, for example) have been shown to be more active than their parent compounds.
It has been demonstrated that copper complexes such as copper aspirinate and copper tryptophanate, markedly increase healing rate of ulcers and wounds. For example, copper complexes heal gastric ulcers five days sooner than other reagents. Further, it has been shown that, whereas non-steroidal anti-inflammatory drugs, such as ibuprofen and enefenamic acid suppress wound healing, copper complexes of these drugs promote normal wound healing while at the same time retaining anti-inflammatory activity.
With reports of seizures in animals and humans who had significant and prolonged copper deficiencies in their diets, researches postulated that copper plays a role in the prevention of seizures. Research uncovered that organic compounds which are not themselves anti-convulsants, exhibit anticonvulsant activity when combined with copper. Further, it was found that copper complexes of all anti-epileptic drugs are more effective and less toxic than their parent drugs.
The 1973 work by Dr. L.M. Klevay at the U.S. Department of Agriculture, Human Nutrition Research Center pointed to a relationship between copper and cholesterol. In subsequent work, published in 1975, Dr. Klevay theorized that a metabolic imbalance between zinc and copper — with more emphasis on copper deficiency than zinc excess – is a major contributing factor in coronary heart disease.
Subsequent work by other investigators has shown that copper complexes also can have a valuable role in the minimization of damage to the aorta and heart muscle as oxygenated blood reperfuses into tissues following myocardial infarction. This action is based on the anti-inflammatory action of copper complexes.
It has been speculated that the reason that the heart attack rate in France is lower than in the rest of Europe is because of the significant consumption by the French of red wine, which has a higher copper content than white wine because it is prepared with the skin of the grape intact.
Copper’s role in the immune system has recently been supported by observations that individuals suffering from Menke’s disease (an inherited disease in which there is defective copper absorption and metabolism) generally die of immune system-related phenomena and other infections. Further, animals deficient in copper have been shown to have increased susceptibility to bacterial pathogens such as salmonella and listeria. This kind of evidence has led researchers to suggest that copper compounds not only can cure various conditions, but can aid in the prevention of disease.
Copper in the 21st Century
Copper jewelry worn directly on skin has been used for a hundred years or more as a remedy for many ailments, including arthritis. Now, copper bracelets to ease joint and arthritis pain are ubiquitous in health food stores, and health magazines and catalogues.
With the understanding that copper deficiency can result in gray hair, skin wrinkles, crow’s feet, varicose veins and saggy skin, copper has recently been touted as a “Fountain of Youth” for its ability to improve the elastic fiber in skin, increase skin flexibility, and act as an anti-wrinkle treatment. It has even been said to be able to return gray hair back to its natural color.
As modern researches continue to investigate the role of copper in the functioning of the human body, the efficacy of copper as a trace element critical to human health and wellness is slowly but surely being discovered . . . or, shall we say, rediscovered, since the incredible healing properties of copper have been understood and used throughout human history.
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Copper sulphate as a fish disease treatment
Copper sulphate (sulfate) can be used to treat a range of parasites affecting marine aquarium fish. Protozoan parasites such as Crytocaryon (marine Ich), Trichodina, Amyloodium (marine velvet disease) as well as monogenean flukes – Dactylogyrus (gill flukes) and Gyrodactylus (skin fluke). It is not recommended for treating freshwater fish.
Using copper
Copper is active against many marine protozoan and monogenean parasites, but its use can be complicated. Copper is easily de-activated because it reacts with calcareous material often found in marine aquariums, i.e. coral and limestone, to form insoluble copper carbonate.
The solubility of copper is highly dependent on pH. As pH increases above 7, copper precipitates out of solution – 100x increase for every one-unit increase in pH. The danger is that should the pH of the tank drop, that is become more acidic, then the level of ‘free’ copper can quickly rise to toxic levels as the precipitated copper is re-dissolved. In addition, organic matter also binds up copper.
When treating parasite disease, the free copper level must be maintained between 0.15 – 0.20 mg/litre. If the concentration drops below this range it will not kill the parasites. If it rises above this level then it will kill the fish! Copper will also adversely affect invertebrates. Because of these complications it is advised never to treat the community tank but instead treat affected fish in a separate hospital tank.
Dosages
A stock solution is prepared using 1 gram of copper sulphate (CuSO4.5H2O) to 250 mls distilled water. This solution now contains 1 mg copper per millilitre. The initial dose is 0.15 mg copper per litre. Therefore if the tank contains say 200 litres then the dose required will be 200 x 0.15 mgs copper = 30 grams = 30 mls of stock solution.
The copper level of the tank should be measured immediately and thereafter twice daily using a test-kit that measures in increments of at least 0.05 mg/litre. If the residual copper level in the tank drops below 0.15 mg/litre – then add additional doses of 0/05 mg/ litre of the stock solution until the optimum level is restored. Using the same example 200 x 0.05 mgs copper = 10 mgs copper = 10 mls stock solution
Copper can easily be removed by activated carbon– Charcoal
Useful conversions are:
ppm = mg/litre i.e. 5 ppm = 5 mg / litre
mg / litre x 3.785 = mg / gall (US) i.e 5 mg / litre = 18.9 mg / gall (US)
mg/ litre x 4.546 = mg / gall (UK) i.e 5 mg / litre = 22.7 mg / gall (UK)
To convert imperial gallons to US gallons multiply by 1.2
Other useful figures:
1 ounce = 28.35 grams
1% solution =
10 ml per litre
10 gram per litre
38 gram per gall (US)
45 gram per gall (UK)
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Disinfectant and method of making
The process of making a disinfectant comprises electrolytically generating silver ions in a solution of citric acid and water to form an aqueous solution of silver citrate. Preferably, the solution of citric acid and water comprises a solution of approximately 5.0% to 10% citric acid in water by volume. A potential difference of 12 volts to 50 volts provides a flow of silver ions in the range of 0.1 amperes to 0.5 amperes per square inch. A more fuller explanation of the content of the solution within the ion chamber 170 will be described in greater detail hereinafter
The silver and citric acid formulations were prepared using 100/100 silver:silver electrodes. The electrodes were immersed in 1.0, 5.0 and 10% citric acid solutions and a current was applied for approximately two hours. The solutions were stored for 24 hours to allow for precipitation. The solutions were filtered using #2 Whatman filter paper. The final pH was adjusted to 6.0 with sodium carbonate and sodium bicarbonate
US 6197814 B1
Abstract
A non-toxic environmentally friendly aqueous disinfectant is disclosed for specific use as prevention against contamination by potentially pathogenic bacteria and virus. The aqueous disinfectant is formulated by electrolytically generating silver ions in water in combination with a citric acid. The aqueous disinfectant may include a suitable alcohol and/or a detergent. The aqueous disinfectant has been shown to be very effective at eliminating standard indicator organisms such as staphylococcus aureus, samonella cholerasuis and Pseudomonas aeruginosa.
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[F1]More then likely made in a lab in Canada and the USA—since they deal with this type of technology by bioengineering the insects to attack and disable people
[F2]Limited exposure—
[F3]INTERESTING COMMENT you have to wonder with this statement —if they know something no one else knows— is it going to spread because they spread it— why would the bug not die off or subside??? See these are the things that make one go hmm
[F4]Another part of this —makes one go hmmm — gm organism—to fight another type of gm organism—hmmm did we just step into a different time line where people are being victoms of genetically engineered warfare??makes you wonder
[F5]Africa and asia and now it iis finding fertile ground in latin America—hmm that is a huge huge flight from that part of the planet to the latin American countries
[F6]SO the US mosquitos did not have the pathogen and the Mexican side did??good genetic engineering and a good double blind study—this is what it appears to me..
[F7]Does sound encouraging
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Show of the Month October 18 2014
“And those who were seen dancing were thought to be insane by those who could not hear the music.”
Human genetic research uncovers how omega-6 fatty acids lower bad cholesterol
Olive oil more stable and healthful than seed oils for frying food
Has selenium loading as part treatment/prevention of Ebola been suppressed since 1995
Addiction Therapy for Drugs, Alcohol, Caffeine, and Sugar
Parkinson’s disease can migrate from gut to brain
Altering gut bacteria might mitigate lupus
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Human genetic research uncovers how omega-6 fatty acids lower bad cholesterol
Date:
October 16, 2014
Source:
Cell Press
Supplementing the diet with omega-6 polyunsaturated fatty acids has beneficial effects on heart health by lowering “bad” LDL cholesterol and raising “good” HDL cholesterol,[F1] but the underlying mechanisms involved are poorly understood. Now research based on the genetic information from over 100,000 individuals of European ancestry has uncovered a gene that affects blood cholesterol levels through the generation of a compound from omega-6 polyunsaturated fatty acids, called lipoxins. The study, publishing online October 16 in the Cell Press journal Cell Metabolism, also provides additional evidence that aspirin assists in preventing heart attacks by promoting lipoxin production. These insights could change the way doctors care for patients at increased risk for heart disease.—“Our findings could help pave the way for novel therapeutic approaches to prevent cardiovascular disease and its associated clinical sequelae, including heart attacks and stroke,” says senior author Dr. Ivan Tancevski, of the Innsbruck Medical University, in Austria.–In assessing the genetic information from the study participants of European descent, Dr. Tancevski and his colleagues identified one gene, called Alox5, that codes for an enzyme that generates lipoxins from omega-6 polyunsaturated fatty acids to help the body get rid of bad cholesterol. Lipoxins have anti-inflammatory properties.—The team found that aspirin, which is widely used to prevent heart attacks and stroke, also acts on this pathway. In experiments conducted in mice, aspirin stimulated production of lipoxins that then promoted the transport of excess cholesterol to the liver, where it is excreted through bile. Treating mice that had atherosclerotic plaques in their blood vessels with aspirin even caused the plaques to regress[F2]. “Aspirin is known to prevent cardiovascular disease due to its antithrombotic and anti-inflammatory effects. We now identified a third mechanism by which aspirin may confer protection,” says Dr. Tancevski.–The researchers went a step further in generating and testing chemically modified lipoxins mimetics that were even more effective at lowering LDL cholesterol, suggesting that new lipoxin-based specific drugs could provide greater benefits for patients.–Story Source–The above story is based on HYPERLINK “http://www.eurekalert.org/pub_releases/2014-10/cp-hgr100814.php” \t “_blank” materials provided by HYPERLINK “http://www.cellpress.com” \t “_blank” Cell Press. Note: Materials may be edited for content and length.–Journal Reference-Ivan Tancevski et al. The Arachidonic Acid Metabolome Serves as a Conserved Regulator of Cholesterol Metabolism. Cell Metabolism, 2014; DOI: HYPERLINK “http://dx.doi.org/10.1016/j.cmet.2014.09.004” \t “_blank” 10.1016/j.cmet.2014.09.004
Good sources of Omega 6 – Almond oil-peanut oil-sesame seed oil ( unroasted) sunflower oil—evening primrose oil—wheat germ oil—
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Olive oil more stable and healthful than seed oils for frying food
Date:
October 22, 2014
Source:
American Chemical Society
Frying is one of the world’s most popular ways to prepare food — think fried chicken and french fries. Even candy bars and whole turkeys have joined the list. But before dunking your favorite food in a vat of just any old oil, consider using olive. Scientists report in ACS’ Journal of Agricultural and Food Chemistry that olive oil withstands the heat of the fryer or pan better than several seed oils to yield more healthful food.–Mohamed Bouaziz and colleagues note that different oils have a range of physical, chemical and nutritional properties that can degrade oil quality when heated. Some of these changes can lead to the formation of new compounds that are potentially toxic. By-products of heating oil can also lower the nutritional value of the food being fried. Bouaziz’s team wanted to find out which cooking oil can maintain its quality under high heat and repeated use.–The researchers deep- and pan-fried raw potato pieces in four different refined oils — olive, corn, soybean and sunflower — and reused the oil 10 times. They found that olive oil was the most stable oil for deep-frying at 320 and 374 degrees Fahrenheit, while sunflower oil degraded the fastest when pan-fried at 356 degrees. They conclude that for frying foods, olive oil maintains quality and nutrition better than seed oils.–The authors acknowledge funding from the Ministère de l’Enseignement Supérieur et de la Recherche Scientifique and the Ministère de l’Agriculture, Tunisia.
Story Source–The above story is based on HYPERLINK “http://www.acs.org/content/acs/en/pressroom/presspacs/2014/acs-presspac-october-22-2014/olive-oil-more-stable-and-healthful-than-seed-oils-for-frying-food.html” \t “_blank” materials provided by HYPERLINK “http://www.acs.org” \t “_blank” American Chemical Society. Note: Materials may be edited for content and length.-Journal Reference–Akram Zribi, Hazem Jabeur, Felix Aladedunye, Ahmed Rebai, Bertrand Matthäus, Mohamed Bouaziz. Monitoring of Quality and Stability Characteristics and Fatty Acid Compositions of Refined Olive and Seed Oils during Repeated Pan- and Deep-Frying Using GC, FT-NIRS, and Chemometrics. Journal of Agricultural and Food Chemistry, 2014; 62 (42): 10357 DOI: HYPERLINK “http://dx.doi.org/10.1021/jf503146f” \t “_blank” 10.1021/jf503146f
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Has selenium loading as part treatment/prevention of Ebola been suppressed since 1995?
(There are ONLY three articles in Pubmed for Selenium & Ebola)
Computational genomic analysis of hemorrhagic fever viruses. Viral selenoproteins as a potential factor in pathogenesis – 1997
A number of distinct viruses are known as hemorrhagic fever viruses based on a shared ability to induce hemorrhage by poorly understood mechanisms, typically involving the formation of blood clots (“disseminated intravascular coagulation”). It is well documented that selenium plays a significant role in the regulation of blood clotting via its effects on the thromboxane/prostacyclin ratio, and effects on the complement system.
Selenium has an anticlotting effect, whereas selenium deficiency has a proclotting or thrombotic effect. It is also well documented that extreme dietary selenium deficiency, which is almost never seen in humans, has been associated with hemorrhagic effects in animals.
Thus, the possibility that viral selenoprotein synthesis might contribute to hemorrhagic symptoms merits further consideration. Computational genomic analysis of certain hemorrhagic fever viruses reveals the presence of potential protein coding regions (PPCRs) containing large numbers of in-frame UGA codons, particularly in the -1 reading frame. In some cases, these clusterings of UGA codons are very unlikely to have arisen by chance, suggesting that these UGAs may have some function other than being a stop codon, such as encoding selenocysteine.
For this to be possible, a downstream selenocysteine insertion element (SECIS) is required. Ebola Zaire, the most notorious hemorrhagic fever virus, has a PCR with 17 UGA codons, and several potential SECIS elements can be identified in the viral genome. One potential viral selenoprotein may contain up to 16 selenium atoms per molecule. Biosynthesis of this protein could impose an unprecedented selenium demand on the host, potentially, leading to severe lipid peroxidation and cell membrane destruction, and contributing to hemorrhagic symptoms. Alternatively, even in the absence of programmed selenoprotein synthesis, it is possible that random slippage errors would lead to increased encounters with UGA codons in overlapping reading frames, and thus potentially to nonspecific depletion of SeC in the host.
HYPERLINK “http://www.ncbi.nlm.nih.gov/pubmed/9152513” \t “_blank” http://www.ncbi.nlm.nih.gov/pubmed/9152513
Review: micronutrient selenium deficiency influences evolution of some viral infectious
Recently emerged viral infectious diseases (VIDs) include HIV/AIDS, influenzas H5N1 and 2009 H1N1, SARS, and Ebola hemorrhagic fevers. Earlier research determined metabolic oxidative stress in hosts deficient in antioxidant selenium (Se) (<1 μMol Se/L of blood) induces both impaired human host immunocompetence and rapidly mutated benign variants of RNA viruses to virulence. These viral mutations are consistent, rather than stochastic, and long-lived. When Se-deficient virus-infected hosts were supplemented with dietary Se, viral mutation rates diminished and immunocompetence improved. Herein is described the role of micronutrient Se deficiency on the evolution of some contemporary RNA viruses and their subsequent VIDs. Distinguishing cellular and biomolecular evidence for several VIDs suggests that environmental conditions conducive to chronic dietary Se deprivation could be monitored for bioindicators of incipient viral virulence and subsequent pathogenesis.
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Selenium Medicine: And the Rising Tide of Mercury
HYPERLINK “http://drsircus.com/books/e-book/selenium-medicine/” \t “_blank” http://drsircus.com/books/e-book/selenium-medicine/
Using Glutathione and Selenium to Treat Viral Infections
HYPERLINK “http://drsircus.com/medicine/glutathione-selenium-viral-infections” \t “_blank” http://drsircus.com/medicine/glutathione…infections
Selenium Deficiency and Ebola Virus
During the spring of 1995 Ebola virus created havoc in the African nation of Zaire. Researchers studying the ebola virus found many similarities between it and the HIV virus. For example, like HIV, Ebola has the potential to create several proteins requiring selenium. However, in the case of Ebola, the selenium content appears much higher than in HIV. It could be as much as ten times higher. (17)
According to Dr. Taylor, the Ebola virus behaves very much like HIV. When selenium levels in infected cells drop, Ebola reproduces and aggressively searches for cells with more selenium, spreading the infection throughout the body. The population of Zaire was found to be deficient in selenium (may be because the soil in this country is deficient in selenium.) This may partially explain why both HIV virus and Ebola virus are rampant in Zaire. Normal immune defenses against the virus is handicapped by selenium deficiency.
Selenium Reduces Bacterial Blood Poisoning
When selenium was used in large dosages with other antioxidants such as vitamins C and E it was found to reduce the hospital-induced sepsis (bacterial blood poisoning) and acute respiratory distress syndrome by 50 percent. (18)
HYPERLINK “http://www.holistic-online.com/Remedies/Biot/biot_anthrax-selenium-6-nat-rem.htm” \t “_blank” http://www.holistic-online.com/Remedies/…at-rem.htm
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Theoretical Evidence that the Ebola Virus Zaire Strain May Be Selenium-Dependent: A Factor in Pathogenesis and Viral Outbreaks?
Ethan Will Taylor1 and Chandra Sekar Ramanathan
Abstract
A theoretical analysis of the genomic structure of the Ebola virus Zaire strain reveals the existence of several open reading frames (ORFs) containing large numbers of inframe UGA codons. This clustering of UGA codons is very unlikely to have arisen by chance, and raises the possibility that these ORFs may encode selenoproteins, since, in addition to its usual role as a stop codon, UGA can under certain conditions encode selenocysteine. The other major requirement for selenocysteine insertion at UGA codons appears to be met in this case, due to the presence of selenocysteine insertion sequences (SECIS) in stable stem-loop structures in the appropriate Ebola Zaire mRNAs. Specifically, there is a SECIS in the 3’untranslated region of the nucleoprotein mRNA, where the largest potential selenoproteins are encoded, one of which may contain up to 16 selenium atoms per molecule. The expression of this hypothetical protein could impose an unprecedented selenium demand upon the host, potentially leading to severe lipid peroxidation and cell membrane destruction. This could also contribute to the characteristic hemorrhaging caused by intravascular blood clotting, due to the thrombotic effect of Se deficiency. The possibility that this gene might contribute to the extreme pathogenicity of the Zaire strain of Ebola virus by this mechanism is also consistent with the observation that this potential selenoprotein gene is not present in the Ebola Reston strain, which was not pathogenic in humans. ———It has long been apparent that an increased susceptibility to infectious diseases is common in malnourished human populations. This has traditionally been viewed as simply a consequence of the fact that the immune system must be maintained by adequate nutrition in order to function optimally. Only recently has data begun to accumulate in support of the idea that nutritional factors may sometimes have a direct effect on pathogens, and that passage through nutritionally deficient hosts may facilitate evolutionary changes in infectious agents. In this communication, we present theoretical molecular evidence that the highly pathogenic Zaire strain of the Ebola virus may be dependent on the trace mineral selenium (Se), due to the presence in the Ebola genome of several open reading frames (ORFs) containing clusters of up to 17 inframe UGA codons, which potentially encode the rare amino acid selenocysteine (SeC). We will argue that, by analogy to other known examples, this raises the possibility that Se deficiency in host populations may actually foster viral replication, possibly triggering outbreaks and perhaps even facilitating the emergence of more virulent viral strains. —-This concept is not unprecedented: a classical example of a nutrient effect on viral replication is the well documented induction of endogenous retrovirus expression in cells cultured in arginine-deficient media (recently reviewed by Becker1). Note that arginine is an essential component of many viral proteins. Thus, paradoxically, in this case viral replication appears to be triggered by a deficiency of something the virus requires. This would most likely involve some sort of repressor type of mechanism. Based on the data that we will review here, we suggest that, for some viruses, an analogous situation may exist in the case of Se. —-Aside from the nonspecific protection that can be achieved in vivo by a nutritional boost in immune function, specific antiviral effects have been claimed for various antioxidant nutrients, and Se in particular. A surprising range of in vitro and in vivo antiviral activities has been reported for various simple Se compounds, including inhibition of hepatitis B in humans, influenza virus in culture, and retroviruses like the mouse mammary tumor virus and bovine leukemia virus (reviewed by Schrauzer and Sacher2 and by Taylor et al.3). Recent work has also demonstrated the in vitro activity of Se compounds against the human immunodeficiency virus, HIV-1.4,5 —The most compelling data pertain to Keshan disease, a classical Se-deficiency disease manifested as a non-obstructive cardiomyopathy. Chinese investigators suspected an infectious agent might be a cofactor, and eventually isolated coxsackievirus from the hearts of Keshan disease victims; the combination of the virus and Se deficiency produced cardiomyopathy in mice.6 Recently, Beck and coworkers have shown that in Se-deficient mice, even a normally nonvirulent strain of coxsackievirus B3 can produce myocarditis similar to that seen in Keshan disease7 (and references therein). Significantly, during passage through Se-deficient mice, the virus mutates into a more virulent strain that is pathogenic even in normal animals on Se-adequate diets. —–Along similar lines, it is of considerable interest that Ziegler has pointed out a correlation between high rates of endemic Kaposi’s sarcoma (KS) in African subsistence farmers and geographic regions in Africa where the soils are of volcanic origin.8 These include regions surrounding the entire East African Rift Valley and the Nigeria-Cameroon border. It is widely documented that low Se levels in plants and Se deficiency syndromes of livestock are common in areas with soils of volcanic origin: the Rift Valley is a typical example. Furthermore, Se deficiency in humans has been specifically documented in northern Zaire (e.g.9). Since recent evidence strongly suggests that KS involves a novel herpes virus, this association of KS in Africa with low Se areas suggests a possible analogy to Keshan disease and coxsackievirus. Significantly, we have also found very large ORFs with start codons and up to 11 in-frame UGA codons in herpesviruses like cytomegalovirus and Epstein Barr virus (reported at 8th ICAR, Taylor et al.5), suggesting that some herpesviruses may also be “Se-dependent”.—Rather than being indirect (e.g. involving a nonspecific antioxidant effect), the possibility that some antiviral effects of Se might involve virally-encoded selenoproteins has apparently not been considered until very recently.3,5 Even though first demonstrated about ten years ago, it has still has not become widely appreciated that SeC can be encoded by the UGA codon, which usually serves as a stop codon in the genetic code. Conventional analyses of potential protein coding regions in genes still do not usually discriminate UGA from the other two stop codons, and thus they fail to reveal that proteins might be encoded in regions containing UGA codons. Such regions are routinely assumed to be inactive due to the presence of stop codons, which is probably true in the vast majority of cases, because efficient SeC incorporation is only possible when the mRNA contains a cis-acting signal known as a SeC insertion sequence.10 However, as shown in Figure 2, such consensus SeC insertion sequences capable of forming the required characteristic stem-loop RNA structures are present in several Ebola mRNAs that also encode UGA-rich ORFs. —We recently reported a similar potential for selenoproteins to be encoded in HIV-13,5,11 and in coxsackievirus B3,11 in regions overlapping known genes. In both cases, the link between Se deficiency and the associated viral diseases (AIDS and viral myocarditis, respectively) is strongly supported by an extensive body of literature (reviewed in2,3,7,12). –In the Ebola virus genome (Zaire strain), there are several ORFs with highly significant clusters of inframe UGA codons. Overlapping the major nucleoprotein (NP) gene, there are two ORFs in the -1 reading frame, containing 17 and 11 UGA codons, respectively (Figure 1). The first ORF has excellent potential to be expressed by a ribosomal frameshift from the NP coding region, due to the presence of an “ideal” heptameric shift sequence and an RNA pseudoknot (PK) 8 bases downstream (Figure 3A). This frameshift site comes very near the beginning of the ORF, and could permit the formation of a fusion protein consisting of the N-terminal 314 residues of NP fused to a 181 residue C-terminal module potentially containing 16 SeC residues, encoded in the -1
Potential Selenoprotein Genes in Ebola Virus
Figure 1. UGA-rich open reading frames (ORFs) overlapping the Ebola Zaire nucleoprotein (NP) coding region. The figure shows a schematic of the three reading frames for a portion of the NP gene, with stop codons shown as vertical lines. The dotted lines are UGA stop codons, which can potentially encode selenocysteine. There are two UGA-rich ORFs -1 to the main NP reading frame, ORF1 with 17 and ORF2 with 11 inframe UGA codons. Neither ORF1 or ORF2 has a start codon. ORF1 could be expressed as an NP fusion protein containing a selenoprotein module, by means of a frameshift at either one of two potential -1 frameshift sites, shown with an arrow symbol as A and B. These frameshift sites are shown in detail in Figure 3. ORF2 is less likely to be a functional gene, because it could only be expressed from an edited or spliced NP mRNA, and splicing has never been demonstrated in filoviruses (see text). However, there is a complete splice acceptor (SA) site at the very beginning of the ORF, and several potential upstream splice donor sites (not shown). The only other requirement for selenoprotein synthesis, a selenocysteine insertion sequence (SECIS) in the required stem-loop structure, is present in the 3’-untranslated region of the NP mRNA (Figure 2A). (Figure produced using the beta version of the gene finder program, developed in collaboration with Dr. Dan Everett, University of Georgia).
Figure 2. Schematic RNA secondary structures predicted for selenocysteine insertion sequences (AUG…AAA…UGA) in the Ebola virus RNA with potential to form the required stemloop structures.10 A: In the 3′-untranslated region of the nucleoprotein mRNA, bases 2758-2836 in GenBank #L11365; E = – 10.1 kcal/mole. B: At the 3′ end of the vp35 mRNA, bases 4094-4160; E = – 13.4 kcal/mole. C: At the 3′ end of the vp30 mRNA, bases 9029-9087; E = – 9.4 kcal/mole. Note that the computed stability of these structures is comparable to that determined by Sanchez et al.19 for the 5′-end stem-loop structures in the Ebola mRNAs (average E = -13.3 kcal/mole, range = -7.6 to -20). All base pairs (shown as ladder rungs) are Watson-Crick except those marked by a slash, which are GU base pairs. These structures were predicted using the Zuker FOLD program20 as implemented in the GCG software package (Program Manual for the Wisconsin Package, Ver. 8, September 1994, Genetics Computer Group, 575 Science Drive, Madison, WI 53711).
Figure 3. Potential -1 frameshift sites near the beginning of the major UGA-rich ORF in the Ebola Zaire nucleoprotein (NP) coding region, consisting of slippery sequences (underlined) and potential RNA pseudoknots. The location of these sites are indicated by A and B in Figure 1. Codonanticodon interactions of the P- and A-site tRNAs are shown schematically both before (below sequence) and after slippage (above sequence). A: An “ideal” (XXXYYYZ) heptameric -1 frameshift sequence beginning at position 1405 in GenBank #L11365, located 8 nucleotides upstream from a potential pseudoknot. The A-C bulge shown in the major stem probably forms a hydrogen bonded purine-pyrimidine A:C base pair, as these have been observed in some experimental RNA stem structures. The ORF in the -1 reading frame has a total of 17 in-frame UGA codons, 16 of which are downstream from this frameshift site. B: A second near-ideal frameshift site and potential pseudoknot in the NP coding region beginning at position 1582, 178 bases downstream from that shown in A. This could produce a shift into the same ORF with 17 UGA codons, but the potential selenoprotein module would contain only 11 SeC residues (Figure 1).
frame (bases 1411 to 1953 in GenBank PKs are mere “artifacts”, the chance of the #L11365; subsequent numbering refers to next 16 stop codons following shift site A in the same sequence). Slightly downstream the “blocked” -1 reading frame (Figure 1) all there is a second near-ideal frameshift site being UGA could be estimated as (1/3)16, or and potential PK, also in the NP coding less than one in 43 million. Thus, the high region beginning at position 1582 (Figure significance of this clustering of UGA 3B). This could provide a “second chance” codons, combined with the presence of the to express the selenoprotein module, when-frameshift signals and the distinctive SeC ever the first frameshift failed. This second insertion sequence in the 3′-untranslated resite follows the sixth UGA codon in the gion of the Ebola NP mRNA, argues over-ORF, so a frameshift here would yield a whelmingly that this must be the gene of an potential selenoprotein module with only actual selenoprotein. However, one cannot 11 SeC residues. These redundant frameshift completely rule out the possibility that it sites could provide for either an increased could be a vestigial gene that may have only probability of translating the selenoprotein recently become inactive. module, or for two alternate forms of the NP A second UGA-rich ORF overlapping the fusion protein. Ebola NP gene, encoded between bases 2212
Because there are three different stop and 2598, contains 11 UGA codons over 129 codons (UGA, UAA and UAG), if this is not residues (ORF2 in Figure 1). This ORF a real gene and the potential shift sites and lacks a start codon, but could be expressed
Potential Selenoprotein Genes in Ebola Virus
from an edited or spliced RNA. There is a definite splice acceptor site very near the beginning of the ORF, a CAGA sequence preceded by a pyrimidine rich sequence and an upstream “CURAY” sequence (CUGAC). There are various potential splice donors in the large NP mRNA that could bring this region inframe to the main NP ORF or the upstream selenoprotein ORF with 16 UGAs. Since there are no reports of Ebola replication and transcription in the nuclei of infected cells, this ORF and the associated potential splice sites may be mere artifacts. However, Borna disease virus provides a precedent for nuclear replication/transcription and RNA splicing of a negative non-segmented single stranded RNA virus.13 Thus, we cannot rule out the possibility that splicing of this Ebola mRNA could occur,
e.g. in the unknown “reservoir” species that is the natural host for Ebola virus. Furthermore, RNA editing can also bring such an “out of frame” ORF into frame, and RNA editing is known to occur in a number of viruses, including Ebola Zaire.
There are several additional potential selenoprotein ORFs overlapping the first 6 genes of Ebola virus, including the vp24, vp30, vp35 and vp40 regions, all of which have potential SeC insertion sequences in their mRNAs (shown for vp30 and vp35 in Figure 2). Because the sequence has not yet been released, we are unable to report on the polymerase coding region, where we have consistently found potential overlapping selenoprotein genes in a number of other viruses. On the Ebola minus strand genomic RNA there are also potential SeC insertion sequences and several UGA-rich ORFs (up to 9 UGAs), some with start codons, and some potentially expressed from spliced genomic RNAs. On both plus and minus strands, some of these potential genes have start codons in the context of Kozak-like sequences, suggesting they may be programmed to bind ribosomes and initiate protein synthesis. All these data will be presented in detail in a subsequent publication.
If viruses like HIV-1, coxsackievirus B3 and Ebola do encode selenoproteins, why does all the evidence suggest that dietary Se inhibits viral replication, whereas Se deficiency triggers replication? Why would Se not “feed” the virus? The answer must lie in how viruses use Se.
As discussed previously,3 due to the inefficiency of frameshifting and SeC insertion mechanisms, these hypothetical viral selenoproteins could only be formed in very small amounts. Thus, in most cases they are not likely to be major structural proteins; some might have regulatory roles, acting in the midphase of the life cycle, and might not even be packaged in virions. If even one such selenoprotein were involved in negative feedback on replication (a repressor type function), decreased levels of that protein would provide the virus a way to respond to low Se levels by leaving the cell in search of a new host. By such a mechanism, the virus could satisfy a basal dependence on Se by escaping from a cell where Se levels had become dangerously low.
Since Se is an essential antioxidant, critical as a component of glutathione peroxidase in blood cells and liver cells (the very cell types that Ebola and many other viruses prefer to infect), very low Se levels are potentially associated with oxidative stress, lipid peroxidation and cell death. Thus, viral survival might be enhanced by the stimulation of replication under low Se conditions.
At the same time, host/viral competition for a limited amount of Se – particularly in a malnourished host – could significantly contribute to pathogenesis. This could be particularly acute with Ebola virus, due to the unprecedented high Se requirement implicit in the ORF with 16 UGA codons.
Dietary Se is also known to have immunopotentiating effects (reviewed in12). Thus, in addition to any direct effects exerted via (hypothetical) viral selenoproteins, Se deficiency can also weaken the immune system’s ability to fight viral infection, permitting increased replication, rapid mutation, and facilitating the emergence of more virulent strains, as Beck et al. suggest in the case of coxsackievirus.7
Given the unique dependence of selenoprotein genes upon a trace nutrient whose availability varies widely in geographical areas and host populations, the presence and activity of such genes would very likely be strain specific, as we suggested for coxsackievirus.11 This could help explain why some viral strains can be very virulent, even when significant subsets of indigenous populations have antibodies to a similar, presumably much less virulent viral strain, which appears to be true even for filoviruses.14,15
Certainly, prolonged Se deficiency in a host population could eventually lead to the inactivation and loss of any viral seleno-protein genes. Whether that loss would lead to more virulent strains, or whether those strains might undergo a compensatory attenuation by passage through the host population, would be difficult to predict.
However, in the case of Ebola virus, there is some reason to think that the presence of a gene with an exceptionally high Se demand could be a factor in the pathogenicity of specific viral strains. This is supported by the striking observation that in the Ebola Reston strain, which was devoid of pathogenicity in the 3 humans that were infected, there is no equivalent to the major potential selenoprotein gene overlapping the NP gene in Ebola Zaire (ORF1 in Figure 1). In the Ebola Reston NP mRNA, the UGA-rich ORFs are disrupted by non-UGA stop codons, there are fewer UGA codons, no analogous frameshift sites or PKs, and no SECIS element in the 3′-UTR. Thus there is no way that this potential selenoprotein gene could be expressed in Ebola Reston. This is a definite major difference at the gene level between these strains, which have previously been considered to be very close genetically. This potential NP-associated selenoprotein gene is also absent in Marburg virus, which also has a lower mortality rate than Ebola Zaire.
Since the hypothetical selenoprotein overlapping the Ebola Zaire NP gene could only be expressed as an NP fusion protein, it is possible that it could be formed as an NP variant comprising as much as a few percent of the total NP present in virions (more likely a fraction of a percent), in which case it might be possible to detect selenium in Ebola Zaire virions. This percentage would be expected to decrease in late infections if cellular stores of SeC became depleted. In regard to the possible function of such a viral selenoprotein, it is tempting to speculate that it might provide some type of antioxidant protection to the Ebola virions in a rapidly degenerating cellular environment.
Ebola is classified as a “hemorrhagic fever” virus, and produces the characteristic hemorrhaging due to the formation of blood clots (“disseminated intravascular coagulation”), leading to the obstruction and rupture of small blood capillaries. For this reason, counterintuitively, the anticoagulant drug heparin has been used to reduce the bleeding in Ebola patients.
It is very well documented that Se plays a significant role in the regulation of blood clotting via its effects on the thromboxane/ prostacyclin ratio. Se has an anti-clotting effect, whereas Se deficiency has a pro-clotting or thrombotic effect.16 Se deficiency has been associated with thrombosis and even hemorrhaging, which has been documented in a number of animals with severe Se deficiency (often artificially induced), but is almost never seen in humans, probably because such an extreme Se deficiency is rarely attained due to the diversity of human diets.
Thus, the possibility that a rapid depletion of Se due to the formation of viral selenoproteins could be a factor contributing to the severity of the hemorrhagic symptoms is mechanistically very feasible. Our analysis suggests that severe Ebola infections could produce an artificial and extreme Se depletion, resulting in extensive cellular damage due to lipid peroxidation, combined with enhanced thrombosis. This could also contribute to the associated immune deficiency that has been observed in Ebola infections.
To our knowledge, indicators of Se status and lipid peroxidation have never been examined in Ebola patients. However, Se has apparently been used with great success by the Chinese in the palliative treatment of an infectious hemorrhagic fever.17 Although this did not involve Ebola virus, there are a number of different hemorrhagic fever viruses, and they may share common mechanisms. This example provides yet another reason to expect that pharmacological doses of Se may also have some benefit in Ebola infections.
In the light of the extensive data on the antiviral effects of Se, the association between coxsackievirus and Keshan disease, and the geographic correlation for KS proposed by Ziegler, it is certainly intriguing that a number of emerging viruses have emanated from these same regions of Africa, that are potentially low in Se. By providing compelling theoretical evidence for the existence of selenoprotein genes in a number of viruses, now including Ebola virus, we have attempted to provide a unifying theoretical model to explain some of these disparate observations.
Taken as a whole, these observations and theoretical findings suggest the basis for a new paradigm in antiviral chemotherapy: the use of nutritional factors to alter the dynamics of the virus-host interaction so as to reestablish a balance in which the natural host defenses can be more effective. In essence, this is the fundamental concept of orthomolecular medicine, so perhaps this is not such a “new” paradigm after all. What is new and exciting is that this simple concept may be more widely applicable, to more virulent viral diseases, and a broader range of vitamins and minerals – in this case Se -than previously thought possible.
Finally, because SO2 reacts with Se compounds in soil, making it more difficult for plants to absorb, it has long been suspected that fossil fuel burning and acid rain may be contributing to a gradual decrease of Se in the food chain.18 Thus, like deforestation in jungles and rain forests, the resulting alterations in global Se cycling and distribution may be yet another example of how human activity possibly contributes to the emergence of new viral diseases. Ultimately, it is only a deeper understanding of the impact of these human activities on both microbes and their hosts that will empower us to rectify the resulting imbalances in our shared ecosystem.
Acknowledgments
The authors would like to thank Dr. Anthony Sanchez of the Centers for Disease Control and Prevention, Atlanta, GA, for providing the sequence of the Ebola Reston nucleoprotein gene, as well as other unpublished sequences. We are also grateful to Dr. Gerhard Schrauzer of the University of California, San Diego, for making us aware of the previous use of Se to treat an Asian epidemic hemorrhagic fever.17
Potential Selenoprotein Genes in Ebola Virus
References
Becker Y. (1995) Endogenous retroviruses in the human genome – a point of view. Virus Genes 9:211-218.
Schrauzer G.N., Sacher J. (1994) Selenium in the maintenance and therapy of HIV-infected patients. Chem-Biol Interact 91:199-
205.
Taylor E.W., Ramanathan C.S., Jalluri R.K., Nadimpalli R.G. (1994) A basis for new approaches to the chemotherapy of AIDS: novel genes in HIV-1 potentially encode selenoproteins expressed by ribosomal frameshifting and termination suppression. J Med Chem 37:2637-2654.
Sappey C., Legrand-Poels S., Best-Belpomme M., Favier A., Rentier B., Piette J. (1994) Stimulation of glutathione peroxidase activity decreases HIV type 1 activation after oxidative stress. AIDS Res Human Retrovir 10:1451-1461.
Taylor E.W., Ramanathan C.S., Nadimpalli R.G., Schinazi R.F. (1995) Do some viruses encode selenoproteins? Evaluation of the theory in the light of current theoretical, experimental and clinical data. Antiviral Res 26:A271-86.
Bai J., Wu S., Ge K., Deng X., Su C. (1980) The combined effect of selenium deficiency and viral infection on the myocardium of mice. Acta Acad Med Sin 2:29-31.
Beck M.A., Shi Q., Morris V.C., Levander
O.A. (1995) Rapid genomic evolution of a non-virulent Coxsackievirus B3 in selenium-deficient mice results in selection of identical virulent isolates. Nature Med 1:433-436.
Ziegler J.L. (1993) Endemic Kaposi’s sarcoma in Africa and local volcanic soils. Lancet 342:1348-1351.
Vanderpas J.B., Contempre B., Duale N.L., Goossens W., Bebe N., Thorpe R., Ntambue K.,Dumont J., Thilly C.H., Diplock A.T. (1990) Iodine and selenium deficiency associated with cretinism in northern Zaire. Am J Clin Nutr 52:1083-1086.
10.Berry M.J., Larsen P.R. (1993) Recognition of UGA as a selenocysteine codon in eukaryotes: a review of recent progress. Biochem Soc Trans 21:827-32.
11.Taylor E.W., Ramanathan C.S., Nadimpalli
R.G. (1995) A general approach to predicting potential new genes in nucleic acid sequences: application to the human immunodeficiency virus. In: Proceedings of the First World Congress on Computational Biomedicine, Public Health and Biotechnology. Austin, TX: World Scientific, Tokyo, in press.
12.Taylor E.W. (1995) Selenium and cellular immunity: evidence that selenoproteins may be encoded in the +1 reading frame overlapping the human CD4, CD8 and HLA-DR genes. Biol Trace Elem Res 49:85-95.
13.Cubitt B., Oldstone C., Valcarcel J., de la Torre J.C. (1994) RNA splicing contributes to the generation of mature mRNAs of Borna disease virus, a non-segmented negative strand RNA virus. Virus Res 34:69-79.
14.Johnson E.D., Gonzales J.P., Georges A. (1993) Filovirus activity among selected ethnic groups inhabiting the tropical forest of equatorial Africa. Trans R Soc Trop Med Hyg 87:536-538.
15.Becker S., Feldmann H., Will C., Slenczka
W. (1992) Evidence for occurrence of filovirus antibodies in humans and imported monkies: do subclinical filovirus infections occur worldwide? Med Microbiol Immunol Berl 181:43-55.
16.Meydani M. (1992) Modulation of the platelet thromboxane A2 and aortic prostacyclin synthesis by dietary selenium and vitamin E.
BiolTrace Elem Res 33:79-86.
17.Hou J.C., Jang Z.F., He, Z.F. (1993) Inhibitory effect of selenite on complement activation and its clinical significance. Chung Hua I Hsueh Tsa Chih 73:645-646.
18.Frost D.V. (1987) Why the level of selenium in the food chain appears to be decreasing. In:Selenium in Biology and Medicine, G.F. Combs, Jr., J.E. Spallholz, O.A. Levander,
J.E. Oldfield, Eds. AVI Van Nostrand, New York. Part A, pp. 534-547.
19.Sanchez A., Kiley M.P., Holloway B.P., Aupern D.D. (1993) Sequence analysis of the Ebola virus genome: organization, genetic elements, and comparison with the genome of Marburg virus. Virus Res 29:215-240.
20. Zuker M., Steigler P. (1981) Optimal computer folding of large RNA sequences using thermodynamics and auxillary information. Nucl Acids Res 9:133-148.
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Addiction Therapy for Drugs, Alcohol, Caffeine, and Sugar
by Reagan Houston
(OMNS Oct 21, 2014) In 1977, Alfred Libby and Irwin Stone (1, 2) realized that addiction is both a disease and poor nutrition. Having lost their appetite, addicts are deficient in vitamin C, other vitamins, minerals, and protein. Genetics and certainly bad lifestyle may have contributed to the disease, but conventional medical therapy is almost useless until their nutrition is restored. In one test, very high doses of vitamin C gave a temporary cure to 30 out of 30 drug addicts. Vitamin C was observed to be an easy, quick, and painless remedy. Ewan Cameron (3) treated cancer patients on heavy doses of opiate-type painkillers. When vitamin C stopped the pain for five cancer patients, the patients wanted no morphine. Importantly, they had no withdrawal symptoms. Stone suggested that ascorbate mimics morphine and probably fits into the opiate receptor sites.
Libby and Stone’s Protocol for Drug Addicts:
Work with your physician and stop intake of all drugs or Methadone.
Dissolve 25 to 85 grams (25,000-85,000 milligrams) of sodium ascorbate powder in milk and have the patient drink it during the day.
Adjust ascorbate dose up or down according to the estimated drug intake. Continued to adjust dose to almost cause loose stools.
Give multivitamins, a mineral tablet, and vitamin E and protein powder. Doses were widely variable and adjusted for each patient.
The vitamin C was started as soon as possible in many divided doses through the day. Other items were also given in divided doses.
Continued full dose for 4 to 6 days and then slowly decreased the vitamin C down to 10,000 to 30,000 mg/day. Continued the lower doses indefinitely or as needed.
What Happened to Patients after Starting Vitamin C?
One incoherent patient received 30,000 mg of vitamin C. In 45 minutes he could hold a normal conversation.
After 12 to 24 hours, appetite started to return, mental alertness and visual acuity were improved.
Patient was often amazed that treatment worked without another narcotic.
After 2 or 3 days, patient felt fine, and he or she could sleep.
One patient took 45,000 mg of sodium ascorbate in milk. Five hours later, he took a heavy dose of heroin but felt no drug effect. Remarkably, vitamin C had stopped the desire for drugs. (1)
To repeat: Libby and Stone demonstrated a simple but effective method of temporarily curing 30 out of 30 drug addicts regardless of the type of drug. Their cure is temporary since patients could be followed for only about 30 days. This did not give time to evaluate and treat the basic causes of the addictions. However, treatment for basic causes can proceed with greater expectation of success since the patients have become properly nourished.
(Reagan Houston, MS, PE (Professional Chemical Engineer), age 91, takes his vitamins. His daily exercise usually includes three flights of stairs in about 50 seconds. His web site is HYPERLINK “http://orthomolecular.emlnk6.com/lt.php?s=915ac1de175031fe3825bd4ab478a726&i=8A12A1A94” \t “_blank” http://www.cancertherapies.org .)
References:
1. Libby AF and Stone I. The Hypoascorbemia-Kwashiorkor approach to drug addiction: a pilot study. Orthomolecular Psychiatry. 1977; 6(4): 300-308. Read the complete article at HYPERLINK “http://orthomolecular.emlnk6.com/lt.php?s=915ac1de175031fe3825bd4ab478a726&i=8A12A1A95” \t “_blank” http://orthomolecular.org/library/jom/1977/pdf/1977-v06n04-p300.pdf or Google: “Libby Stone drug addiction 1977.”
2. Stone I. The Healing Factor: Vitamin C against Disease. 1972, New York. Free full text at HYPERLINK “http://orthomolecular.emlnk6.com/lt.php?s=915ac1de175031fe3825bd4ab478a726&i=8A12A1A96” \t “_blank” http://vitamincfoundation.org/stone/ .
3. Cameron E & Baird GM. Ascorbic acid and dependence on opiates in patients with advanced disseminated cancer. J International Research Communication. 1973; 1(6):33.
Nutritional Medicine is Orthomolecular Medicine
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Carolyn Dean, M.D., N.D. (USA)
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Michael Ellis, M.D. (Australia)
Martin P. Gallagher, M.D., D.C. (USA)
Michael Gonzalez, D.Sc., Ph.D. (Puerto Rico)
William B. Grant, Ph.D. (USA)
Michael Janson, M.D. (USA)
Robert E. Jenkins, D.C. (USA)
Bo H. Jonsson, M.D., Ph.D. (Sweden)
Peter H. Lauda, M.D. (Austria)
Thomas Levy, M.D., J.D. (USA)
Stuart Lindsey, Pharm.D. (USA)
Jorge R. Miranda-Massari, Pharm.D. (Puerto Rico)
Karin Munsterhjelm-Ahumada, M.D. (Finland)
Erik Paterson, M.D. (Canada)
W. Todd Penberthy, Ph.D. (USA)
Gert E. Schuitemaker, Ph.D. (Netherlands)
Robert G. Smith, Ph.D. (USA)
Jagan Nathan Vamanan, M.D. (India)
Atsuo Yanagisawa, M.D., Ph.D. (Japan)
Andrew W. Saul, Ph.D. (USA), Editor and contact person. Email: HYPERLINK “mailto:[email protected]” \t “_blank” [email protected] This is a comments-only address; OMNS is unable to respond to individual reader emails. However, readers are encouraged to write in with their viewpoints. Reader comments become the property of OMNS and may or may not be used for publicationEK
Parkinson’s disease can migrate from gut to brain
Parkinson’s disease may start in the gut
Parkinson’s disease is strongly linked to the degeneration of the brain’s movement center. In the last decade, the question of where the disease begins has led researchers to a different part of the human anatomy. In 2003, the German neuropathologist Heiko Braak presented a theory suggesting that the disease begins in the gut and spreads to the brain. The idea has since, despite vocal critics, gained a lot of ground. Researchers at Lund University in Sweden now present the first direct evidence that the disease can actually migrate from the gut to the brain.—The so-called Braak’s hypothesis proposes that the disease process begins in the digestive tract and in the brain’s center of smell. The theory is supported by the fact that symptoms associated with digestion and smell occur very early on in the disease.–Researchers at Lund University have previously mapped the spread of Parkinson’s in the brain. The disease progression is believed to be driven by a misfolded protein that clumps together and “infects” neighboring cells. Professor Jia-Yi Li’s research team has now been able to track this process further, from the gut to the brain in rat models. The experiment shows how the toxic protein, alpha-synuclein, is transported from one cell to another before ultimately reaching the brain’s movement center, giving rise to the characteristic movement disorders in Parkinson’s disease.—“We have now been able to prove that the disease process actually can travel from the peripheral nervous system to the central nervous system, in this case from the wall of the gut to the brain. In the longer term, this may give us new therapeutic targets to try to slow or stop the disease at an earlier stage”, says Professor Jia-Yi Li, research group leader for Neural Plasticity and Repair at Lund University.–The research team will now carry out further studies in which the mechanisms behind the transport of the harmful protein will be examined in detail. The current study suggests that the protein is transferred during nerve cell communication. It is at this point of interaction that the researchers want to intervene in order to put a stop to the further spread of the disease.
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Altering gut bacteria might mitigate lupus, study suggests
Date: October 20, 2014
Source: American Society for Microbiology
Lactobacillus species, commonly seen in yogurt cultures, correlate, in the guts of mouse models, with mitigation of lupus symptoms, while Lachnospiraceae, a type of Clostridia, correlate with worsening, according to research published ahead of print in Applied and Environmental Microbiology. “Our results suggest that the same investigation shold be performed in human subjects with lupus,” says principal investigator Xin Luo of Virginia Tech, Blacksburg, VA.–In the study, the investigators first showed that mouse models of lupus had higher levels of Lachnospiraceae (a type of Clostridia), and lower Lactobacillus than control mice. They also compared male and female mice, and found that the differences were present only in females. These results suggest that the gut bacteria may contribute to lupus, a disease which is nine times as prevalent in women as in men, says first author Husen Zhang.–They also monitored the gut microbiota over time in both lupus and control mice, and found that in the former, Clostridia increased in both early and late stages of the disease.–In further experiments, the investigators treated the symptoms in the lupus mice with either retinoic acid alone or vitamin A plus retinoic acid. The latter worsened the symptoms — surprisingly, Luo says, because it had been expected to reduce them — and in those mice, Clostridia increased, while Lactobacillus declined. Retinoic acid alone improved the symptoms, with opposite population changes in the gut bacteria.–The research suggests, but does not prove that altering the gut microbiota could mitigate lupus. Nonetheless, Luo suggests that people with lupus should eat Lactobacillus-containing probiotics, such as live culture yogurts, to reduce lupus flares. More generally, “The use of probiotics, prebiotics, and antibiotics has the potential to alter microbiota dysbiosis, which in turn could improve lupus symptoms,” says co-principal investigator Husen Zhang. Ultimately, says Luo, fecal transplant might prove valuable as a treatment for lupus.–“We were inspired in part to perform this research by a study on type 1 diabetes, which found that that disease is dependent on gut microbiota,” says Zhang. “Like type 1 diabetes, lupus is an autoimmune disease that is even more prevalent [than type 1 diabetes] in women.”–Story Source-The above story is based on materials provided by American Society for Microbiology. Note: Materials may be -edited for content and length.–Journal Reference- H. Zhang, X. Liao, J. B. Sparks, X. M. Luo. Dynamics of gut microbiota in autoimmune lupus. Applied and Environmental Microbiology, 2014; DOI: 10.1128/AEM.02676-14
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[F1]There is no such thing as good and bad cholesterol but what maybe happening is the omega 6 either through an antioxidant or anti inflammatory profiles maybe protecting the proteins in the cholesterol from causing oxidative damage to the fats
[F2]So with Omega 6’s your getting an anti inflammatory due to the lipoxin conversion—this is why rubbing peanut oil on arthritic points seems to have a anti inflammatory effect on pain and reduces the inflammation of the area
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Show of the Month October 25 2014
Fight against Alzheimer’s disease- New research on walnuts
Exposure to aluminum may impact on male fertility, research suggests
Why Are the Farmers Depressed and Suicidal
Anti Virals—Uses
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Fight against Alzheimer’s disease- New research on walnuts
Date:October 21, 2014 –Source:IOS Press BV
A new animal study published in the Journal of Alzheimer’s Disease indicates that a diet including walnuts may have a beneficial effect in reducing the risk, delaying the onset, slowing the progression of, or preventing Alzheimer’s disease.—-Research led by Abha Chauhan, PhD, head of the Developmental Neuroscience Laboratory at the New York State Institute for Basic Research in Developmental Disabilities (IBR), found significant improvement in learning skills, memory, reducing anxiety, and motor development in mice fed a walnut-enriched diet.-The researchers suggest that the high antioxidant content of walnuts (3.7 mmol/ounce) may have been a contributing factor in protecting the mouse brain from the degeneration typically seen in Alzheimer’s disease. Oxidative stress and inflammation are prominent features in this disease, which affects more than five million Americans.–“These findings are very promising and help lay the groundwork for future human studies on walnuts and Alzheimer’s disease — a disease for which there is no known cure[F1],” said lead researcher Dr. Abha Chauhan, PhD. “Our study adds to the growing body of research that demonstrates the protective effects of walnuts on cognitive functioning.”–The research group examined the effects of dietary supplementation on mice with 6 percent or 9 percent walnuts, which are equivalent to 1 ounce and 1.5 ounces per day, respectively, of walnuts in humans. This research stemmed from a previous cell culture study led by Dr. Chauhan that highlighted the protective effects of walnut extract against the oxidative damage caused by amyloid beta protein. This protein is the major component of amyloid plaques that form in the brains of those with Alzheimer’s disease.—Someone in the United States develops Alzheimer’s disease every 67 seconds, and the number of Americans with Alzheimer’s disease and other dementias are expected to rapidly escalate in coming years as the baby boom generation ages. By 2050, the number of people age 65 and older with Alzheimer’s disease may nearly triple, from five million to as many as 16 million, emphasizing the importance of determining ways to prevent, slow or stop the disease. Estimated total payments in 2014 for all individuals with Alzheimer’s disease and other dementias are $214 billion.–Walnuts have other nutritional benefits as they contain numerous vitamins and minerals and are the only nut that contains a significant source of alpha-linolenic acid (ALA) (2.5 grams per ounce), an omega-3 fatty acid with heart and brain-health benefits. The researchers also suggest that ALA may have played a role in improving the behavioral symptoms seen in the study.–Story Source-The above story is based on materials provided by IOS Press BV. Note: Materials may be edited for content and length. –Journal Reference- Abha Chauhan, PhD et al. Dietary Supplementation of Walnuts Improves Memory Deficits and Learning Skills in Transgenic Mouse Model of Alzheimer’s Disease. Journal of Alzheimer’s Disease, Volume 42, Number 4 / 2014 DOI: 10.3233/JAD-140675
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Exposure to aluminum may impact on male fertility, research suggests
Date:
October 21, 2014 Source: Keele University
Aluminium symbol from the periodic table. Human exposure to aluminum has increased significantly in recent times, experts say. The observation of “significant contamination of male semen by aluminum must implicate aluminum as a potential contributor to these changes in reproductive fertility.” New research from scientists in the UK and France suggests that human exposure to aluminum may be a significant factor in falling sperm counts and reduced male fertility. Fluorescence microscopy using an aluminum-specific stain confirmed the presence of aluminum in semen and showed aluminum inside individual sperm. And the team of scientists, at the universities of Lyon and Saint-Etienne in France and Keele in the UK, found that the higher the aluminum, the lower sperm count. The research, led by Professor Christopher Exley, a leading authority on human exposure to aluminum at Keele, and Professor Michele Cottier, a specialist in cytology and histology at Saint-Etienne, measured the aluminum content of semen from 62 donors at a French clinic. Professor Exley said: “There has been a significant decline in male fertility, including sperm count, throughout the developed world over the past several decades and previous research has linked this to environmental factors such as endocrine disruptors. [F2]”Human exposure to aluminum has increased significantly over the same time period and our observation of significant contamination of male semen by aluminum must implicate aluminum as a potential contributor to these changes in reproductive fertility.” The mean aluminum content for all 62 donors was found to be very high at 339 ppb [F3]with the aluminum content of semen from several donors being in excess of 500 ppb. A statistically significant inverse relationship was found between the aluminum content of semen and the sperm count. Higher aluminum resulted in a lower sperm count. Story Source-The above story is based on materials provided by Keele University. Note-Materials may be edited for content and length. Journal Reference-J.P. Klein, M. Mold, L. Mery, M. Cottier, C. Exley. Aluminium content of human semen: implications for semen quality. Reproductive Toxicology, 2014; DOI: 10.1016/j.reprotox.2014.10.001
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Why Are the Farmers Depressed and Suicidal?
Is the same thing that’s destroying the bees also crippling our farmers?–When Ginnie Peters’ farmer husband took his own life after a sudden mood shift, she really hit the nail on the head when she said: These chemicals that farmers use, look what they do to an insect. It ruins their nervous system. What is it doing to the farmer? No one can deny that farming is drastically different than it was in the 1950s, and today it requires extra demand, complete expertise and the stress of uncertainty. Most farmers don’t go into it for high profits. The EPA, however, has long denied that the pesticide exposure they experience is directly tied to psychological symptoms, mental illness, behavioral changes and higher rates of suicide. Even though those are the very symptoms caused by such exposure, and the results of the EPA’s own studies, decades and decades ago, have arrived at the very same conclusion. Farmers serve our country too – has our government left these unsuspecting service men in a dangerous lurch, the same as military people who come back with mystery illnesses? Lorann Stallones, an epidemiologist and psychology professor at Colorado State University says: For years there was a high level of denial in the farming community that mental illness exists, period. But there’s been a shift – partly because there’s more people talking about being mentally incapacitated. Scientific American has recently reported: Some research suggests that the chemicals that farmers and their workers spread on fields may alter some of these brain chemicals.–Peters and his wife were among 89,000 farmers and other pesticide applicators in Iowa and North Carolina who have participated in the Agricultural Health Study led by the National Institute of Environmental Health Sciences. –Last month, epidemiologist Freya Kamel and her colleagues reported that among 19,000 studied, those who used two classes of pesticides and seven individual pesticides were more likely to have been diagnosed with depression. Those who used organochlorine insecticides were up to 90 percent more likely to have been diagnosed with depression than those who hadn’t used them. For fumigants, the increased risk was up to 80 percent.–The authors who wrote in the journal Environmental Health Perspectives say: Our study supports a positive association between depression and occupational pesticide use among applicators… and suggests several specific pesticides that deserve further investigation in animal studies and other human populations, While previous studies have only asked participants once about their depression – this one asked twice – once years back and again in 2010. It also included a large pool of farmers, meaning that people couldn’t really dismiss the study later for saying it was too small for consequence. The group came to the same conclusions when they studied the group between 1993 – 1997.
Startlingly: Farmers with the highest number of lifetime exposure days to pesticides were 50 percent more likely to later have a depression diagnosis. Of course, after all these years, no one’s brave enough to say the P-word – Proof. Even though they show that psychological issues in rats is possible with exposure. For instance: tests on rats show altered brain cells, neurotransmitters and production of a protective acid. All important aspects of the complexity of brain and hormone health.[F4] Last year, it became glaringly apparent to researchers that French farmers were twice as likely to seek treatment for depression than those who don’t use herbicides. The rate increases with the increase of years using herbicides. –These are not just acute high exposures, either, like chemical companies like to ‘claim and blame.’ Many past studies have shown that chronic low exposure leads to problems that aren’t obviously until years later. Stallones, who wasn’t part of the main study says “but the association [with depression] held true for those that didn’t report poisoning.”–When there were larger dose poisonings in a short period, the rate of Colorado farmers risk for depression doubled in the next few years and North Carolina and Iowa farmers were 2.5 times more likely in the same situation. –Other health problems linked to depression are also linked to pesticide exposure.
From Scientific American:
For instance, Dr. Beate Ritz, a neurologist and professor at the University of California, Los Angeles, found that Californians exposed to pesticides are more likely to have Parkinson’s disease. One effect of the neurological disease, characterized by a lack of the chemical dopamine, is depression.
[…]
Several studies have linked suicide to pesticide use. In Brazil, workers that used more pesticides were more likely to commit suicide, and in China, a World Health Organization survey of 9,800 people in the rural Zhejiang province revealed that those who stored pesticides in their homes had more than double the risk of having suicidal thoughts.
Wendy Ringgenberg, an assistant professor at the University of Iowa, combed through 19 years of national data and reported that farmers and farm workers were 3.6 times more likely to die of suicide than other professions. However, the study did not examine the causes of suicide.
Interestingly, some of the pesticides linked to depression and suicide in the study are not supposed to be in use[F5]. Chemical company giants like Monsanto, Bayer Cropscience and Syngenta say that their products were not included in the study and won’t comment on the bigger picture of brain health and long-term pesticide use. Also left from the study were the newer class of pesticides – neonicotinoids, which are implicated for mass bee die-off as they kill the nervous system of exposed insects.
Ginnie Peters’ husband was using neonicotinoids – his father had chronic depression as well. Peters was exposed to organophosphates by doing his own crop spraying. Peters had chronic insomnia too.
Ginnie is trying to bring awareness about suicide in farmers, linked to exposure to pesticides.
I don’t have ability to do the science, but I have my gut, and what happened to Matt, it had to be the chemicals.
What the researchers of new studies aren’t saying, or do not know, is that this supposed phenomenon has gone on, vastly under the radar for a long, long time.
If you are interested in going down this dark rabbit hole, there are a couple rare and out-of-print books to help start connecting dots. Brain Fog by the late Bruce Haney, who himself was one such horticulturist with depression and behavioral changes that he noticed in his friendly competitors too. He tried desperately to get the attention of Congress in the 1990s and nursed many farmers and servicemen back to health. He cited all the notable EPA studies that knew the psychological connection, but which never led to any thoughtful halt on chemical approval.
Then there is Environmental and Chemical Toxins and Psychiatric Illness by James S. Brown Jr., M.D. The symptomology and research is vast – the title aptly describes every piece of information found therein. If you are interested in the effects of chemical exposure on your own health, then please check out Our Chemical Lives and the Hijacking of our DNA: A Probe Into What’s Probably Making Us Sick.
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Anti Virals—Uses
Allium sativum, apple juice, Andrographis paniculata, HYPERLINK “http://www.healthline.com/natstandardcontent/arabinoxylan” arabinoxylan, astragalus, HYPERLINK “http://www.healthline.com/adamcontent/avian-influenza” avian flu, HYPERLINK “http://www.healthline.com/adamcontent/avian-influenza” bird flu, HYPERLINK “http://www.healthline.com/natstandardcontent/cats-claw” cat’s claw, HYPERLINK “http://www.healthline.com/natstandardcontent/clove” cloves, HYPERLINK “http://www.healthline.com/goldcontent/co-enzyme-q10” coenzyme Q10, HYPERLINK “http://www.healthline.com/natstandardcontent/cranberry” cranberry, HYPERLINK “http://www.healthline.com/goldcontent/echinacea” echinacea, Echinacea HYPERLINK “http://www.healthline.com/adamcontent/purpura” purpura, HYPERLINK “http://www.healthline.com/natstandardcontent/elder” elderberry, forsythia, Forsythia suspense, honeysuckle, HYPERLINK “http://www.healthline.com/goldcontent/garlic” garlic, ginger, ginseng, HYPERLINK “http://www.healthline.com/galecontent/licorice” Glycyrrhiza glabra, grape seed extract (GSE), HYPERLINK “http://www.healthline.com/natstandardcontent/green-tea” green tea, infection, influenza, Isatis tinctora, HYPERLINK “http://www.healthline.com/galecontent/lemon-balm” lemon balm, leptotaenia, Leptotaenia dissecta Nutt., HYPERLINK “http://www.healthline.com/galecontent/licorice” licorice, Lonicera japonica, HYPERLINK “http://www.healthline.com/natstandardcontent/mullein” mullein, HYPERLINK “http://www.healthline.com/goldcontent/acetylcysteine” N-acetyl-cysteine, Olea europea, olive leaf, HYPERLINK “http://www.healthline.com/natstandardcontent/propolis” propolis, HYPERLINK “http://www.healthline.com/natstandardcontent/reishi-mushroom” reishi, HYPERLINK “http://www.healthline.com/natstandardcontent/resveratrol” resveratrol, Sambucas nigra L., HYPERLINK “http://www.healthline.com/galecontent/schisandra” schizandra, Schizandra chinensis, scullcap, shiitake, HYPERLINK “http://www.healthline.com/natstandardcontent/ginseng” Siberian ginseng, St. John’s wort, HYPERLINK “http://www.healthline.com/goldcontent/vitamin-e” vitamin e.
Evidence of antiviral activity of selected herbals:
Andrographis paniculata : The leaves of Andrographis paniculata, an annual herb, have been used widely as part of Indian HYPERLINK “http://www.healthline.com/galecontent/folk-medicine” folk medicine and HYPERLINK “http://www.healthline.com/galecontent/ayurvedic-medicine-1” Ayurveda for centuries. The Chinese and Thai herbal medicine systems have also incorporated this herb, valued mostly for its “bitter” properties as a treatment for HYPERLINK “http://www.healthline.com/galecontent/digestive-disorders” digestive problems and a variety of febrile illnesses. More recently, this herb, in its standardized extract form, has become popular in Scandinavia as a remedy for HYPERLINK “http://www.healthline.com/galecontent/acute-respiratory-diseases” upper respiratory infection ( HYPERLINK “http://www.healthline.com/galecontent/acute-respiratory-diseases” URI) and HYPERLINK “http://www.healthline.com/adamcontent/flu” influenza. For example, a 300 milligram Kan Jang tablet containing 4% andrographolides has been recommended to be taken four times daily for cold treatment (for a total daily dose of 48 milligrams andrographolides). Lower doses have been evaluated for respiratory infection prevention; for example, a single 200-300 milligram standardized tablet taken daily. Use appears to be safe for up to two weeks. Higher doses may be unsafe, leading to significant side effects. Kulichenko et al. carried out two randomized parallel-group trials of the SHA-10 extract of HYPERLINK “http://www.healthline.com/galecontent/andrographis” andrographis (Kan Jang, Swedish Herbal Institute) in adults diagnosed with influenza. Both studies found significant improvements in reduction of duration of influenza symptoms (1-2.5 days sooner, depending on particular symptom, p< 0.01). Although the study suffers from a poorly described randomization procedure and a lack of a standardized outcome measure for symptoms, it does seem to provide preliminary evidence that andrographis extract may be effective not only for standard URI treatment but also specifically for influenza treatment.
Apple juice: Freshly prepared apple juice has appreciable antiviral activity, but the activity may decline more readily than that of commercial juice in response to heat and storage.
: Astragalus is an extremely versatile herb which may act as an immune strengthener. It is a commonly used herb in HYPERLINK “http://www.healthline.com/galecontent/traditional-chinese-medicine” traditional Chinese medicine and is used as a component of many immune-supporting formulas, whether prepared as a sliced and boiled herb in food preparations, in extracts, or in capsules. The IL-2 inducing activity of the triterpene saponins found in astragalus might be the mechanism involved in the immunomodulatory and anticancer effects of astragalus species.
: Echinacea may boost the immune defenses in various ways. It contains three compounds with specific antiviral activity: caffeic acid, chicoric acid, and echinacin. It strengthens the body’s local defenses by use of a substance, echinacein, that deactivates germs’ tissue-dissolving HYPERLINK “http://www.healthline.com/adamcontent/enzyme” enzyme. This prevents germs from spreading and infecting other body tissues. In one study, echinacea stimulated production of white blood cells and phagocytes, and increased macrophage germ-killing activity. A University of Munich study demonstrated that echinacea boosted production of infection-fighting T-lymphocytes up to 30% more than standard immune-supportive drugs. In Germany echinacea is used to treat HYPERLINK “http://www.healthline.com/adamcontent/flu” flu, HYPERLINK “http://www.healthline.com/adamcontent/common-cold” colds, HYPERLINK “http://www.healthline.com/adamcontent/bronchitis” bronchitis, HYPERLINK “http://www.healthline.com/adamcontent/tonsillitis” tonsillitis, HYPERLINK “http://www.healthline.com/adamcontent/otitis” ear infections and HYPERLINK “http://www.healthline.com/adamcontent/pertussis” whooping cough. Root extracts of echinacea are believed to boost HYPERLINK “http://www.healthline.com/galecontent/interferons-1” interferon levels, vital to the body’s defenses.
: HYPERLINK “http://www.healthline.com/natstandardcontent/elder” Elderberry has been used has been used as a remedy for flu, cough, colds, and upper respiratory infections for over 2500 years. Recent studies demonstrate black elderberry’s effectiveness against all strains of influenza virus. A constituent present in black elderberry (with actions similar to neuraminidase inhibitors HYPERLINK “http://www.healthline.com/goldcontent/oseltamivir” oseltamivir and HYPERLINK “http://www.healthline.com/goldcontent/zanamivir” zanamivir) prevents the spread of virions from infected cells to new cells. Black elderberry is most effective in either a syrup form or in lozenges.
Forsythia ( Forsythia suspensa ): Forsythia is a traditional Chinese herb used for treating colds, flu, and other viruses. It is often mixed with honeysuckle and sometimes HYPERLINK “http://www.healthline.com/galecontent/lemon-balm” lemon balm and/or ginger as a tea.
: HYPERLINK “http://www.healthline.com/goldcontent/garlic” Garlic may possess antiviral activity. Experts claim it is most effective in its natural form, and they recommend juicing and drinking several HYPERLINK “http://www.healthline.com/natstandardcontent/clove” cloves as needed. Garlic capsules are available and are preferred by those who find the taste of fresh garlic unpleasant. Experts recommend taking 2 capsules daily for prevention of infection. Garlic contains several antimicrobial compounds including allicin, reportedly one of nature’s strongest broad-spectrum HYPERLINK “http://www.healthline.com/galecontent/antibiotics-3” antibiotics. Studies have shown that garlic inhibits the growth of many types of bacteria, including HYPERLINK “http://www.healthline.com/natstandardcontent/alt-probiotics-1” Bacillus, Brucella, Citrobacter, E. Coli, Hafnia, Klebsiella, Salmonella typhi, Shigella, Vibrio cholerae, and various forms of Staphylococcus and Streptococcus. Further studies are needed before any firm recommendations can be made.
Grape seed extract (GSE): GSE is a general antimicrobial agent with specific antiviral properties. It is best known for its application against Candida albicans, an organism responsible for HYPERLINK “http://www.healthline.com/galecontent/fungal-infections-1” fungal infections. Although not proven by scientific research, it may be effective against a long list of other microorganisms as well, including HYPERLINK “http://www.healthline.com/adamcontent/herpes-simplex” herpes simplex type 1 virus, and influenza A virus. GSE may be used in liquid concentrate form or in capsules. GSE may be taken internally, in minute doses such as 2 to 4 drops twice daily diluted in at least 4 ounces of carrot, orange, pineapple or grapefruit juice.
: Certain constituents called catechins found in HYPERLINK “http://www.healthline.com/natstandardcontent/green-tea” green tea have been studied for their ability to inhibit influenza virus replication and their direct virucidal effects. One study evaluated polyphenolic compound catechins ((-)-epigallocatechin gallate (EGCG), (-)-epicatechin gallate (ECG) and (-)-epigallocatechin (EGC)) from green tea for their ability to inhibit influenza virus replication in cell culture and for potential direct virucidal effect. Among the test compounds, the EGCG and ECG were found to be potent inhibitors of influenza virus replication. It has been suggested that the antiviral effect of catechins on influenza virus is mediated not only by specific interaction with HA, but via alteration of the physical properties of the viral membrane.
Honeysuckle ( Lonicera japonica ) is often used in China to treat bacterial and viral conditions. It is taken as a liquid from flower extracts or as a tea.
Isatidis ( Isatis tinctora ): This herb is one of the best-known traditional Chinese medicine antiviral herbs. Isatidis may be a remedy for any virus but appears to be especially good for hepatitis, because it helps reduce both swelling and HYPERLINK “http://www.healthline.com/adamcontent/hepatitis” liver inflammation. Isatidis is mild and can be used in children or those who do not tolerate heat well. Isatidis may also be a good anti-bacterial agent.
Leptotaenia ( Leptotaenia dissecta Nutt.): Available in both capsules or as a liquid extract, leptotaenia is an herb known to be useful in treating HYPERLINK “http://www.healthline.com/adamcontent/pneumonia” pneumonia, flu, colds, and bronchitis, as well as viruses such as Herpes simplex I and II and HYPERLINK “http://www.healthline.com/adamcontent/hepatitis-c” hepatitis C.
: HYPERLINK “http://www.healthline.com/galecontent/licorice” Licorice root has been used to prevent and remedy infections, fevers and inflammation. It has broad antimicrobial activity against viruses, bacteria, yeast and fungi. Licorice contains at least eight antiviral and 25 HYPERLINK “http://www.healthline.com/galecontent/antifungal-therapy” antifungal substances. Licorice also possesses antiviral compounds that promote interferon release. By itself, licorice is a dynamic herb that should only be used for short periods of time.
Olive leaf ( Olea europea ): This herb has general antimicrobial and antiviral properties. It usually comes in powder form in capsules.
HYPERLINK “http://www.healthline.com/galecontent/schisandra” Schizandra ( Schizandra chinensis ): This herb has been used in traditional Chinese medicine as an antiviral herb, specifically in cases of viral hepatitis. Schizandra may be taken in capsule form or the dried berries may be found in herb shops.
: Hypericin, a constituent of St. John’s wort, has been extensively studied as an antiviral. While hypericin has been shown to be effective in inactivating enveloped viruses, such as HYPERLINK “http://www.healthline.com/adamcontent/hepatitis-b” hepatitis B and C, and HYPERLINK “http://www.healthline.com/adamcontent/acute-cytomegalovirus-cmv-infection” cytomegalovirus, it has not been effective against non-enveloped viruses, such as HYPERLINK “http://www.healthline.com/adamcontent/hepatitis-a” hepatitis A, or HYPERLINK “http://www.healthline.com/adamcontent/fifth-disease” parvovirus B-19.
: HYPERLINK “http://www.healthline.com/goldcontent/vitamin-e” Vitamin E is a commonly encountered HYPERLINK “http://www.healthline.com/adamcontent/safety-and-vitamins” nutritional supplement with HYPERLINK “http://www.healthline.com/galecontent/antioxidants” antioxidant properties. Based on animal study, vitamin E may reduce PGE2 production, which in turn leads to enhancement of Th1 cytokines.
N-Dimethylglycine- Studies also show DMG:
Provides useful building blocks for the biosynthesis of vitamins, hormones, neurotransmitters, antibodies, nucleic acids, and other metabolically active molecules
Supports all aspects of immune response by acting as an anti-viral, anti-bacterial, and anti-fungal agent
Promotes cardiovascular functions by supporting normal triglyceride and cholesterol levels, reducing angina, improving circulation, and decreasing elevated homocysteine levels
Improves oxygenation, thus reducing fatigue and increasing energy for improved physical and mental performance
Supports neurological function and mental clarity by acting as a precursor to the amino acids that are building blocks for neurotransmitters
Acts as an antioxidant against free radicals
Supports detoxification and enhances liver function, particularly Phase II detoxification (the phase that excretes converted toxic metabolites)
DMG has anti-tumor properties, modulates the immune system, and helps protect DNA.
· Recommended Ranges for Use of DMG to be taken daily in divided doses:
General Use & Anti-Aging 125-500 mg
Sports Practice & Fitness 375-1,000 mg
Endurance Sports 1,000-2,500 mg
Immune Response (Prevention) 375-750 mg
Compromised Immune Response 750-1,200 mg
Cardiovascular & Circulatory Problems 375-1,000 mg
Diabetics & Hypoglycemics 375-1,000 mg
Autism, ADD, & Seizures 375-1,000 mg
Autoimmune Diseases (Lupus) 750-1,000 mg
Chronic Fatigue, Fibromyalgia 1,000-1,500 mg
Liver Detoxification 750-1,000 mg
Respiratory Dysfunction (Asthma/Allergies) 750-1,000 mg
Stress 250-750 mg
Hydrogen Peroxide 3% Virus inactivation by hydrogen peroxide].
[Article in Russian]
HYPERLINK “http://www.ncbi.nlm.nih.gov/pubmed?term=Mentel%27%20R%5BAuthor%5D&cauthor=true&cauthor_uid=203115” Mentel’ R, HYPERLINK “http://www.ncbi.nlm.nih.gov/pubmed?term=Shirrmakher%20R%5BAuthor%5D&cauthor=true&cauthor_uid=203115” Shirrmakher R, HYPERLINK “http://www.ncbi.nlm.nih.gov/pubmed?term=Kevich%20A%5BAuthor%5D&cauthor=true&cauthor_uid=203115” Kevich A, HYPERLINK “http://www.ncbi.nlm.nih.gov/pubmed?term=Dre%C4%ADzin%20RS%5BAuthor%5D&cauthor=true&cauthor_uid=203115” Dreĭzin RS, HYPERLINK “http://www.ncbi.nlm.nih.gov/pubmed?term=Shmidt%20I%5BAuthor%5D&cauthor=true&cauthor_uid=203115” Shmidt I.
Abstract
The effect of H2O2 on adenovirus types 3 and 6, adenoassociated virus type 4, rhinoviruses 1A, 1B, and type 7, myxoviruses, influenza A and B, respiratory syncytial virus, strain Long, and coronavirus strain 229E was studied in vitro, using different H2O2 concentration and timec of exposure. H2O2 in a 3 percent concentration inactivated all the viruses under study within 1–30 min. Coronavirus and influenza viruses were found to be most sensitive. Reoviruses, adenoviruses and adenoassociated virus were relatively stable. H2O2 is a convenient means for virus inactivation.
Selenium- Recent work with selenium has demonstrated that a deficiency in this trace mineral will lead to increased viral pathogenesis. Selenium-deficient animals infected with a viral pathogen demonstrate immune dysfunction, including altered chemokine and cytokine expression patterns. A benign coxsackievirus infection of selenium-deficient mice leads to the development of myocarditis and further experiments demonstrated that the change in virulence was due to point mutations in the viral genome. Thus, replication in a selenium-deficient host led to a normally benign virus acquiring virulence due to viral mutations. A deficiency in selenium is also associated with disease progression in HIV-infected individuals and with hepatitis C virus-induced liver cancers. It appears that adequate levels of selenium help to protect the host against viral infection.—– Coincidentally, I began to study Ebola less than a month before the 1995 outbreak in Kikwit, Zaire that brought this virus so drastically into the public consciousness. I did so because of a poster presentation I had seen that spring in Santa Fe, at a meeting of the International Society for Antiviral Research. A Russian group presented a world map showing the geographic areas where various hemorrhagic viral diseases tended to occur, and I was struck by the fact that the area shown for the filoviruses Ebola and Marburg matched a region in Africa that I suspected might be a low-selenium region. What we found was striking: several gene regions in Ebola contained large numbers of UGA codons, up to 17 in one segment. We later published a paper showing that it might be possible for Ebola to synthesize selenoproteins from these gene regions, and proposed a mechanism whereby this might induce artificial selenium deficiency and contribute to the blood clotting characteristic of Ebola pathology.During the revisions to the final draft of that paper, we learned of a 1993 paper in a Chinese journal that reported the use of selenium to treat an Ebola-like hemorrhagic fever, with remarkable results. Luckily, the English translation of the abstract was available. Using the very high oral dose of 2 mg selenium per day as sodium selenite, for only 9 days, the death rate fell from 100% (untreated) to 37% (treated) in the very severe cases, and from 22% to zero in the less severe cases. Apparently there were about 80 people involved in this outbreak. Dr. Hou of the Chinese Academy of Medical Sciences, the author of this study, has since told me that he thinks more lives could have been saved if he had been permitted to give the selenite by injection, because in many of the more severly affected there is so much organ damage due to internal bleeding that they may have been unable to fully absorb or retain the oral dose of selenium. All in all, this is the closest thing to a curative result in the treatment of hemorrhagic fever that I have ever heard of.
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[F1]So this would indicate there are cures —they just don’t know them
[F2]Soy—Pesticides—herbicides and fluoride and a host of of other nano paricles like nano silver and titanium dioxide
[F3]339 ppb-500pb == nano sized which would by pass the blood barrier of the testicals
[F4]Now imagine the farmer and field hands having these exposures and then you as a consumer eating these chemicals that may not wash out —and then you wonder what is going on with anti anxiety and anti depressing drugs—which only masked the symptoms and further cause imbalances in brain chemistry
[F5]Funny how that is always the case—not supposed to be used— and is out there —makes you wonder about the double standardEK
Tea, citrus products could lower ovarian cancer risk, new research finds
Date:October 28, 2014 –Source-University of East Anglia
Tea and citrus fruits and juices are associated with a lower risk of developing ovarian cancer, according to new research from the University of East Anglia (UEA).–The research reveals that women who consume foods containing flavonols and flavanones (both subclasses of dietary flavonoids) significantly decrease their risk of developing epithelial ovarian cancer, the fifth-leading cause of cancer death among women.–The research team studied the dietary habits of 171,940 women aged between 25 and 55 for more than three decades.–The team found that those who consumed food and drinks high in flavonols (found in tea, red wine, apples and grapes) and flavanones (found in citrus fruit and juices) were less likely to develop the disease.–Ovarian cancer affects more than 6,500 women in the UK each year. In the United States, about 20,000 women are diagnosed with ovarian cancer each year.–Prof Aedin Cassidy, from the Department of Nutrition at UEA’s Norwich Medical School, led the study. She said: “This is the first large-scale study looking into whether habitual intake of different flavonoids can reduce the risk of epithelial ovarian cancer.–“We found that women who consume foods high in two sub-groups of powerful substances called flavonoids — flavonols and flavanones — had a significantly lower risk of developing epithelial ovarian cancer.–“The main sources of these compounds include tea and citrus fruits and juices, which are readily incorporated into the diet, suggesting that simple changes in food intake could have an impact on reducing ovarian cancer risk.–“In particular, just a couple of cups of black tea every day was associated with a 31 per cent reduction in risk.”–The research was the first to comprehensively examine the six major flavonoid subclasses present in the normal diet with ovarian cancer risk, and the first to investigate the impact of polymers and anthocyanins.–The study was led by Prof Cassidy and Prof Shelley Tworoger, from the Brigham and Women’s Hospital and Harvard Medical School. Data was derived from the Nurses’ Health Study.–Story Source-The above story is based on materials provided by University of East Anglia. Note: Materials may be edited for content and length.–Journal Reference–A. Cassidy, T. Huang, M. S. Rice, E. B. Rimm, S. S. Tworoger. Intake of dietary flavonoids and risk of epithelial ovarian cancer. American Journal of Clinical Nutrition, 2014; 100 (5): 1344 DOI: 10.3945/%u200Bajcn.114.088708
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SaskPower CEO resigns after smart meter report
SaskPower CEO Robert Watson speaks at the official opening of a carbon capture and storage facility at the Boundary Dam Power Station in Estevan, Sask. on Thursday, October 2, 2014. (THE CANADIAN PRESS/Michael Bell)– The head of Saskatchewan’s Crown power company resigned Monday following a report into smart-meter fires that said customer safety wasn’t enough of a priority.–Economy Minister Bill Boyd said SaskPower CEO Robert Watson “took responsibility for the problems experienced with this project.”–“(He) felt it was time that there was new leadership at SaskPower,” said Boyd, who added that Mike Marsh, vice-president of operations, will step into the job for the interim.
CIC Smart Meter Review
Smart meters are seen in this photo taken July 31, 2014 in Regina.-Last summer, the province ordered SaskPower to remove more than 100,000 smart meters that had already been installed in homes after at least eight of the devices caught fire in June and July.-Boyd said it was evident for some time that there were problems with the meters.-“There was not enough consideration given to customer safety, the program was rushed and there (were) warning signs that were overlooked. It was clear that there was no one that was in overall charge of the program,” the minister said.-Watson won’t be receiving severance pay, Boyd said.-Saskatchewan’s Crown Investment Corp. was directed to do a review after the fires. The investigation results released Monday found that rain water and contaminants getting into the meters appeared to contribute to them failing.-“In various parts of the province, eight meters failed catastrophically, melting or burning and in some cases damaging the sides of houses,” the report[F1] said. The failures were not related to “hot sockets” or installation issues, it said.-The report also said SaskPower failed to look at the possibility that the meters could short out and catch fire.-It said that the utility looked at 359 returns and found that 18 smart meters were burned and no longer operational. Three more had high temperature errors, while 107 had display problems and 67 showed error codes.-“The (Return Material Authorization) process involves meters that have had issues in the field, and includes the eight meters involved in the destructive failures,” the review said. “The causes of these issues range from broken displays, over-voltage, communication issues, or simply the meters were dropped and no longer function properly.”-Boyd said the government is taking the review’s findings seriously and the Crown corporation will be directed to follow its recommendations. They include replacing all the meters that were provided by U.S. manufacturer Sensus. SaskPower is planning to have removal completed by March 15.–Watson announced in September that Sensus was refunding $24 million for all the smart meters the province purchased. That covered all devices that were installed and had to be removed, as well as those that hadn’t been put in yet.-Watson said Sensus was also giving SaskPower $18 million in credit for new meters, and another $5 million was to go toward developing a device suited to the Saskatchewan climate.–The NDP Opposition is asking for an independent investigation by the provincial auditor. New Democrat finance critic Trent Wotherspoon said the report is “damning.”-“This government simply didn’t have the consideration of the safety of Saskatchewan people, which is appalling in and of itself,” said Wotherspoon, who added that the problems with the meters were “concealed.”-“They rejected looking into the examples in other jurisdictions — Alabama and Philadelphia — where there was meter failure going on with the very meters that this government was putting taxpayers on the hook to pay.”-Wotherspoon said while the government claims to have recouped costs from the program, “millions of dollars (have been) wasted.”-The problems in Saskatchewan prompted officials in Medicine Hat, Alta., to suspend installation of electricity smart meters in August. A spokesman for the city said there had been no reported problems.-In Ontario, smart meters have been linked to 23 reports to Ontario’s fire marshal between 2011 and 2013, including 13 small fires. Karen Cormier, a spokeswoman for the Ontario Energy Board, has said that 36 of 77 utilities in Ontario use smart meters from Sensus, but none of them are the model used in Saskatchewan.-A smart meter records consumption of energy in small intervals and can relay the information electronically to a utilities company. It eliminates the need to estimate bills when a meter reader can’t do an on-site check.
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CIC SMART METER REVIEW MAKES RECOMMENDATIONS TO IMPROVE CROWN PROCUREMENT
Released on October 27, 2014
Review Finds Customer Safety Was Not Given Enough Priority
An investigation into the causes of fires and the procurement practices surrounding SaskPower’s smart meter program has concluded that customer safety was not given a high enough priority by SaskPower. This and other findings have led to a series of recommendations aimed at preventing such problems in the future.-“Customer safety does not appear to have been a consideration until after reports of smart meter fires involving Philadelphia Electric Company (PECO) arose,” independent experts at the law firm Robertston Stromberg found. “It did not become a matter of central importance until June of 2014.”-During June and July of 2014, there were eight different cases where smart meters caught fire, prompting the suspension of the installation program and a later cabinet order to remove the meters.-Crown Investments Corporation (CIC) was directed to conduct a review and commissioned a number of independent experts to examine different aspects of the issue. -PwC was asked to review procurement and contract management. Consulting engineers Ritenburg and Associates of Regina was asked to examine the technical and safety issues and the law firm Robertson Stromberg was commissioned to look at legal and product liability issues.-An initial study of the causes of the fires shows that rainwater and contaminants getting into the meters appear to be a major contributing factor in the failures, not issues related to their installation.[F2] That portion of the CIC review, conducted by Regina’s Ritenburg and Associates, shows that some of the Sensus meters used in Saskatchewan have a tendency to leak. The eight meters in question were completely destroyed and impossible to analyze.[F3] However, others that quit because of other problems and were removed have shown signs of moisture and conductive contaminants getting in.-This will have to be confirmed by other testing now underway by consultants for SaskPower, but Ritenburg found no evidence that the failures were related to “hot sockets” or installation problems[F4]. -The review also identified a number of problems in the procurement and project management processes.–Overall, the company’s risk management process was found to be lacking. While SaskPower did identify a number of risks, the possibility the meters could actually short out and catch fire was not considered until similar fires at the PECO became public.– While contractor and employee safety were considered, customer safety was not given enough priority, the review found.–SaskPower had also received advice that it should buy small batches of smart meters through a “stepped procurement” process, install them gradually and watch for problems. The company did not do that. After some smaller initial purchases, it went on to buy more than 100,000 meters in a three week period and initiated a full-scale installation program. This was done because they had the budget available for it in 2013.-Both PwC and Robertson Stromberg found that there was no single point of control overseeing the smart meter project, making it easier for warning signals to go unheeded.
There were several such warnings:
A suit filed in Alabama in May of 2010 alleged Sensus meters were catching fire;
After losing the SaskPower contract to Sensus in December of 2011, a meter manufacturer warned SaskPower of past problems with Sensus; and
Fires in Philadelphia forced the PECO to remove Sensus meters in October of 2012.
While SaskPower did respond to the PECO fires with changes to the smart meter program, the review questions whether enough was done.-SaskPower did increase its efforts to detect faulty sockets, enabling an extra temperature sensor and seeking assurances from Sensus that the meters were safe. -However, the remote reading function never did work properly and there were so many false alarms for overheating, SaskPower could not investigate them all[F5]. Even after 100,000 installations, SaskPower had to read all of the smart meters manually.-
Ritenburg made several recommendations including:
Given the potential fire hazard, all of the existing Sensus meters should be removed before next spring and potentially rainy weather;
Those meters should be examined for arcing or other problems when they come out, to establish more information;
When installing meters, more site photos should be taken in case the scene has to be analyzed after any future failures; and
All meter incidents should be reported and a data base created.
[F6] PwC made the following recommendations:
SaskPower should have specific guidelines on identifying and operating high-risk procurement projects;
SaskPower needs a more formal “process safety management” program to ensure customer safety is paramount;
There should be a single “contract owner” for such important, complex projects with a specific risk management process built in; and
Clearly identify the roles and responsibilities for the management of enterprise risks relevant to procurement.
Robertson Stromberg also concluded that in large scale procurements of this kind, the vendor should consider buying product liability insurance to cover the buyer, in case of problems.–CIC Minister Don McMorris said the provincial cabinet has reviewed a summary of the findings and the government has directed CIC to:
Ensure that SaskPower removes all Sensus meters by March 15, 2015 at the latest;
Ensure that SaskPower implements all of the consultants’ recommendations; and
Work with all the Crowns to ensure they are applying the lessons from this incident across the Crown sector.
For more information, contact:
Randy Burton
CIC
Regina
Phone: 306-787-5889
Email: [email protected]
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Silver nanoparticle applications and human health.
Ahamed M1, Alsalhi MS, Siddiqui MK.
Author information
Abstract
Nanotechnology is rapidly growing with nanoparticles produced and utilized in a wide range of commercial products throughout the world. For example, silver nanoparticles (Ag NP) are used in electronics, bio-sensing, clothing, food industry, paints, sunscreens, cosmetics and medical devices. These broad applications, however, increase human exposure and thus the potential risk related to their short- and long-term toxicity. A large number of in vitro studies indicate that Ag NPs are toxic to the mammalian cells derived from skin, liver, lung, brain, vascular system and reproductive organs. Interestingly, some studies have shown that this particle has the potential to induce genes associated with cell cycle progression, DNA damage and apoptosis in human cells at non-cytotoxic doses. Furthermore, in vivo bio-distribution and toxicity studies in rats and mice have demonstrated that Ag NP administered by inhalation, ingestion or intra-peritoneal injection were subsequently detected in blood and caused toxicity in several organs including brain. Moreover, Ag NP exerted developmental and structural malformations in non-mammalian model organisms typically used to elucidate human disease and developmental abnormalities. The mechanisms for Ag NP induced toxicity include the effects of this particle on cell membranes, mitochondria and genetic material. This paper summarizes and critically assesses the current studies focusing on adverse effects of Ag NPs on human health.- Copyright © 2010 Elsevier B.V. All rights reserved.
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Purslane weed (Portulaca oleracea): a prospective plant source of nutrition, omega-3 fatty acid, and antioxidant attributes.
ScientificWorldJournal. 2014;2014:951019
Authors: Uddin MK, Juraimi AS, Hossain MS, Nahar MA, Ali ME, Rahman MM
Abstract
Purslane (Portulaca oleracea L.) is an important plant naturally found as a weed in field crops and lawns. Purslane is widely distributed around the globe and is popular as a potherb in many areas of Europe, Asia, and the Mediterranean region. This plant possesses mucilaginous substances which are of medicinal importance. It is a rich source of potassium (494 mg/100 g) followed by magnesium (68 mg/100 g) and calcium (65 mg/100 g) and possesses the potential to be used as vegetable source of omega-3 fatty acid. It is very good source of alpha-linolenic acid (ALA) and gamma-linolenic acid (LNA, 18 : 3 w3) (4 mg/g fresh weight) of any green leafy vegetable. It contained the highest amount (22.2 mg and 130 mg per 100 g of fresh and dry weight, resp.) of alpha-tocopherol and ascorbic acid (26.6 mg and 506 mg per 100 g of fresh and dry weight, resp.). The oxalate content of purslane leaves was reported as 671-869 mg/100 g fresh weight. The antioxidant content and nutritional value of purslane are important for human consumption. It revealed tremendous nutritional potential and has indicated the potential use of this herb for the future.-PMID: 24683365 [PubMed – indexed for MEDLINE]
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PSA test should be abandoned as screen for prostate cancer, task force says
The blood test mostly commonly used to screen men for prostate cancer should be dropped, because it can result in more harm than good, says a Canadian task force. The prostate-specific antigen, or PSA, test measures inflammation that can be elevated for many reasons other than cancer, such as normal enlargement of the prostate with age or an infection. Researchers said over-diagnosis occurs when cancer is detected correctly but would not cause symptoms or death. The main problems are false-positive results and over-diagnosis, the review indicated. A positive PSA test result often leads to more tests such as a biopsy, which carries risks of bleeding, infection, and urinary incontinence. In most men with prostate cancer, the tumour grows slowly, and they’re likely to die of another cause before the prostate tumour causes any symptoms. Prostate cancer is the most commonly diagnosed non-skin cancer in men. The prognosis for most prostate cancers is good, with a 10-year survival rate of 95 per cent.
PSA: to test or not to test?
Routine PSA prostate cancer test not recommended
Screening aims to find cancer before symptoms appear and reduce the chance of dying from cancer with early treatment. In Monday’s issue of the Canadian Medical Association Journal, the Canadian Task Force on Preventive Health Care reviewed the latest evidence and international best practice to weigh the benefits and harms of PSA screening with or without digital rectal exams. “Available evidence does not conclusively show that PSA screening will reduce prostate cancer mortality, but it clearly shows an elevated risk of harm. The task force recommends that the PSA test should not be used to screen for prostate cancer,” Dr. Neil Bell, chair of the prostate cancer guideline working group member, and his team concluded. The guideline is aimed at physicians and other health-care professionals and policymakers. It updates the task force’s recommendation from 1994 on screening with the PSA test.
The new recommendations include:
For men under age 55 and over age 70, the task force recommends not using the PSA test to screen for prostate cancer. This strong recommendation is based on the lack of clear evidence that screening with the PSA test reduces mortality and on the evidence of increased risk of harm.
For men aged 55–69 years, the task force also recommends not screening, although it recognizes that some men may place high value on the small potential reduction in the risk of death and suggests that physicians should discuss the benefits and harms with these patients.
These recommendations apply to men considered high risk — black men and those with a family history of prostate cancer — because the evidence does not indicate that the benefits and harms of screening are different for this group.
The key evidence was from a well-done European study. It showed inconsistent results, with a small potential positive effect over a long period of time, which the reviewers balanced against the clear evidence of harm, said Dr. James Dickinson, a member of the prostate cancer guideline working group and a professor of family medicine at the University of Calgary. “Fundamentally this is not a good enough test to be worth using,” Dickinson said in an interview. “Let’s hope that better things come in the future, but right now it’s not worth using. It’s more likely to cause harm than benefit.”
Watchful waiting advocated
A Canadian specialist, however, takes issue with the recommendation. The task force’s guidelines are flawed for Canada, said Dr. Neil Fleshner, who studies and treats prostate cancer at Princess Margaret Cancer Centre in Toronto. “By using the PSA test, we can absolutely find lethal cancers early and by intervening in those men, we can save their lives. Therefore, these recommendations ndoubtedly will lead to more prostate cancer deaths,” Fleshner said. [F7]–The task force’s Bell said almost one in five men aged 55 to 69 have at least one false-positive PSA test, and about 17 per cent end up with unnecessary biopsies.–“If you screen men [aged 55 to 69] based on the protocol in those trials, every two to four years for 13 years, five out of 1,000 will die from prostate cancer. If you don’t screen, six out of 1,000 men will die from prostate cancer,” Bell said. “So the reduction in prostate cancer mortality is one in 1,000 or about 0.1 per cent.”–“To get the benefit, you’re diagnosing about 27 or 28 men with prostate cancer who would never benefit from the treatment related to prostate cancer because they would never suffer any difficulty from it.”–Bell added that more than half of detected prostate cancers are over-diagnosed. The task force said that separating screening from treatment through watchful waiting or active surveillance, could change the ratio of risks to benefits of PSA screening, but the hypothesis needs to be tested. Dr. Murray Krahn of Toronto’s University Health Network wrote a journal commentary on prostate cancer screening. Krahn said the task force guideline provides a good summary, but he would like to see more emphasis on patient preference, such as whether the harms are important, and shared decision-making.. With files from CBC’s Kas Roussy and The Canadian Press
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Could copper prevent spread of Ebola?
Date:
October 30, 2014
Source:
University of Southampton
“Based on our research on viruses of similar genetic structure, we expect copper surfaces to inactivate Ebola, and to help control the spread of this virus if employed for publicly-used touch surfaces,” explains Professor Keevil, pictured here.–Research from the University of Southampton has indicated that copper could help to prevent the spread of Ebola.–Hand washing, disinfectants and quarantine procedures alone have been found to be insufficient to contain the spread of the virus. Research by Professor Bill Keevil at the University of Southampton has offered promising evidence that antimicrobial copper — engineering materials with intrinsic hygiene benefits — could be a valuable addition to these existing measures.–The US Centers for Disease Control and Prevention (CDC) note the Ebola virus is transmitted through direct contact with the bodily fluids of an infected person, or through exposure to contaminated objects. Viruses similar to Ebola are susceptible to a broad range of surface disinfectants, however testing against Ebola itself cannot currently be conducted due to limited access to laboratories with the required safety clearances. The CDC has therefore instructed hospitals to use disinfectants with proven efficacy against resistant viruses such as norovirus, adenovirus and poliovirus1.–Peer-reviewed and published data from laboratory studies conducted by Professor Bill Keevil, Chair of Environmental Healthcare at the University of Southampton, demonstrates copper’s ability to rapidly and completely inactivate norovirus2. Recent work in Germany has also explored its effectiveness against other viral biothreat agents3. Clinical trials conducted in the UK, US and Chile have shown surfaces made from solid copper or copper alloys — collectively termed ‘antimicrobial copper’ — continuously reduce surface contamination by greater than 80 per cent. These results indicate a potential role for antimicrobial copper touch surfaces in preventing the spread of Ebola.–“Based on our research on viruses of similar genetic structure, we expect copper surfaces to inactivate Ebola, and to help control the spread of this virus if employed for publicly-used touch surfaces,” explains Professor Keevil.-Antimicrobial copper surfaces have been described as a ‘no touch’ solution, meaning that no special measures or human intervention are required for it to continuously kill pathogens, in between regular cleans. Replacing frequently-touched surfaces, such as door handles, taps and light switches, with solid copper or copper alloy equivalents will provide a more hygienic environment, with fewer bacteria and viruses available to spread infections. With this in mind, the use of antimicrobial copper surfaces could offer an additional method of controlling the current spread of Ebola.–Interim Guidance for Environmental Infection Control in Hospitals for Ebola Virus, Centers for Disease Control and Prevention: http://www.cdc.gov/vhf/ebola/hcp/environmental-infection-control-in-hospitals.html—-Story Source-The above story is based on materials provided by University of Southampton. Note: Materials may be edited for content and length.-Journal Reference-Sarah L. Warnes, C. William Keevil. Inactivation of Norovirus on Dry Copper Alloy Surfaces. PLoS ONE, 9(5): e98333 DOI: 10.1371/journal.pone.0098333
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[F1]Reports can be altered to offset and litigation that the company or province or electric company may have to pay out—imagine the electric company installing these things and a house—for a ½ a mill breaks down and burns as a result of this anal technology—that can add up—this was the situation in Vancouver Island when a 250,000 home caught fire and the electrical company went into deniability because of the cost to replace that home would have doubled
[F2]This is such BS and a real uncreative report to show that it was an environmental issue rather then a technical one or even inadequate installation procedures –would be as well curious to see if the backing plates were also removed or replaced—the one on Vancouve island was left on and not repaced and the technician forced the meter on the plate causing a over heating of the plate—technical error down by the installer which would have made the company liable
[F3]As I said BS –these were convienantly destroyed beyond examination—and based on the others –they made a conclusion based on a guess—this is really interesting to make such a claim without a real dissection of the unit and a real examination—chances are the unit was working and it was not compliant to the current tech in the home
[F4]And I wonder how they came to that conclusion since the devixces were convienantly destroyed beyond there capability to examine—would indicate a huge surge or a Hot Socket to me
[F5]This is incredibly alarming they had so many issues before the fires occurred that they should have seen the red flags on this and yanked them right then and there —to have so many problems on going and not being able to maintain or repair the issues would have been a clear sign to pull them off the house
[F6]I love how this is showing incompetence —these things were probably already being implemented—this is normal procedures when something goes wrong –photos—reports and follow through so this is basically a smoke screen to again alleviate responsibilty and litigation
[F7]Here is a Money making Doctor –as you can see he is making hhis dollars by sticking his finger up someone’s arse –and then possibly billing the gov’t for a surgical procedure —yet with all the men who do reach 80+ and have prostate issues—it never kills them—something else usually does —so is the test necessary at all…from the research —only if there is a need to investigate and the procedure itself could cause death to examine the person
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HOME
Show of the Month November 8 2014
Niacin and Schizophrenia– History and Opportunity
Healing the Kidneys with Sodium Bicarbonate (Baking Soda)
Effects of poor eating habits persist even after diet is improved
Alzheimer’s Disease and Parkinson’s Disease. A Dietary Connection
Biological fat with a sugar attached essential to maintaining brain’s supply of stem cells
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Niacin and Schizophrenia– History and Opportunity
by Nick Fortino, PhD Candidate
(OMNS Oct 27, 2014) Schizophrenia is usually treated with prescription antipsychotic drugs, many of which produce severe adverse effects (1-6); are linked to an incentive for monetary profit benefiting pharmaceutical corporations (7-13); lack sufficient evidence for safety and efficacy (9, 14); and have been grossly misused (15-20). Orthomolecular (nutritional) medicine provides another approach to treating schizophrenia, which involves the optimal doses of vitamin B3-also known as niacin, niacinamide, nicotinamide, or nicotinic acid-in conjunction with an individualized protocol of multiple vitamins. The orthomolecular approach involves treating “mental disease by the provision of the optimum molecular environment for the mind, especially the optimum concentrations of substances normally present in the human body” (21).
Evidence for the Niacin Treatment of Schizophrenia
Vitamin B3 as a treatment for schizophrenia is typically overlooked, which is disconcerting considering that historical evidence suggests it effectively reduces symptoms of schizophrenia, and has the added advantage, in contrast to pharmaceuticals, of mild to no adverse effects (22-35). After successful preliminary trials treating schizophrenia patients with niacin, pilot trials of larger samples commenced in 1952-reported in 1957 by Hoffer, Osmond, Callbeck, and Kahan. Dr. Abram Hoffer began an experiment involving 30 patients who had been diagnosed with acute schizophrenia. Participants were given a series of physiological and psychological tests to measure baseline status and were subsequently assigned randomly to treatment groups. Nine subjects received a placebo, 10 received nicotinic acid, and 11 received nicotinamide (the latter two are forms of vitamin B3). All participants received treatment for 42 days, were in the same hospital, and received psychotherapy from the same group of clinicians. The two experimental groups were administered three grams of vitamin B3 per day. Each of the three treatment groups improved, but the two vitamin B3 groups improved more than the placebo group as compared to baseline measures. At one year follow up, 33% of patients in the placebo group remained well, and 88% of patients in the B3 groups remained well. These results inspired many subsequent trials, and those that replicated the original method produced similarly positive results.
Antipsychotic Drugs
That schizophrenia may be caused or aggravated by a deficiency of essential nutrients appears to have eluded the majority of the health care providers serving the schizophrenic population, as evidenced by the fact that “antipsychotic medications represent the cornerstone of pharmacological treatment for patients with schizophrenia” (36). Waves of different antipsychotic drugs have been developed throughout the last 60 years, which have not decreased the prevalence of schizophrenia; in fact it has increased (15, 37).–Although dangerous when taken in high doses and for a long period of time, the value of antipsychotics appears to be that in the short term they can help to bring some control to schizophrenic symptoms, not by curing the condition but by inducing a neurological effect that is qualitatively different from the schizophrenic state. Dr. Hoffer acknowledged their value and in his private practice he would introduce antipsychotics and vitamins simultaneously because antipsychotics work rapidly and vitamins work more slowly, so a person could benefit from the short term relief from symptoms that antipsychotics provide while the vitamins slowly, but surely, healed the deficiency causing the schizophrenic symptoms. This also allowed for a much easier process of tapering from the drugs.
“For schizophrenia, the recovery rate with drug therapy is under 15%. With nutritional therapy, the recovery rate is 80%.” – Abram Hoffer, MD, PhD
More Research Needed
Further research into the orthomolecular treatment of schizophrenia is imperative. Saha, Chant, and McGrath (38) found that mortality rates in schizophrenia have increased in recent decades and warned, “in light of the potential for second-generation antipsychotic medications to further adversely influence mortality rates in the decades to come, optimizing the general health of people with schizophrenia warrants urgent attention.” The orthomolecular approach may be, at least, an integral part of a treatment program that optimizes general health and leads to a life free from schizophrenic symptoms.–Questions abound regarding individuals’ experiences while on these different treatments. Particularly the psychological and relational, or, intrapersonal and interpersonal experience while on antipsychotics versus an orthomolecular treatment must be more thoroughly documented because it is in this domain that a person ascertains his/her quality of life. And only the person who has these experiences can provide such an account; no psychiatrist peering in from outside a one-way mirror on a person hearing voices, nor any brain image, nor any valid and reliable measure can ever reflect the person’s living qualitative experience as accurately as the person can[F1]. This is why I have designed a multiple case study to explore in depth the experiences of individuals successfully treating their schizophrenia using orthomolecular medicine. The central research question is: What is the experience of individuals with schizophrenia who switched from using antipsychotics to orthomolecular medicine to treat their condition?
A Call for Participants
Inclusion criteria for this study are: over age 18, diagnosed as having schizophrenia, treated for a period of time primarily with antipsychotics, and are currently treated by or were cured by an orthomolecular protocol. Participation will consist of three interviews with the researcher (in person or online video conference), each of which will focus on a distinct period: symptomatic but unmedicated, primarily using antipsychotic drugs, and primarily using orthomolecular medicine. The researcher will also request one interview with the orthomolecular practitioner if possible, the diagnosing psychiatrist if possible, and at least two close friends and/or family members about their experiences of relating with the primary participant during these different periods. Anonymity is guaranteed if requested.–I am a Psychology Ph.D. student and this is my dissertation study. I never had the privilege of meeting Dr. Hoffer, but his spirit, conviction, and massive production of great work have inspired my writing this dissertation. Toward that latter part of his career, he commented on the nature of schizophrenia treatment research:
Case histories have disappeared from journal articles, as if living patients no longer existed or counted for very much. Instead, authors describe their methods, describe what criteria they used in selecting their groups of patients which were used in their prospective double blind controlled studies, and provide ample charts and statistics. I have read many papers where it is impossible to get any feeling for a single patient. (29)[F2]
This dissertation attempts to address this deficit of qualitative data. The narrative accounts that multiple case studies yield are invaluable, and can be accessible and relatable for people in a position of gathering information about schizophrenia treatments for themselves or a loved one. This dissertation is not an attempt to prove the legitimacy of the orthomolecular treatment; Dr. Hoffer and others have dedicated their professional lives to that endeavor. This is meant to explore the experience of the treatment, especially as it compares to the experience of the antipsychotic treatment. I am recruiting from a very small population of people, so I ask you to consider participating if you fit the criteria, or pass this invitation along to someone you know who fits the criteria. I can be reached by phone (408) 840-1253 or email ([email protected]) to answer questions and/or to begin the research process.
References:
1. Arana, G. W. (2000). An overview of side effects caused by typical antipsychotics. Journal of Clinical Psychiatry, 61(8), 5-11. http://www.ncbi.nlm.nih.gov/pubmed/10811237.
2. Ciranni, M. A., Kearney, T. E., & Olson, K. R. (2009). Comparing acute toxicity of first- and second-generation antipsychotic drugs: A 10-year, retrospective cohort study. The Journal of Clinical Psychiatry, 70(1), 122-129. http://www.ncbi.nlm.nih.gov/pubmed/19192473
3. Ho, B. C., Andreasen, N. C., Ziebell, S., Pierson, R., & Magnotta, V. (2011). Long-term antipsychotic treatment and brain volumes: A longitudinal study of first-episode schizophrenia. Archives of General Psychiatry, 68(2), 128. http://www.ncbi.nlm.nih.gov/pubmed/21300943
4. Pope, H. G., Keck, P. E., & McElroy, S. L. (1986). Frequency and presentation of neuroleptic malignant syndrome in a large psychiatric hospital. The American Journal of Psychiatry, 143(10), 1227-1233. http://www.ncbi.nlm.nih.gov/pubmed/2876647
5. Saddichha, S., Manjunatha, N., Ameen, S., & Akhtar, S. (2008). Diabetes and schizophrenia-effect of disease or drug? Results from a randomized, double blind, controlled prospective study in first-episode schizophrenia. Acta Psychiatrica Scandinavica, 117, 342-347. http://www.ncbi.nlm.nih.gov/pubmed/18307585
6. Woods, S. W., Morgenstern, H., Saksa, J. R., Walsh, B. C., Sullivan, M. C., Money, R., Hawkins, K. A., Gueorguieva, R. V., & Glazer, W. M. (2010). Incidence of tardive dyskinesia with atypical and conventional antipsychotic medications: Prospective cohort study. The Journal of Clinical Psychiatry, 71(4), 463-475. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3109728/
7. Angell, M. (2004). The truth about the drug companies: How they deceive us and what to do about it. New York, N.Y.: Random House LLC.
8. Berenson, A. (2007, January 05). Lilly settles with 18,000 over zyprexa. The New York Times, pp. 1-2. Retrieved from http://www.nytimes.com/2007/01/05/business/05drug.html?_r=0
9. Kendall, T. (2011). The rise and fall of atypical antipsychotics. The British Journal of Psychiatry, 199(4), 266-268. doi:10.1192/bjp.bp.110.083766 http://www.ncbi.nlm.nih.gov/pubmed/22187726
10. Moynihan, R., & Alan, C. (2005). Selling sickness: How the world’s biggest pharmaceutical companies are turning us all into patients. New York, N.Y.: Nation Books.
11. Moynihan, R., Heath, I., & Henry, D. (2002). Selling sickness: the pharmaceutical industry and disease mongering. British Medical Journal, 324(7342), 886. http://www.ncbi.nlm.nih.gov/pubmed/11950740
12. Scherer, F. M. (1993). Pricing, profits, and technological progress in the pharmaceutical industry. The Journal of Economic Perspectives, 7(3), 97-115. https://www.aeaweb.org/articles.php?doi=10.1257/jep.7.3.97
13. Spielmans, G. I., & Parry, P. I. (2009). From evidence-based medicine to marketing-based medicine: Evidence from internal industry documents. Journal of Bioethical Inquiry, 7(1), 13-29. doi:10.1007/s11673-010-9208-8 http://link.springer.com/article/10.1007%2Fs11673-010-9208-8#page-1
14. Lieberman, J. A., Stroup, T. S., McEvoy, J. P., Swartz, M. S., Rosenback, R. A., Perkins, D. O., Keefe, R. S. E., Davis, S. M., Davis, C. E., Lebowitz, B. D., Severe, J., Hsiao, J. K. (2005). Effectiveness of antipsychotic drugs in patients with chronic schizophrenia. The New England Journal of Medicine, 353(12), 1209-1223. http://www.ncbi.nlm.nih.gov/pubmed/17335312
15. Whitaker, R. (2010). Anatomy of an epidemic: Magic bullets, psychiatric drugs, and the astonishing rise of mental illness in America. New York, N.Y.: Crown Publishers.
16. Kuehn, B. M. (2010). Questionable antipsychotic prescribing remains common, despite serious risks. Journal of the American Medical Association, 303(16), 1582-1584. http://www.ncbi.nlm.nih.gov/pubmed/20424239
17. Moran, M. (2011). Misuse of antipsychotics widespread in nursing homes. Psychiatric News, 46(11), 2. http://psychnews.psychiatryonline.org/newsarticle.aspx?articleid=108671
18. Ray, W. A., Federspiel, C. F., & Schaffner, W. (1980). A study of antipsychotic drug use in nursing homes: Epidemiologic evidence suggesting misuse. American Journal of Public Health, 70(5), 485-491. http://www.ncbi.nlm.nih.gov/pubmed/6103676
19. Stevenson, D. G., Decker, S. L., Dwyer, L. L., Huskamp, H. A., Grabowski, D. C., Metzger, E. D., & Mitchell, S. L. (2010). Antipsychotic and benzodiazepine use among nursing home residents: Findings from the 2004 National Nursing Home Survey. The American journal of Geriatric Psychiatry: Official Journal of the American Association for Geriatric Psychiatry, 18(12), 1078-1092. http://www.ncbi.nlm.nih.gov/pubmed/20808119
20. Szaz, T. (1974). The myth of mental illness: Foundations of a theory of personal conduct. New York, N.Y.: Harper Perennial.
21. Pauling, L. (1968). Orthomolecular psychiatry. Varying the concentrations of substances normally present in the human body may control mental disease. Orthomolecular psychiatry. Science, 160, 265-271. http://www.ncbi.nlm.nih.gov/pubmed/5641253
22. Cleckley, H. M., Sydenstricker, V. P., & Geeslin, L. E. (1939). Nicotinic acid in the treatment of atypical psychotic states. The Journal of the American Medical Association, 112(21), 2107-2110. http://jama.jamanetwork.com/article.aspx?articleid=288714
23. Hoffer, A. (1962). Niacin Therapy in Psychiatry. Springfield, Il: C. C. Thomas.
24. Hoffer, A. (1963). Nicotinic acid: An adjunct in the treatment of schizophrenia. American Journal of Psychiatry, 120, 171-173. http://www.ncbi.nlm.nih.gov/pubmed/13963912
25. Hoffer, A. (1966). The effect of nicotinic acid on the frequency and duration of re-hospitalization of schizophrenic patients: A controlled comparison study. International Journal of Neuropsychiatry, 2(3), 234-240. http://www.ncbi.nlm.nih.gov/pubmed/4225426
26. Hoffer, A. (1970a). Childhood schizophrenia: A case treated with nicotinic acid and nicotinamide. Schizophrenia, 2, 43-53. http://orthomolecular.org/library/jom/1970/pdf/1970-v02n01-p043.pdf
27. Hoffer, A. (1973). A neurological form of schizophrenia. Canadian Medical Association Journal, 108, 186-194. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1941147/
28. Hoffer, A. (1994). Chronic schizophrenic patients treated ten years or more. Journal of Orthomolecular Medicine, 9(1), 7-37. http://orthomolecular.org/library/jom/1994/pdf/1994-v09n01-p007.pdf
29. Hoffer, A. (1996). Inside schizophrenia: Before and after treatment. Journal of Orthomolecular Medicine, 11(1), 45-48. http://orthomolecular.org/library/jom/1996/pdf/1996-v11n01-p045.pdf
30. Hoffer, A. & Fuller, F. (2009). Orthomolecular treatment of schizophrenia. Journal of Orthomolecular Medicine, 24(3,4), 151-159. http://orthomolecular.org/library/jom/2009/pdf/2009-v24n01-p009.pdf
31. Hoffer, A., & Osmond, H. (1964). Treatment of schizophrenia with nicotinic acid: A ten year follow up. Acta Psychiatrica Scandinavica, 40, 171-189. doi:10.1111/j.1600-0447.1964.tb05744.x http://www.ncbi.nlm.nih.gov/pubmed/14235254.
32. Hoffer, A., & Osmond, H. (1980). Schizophrenia: Another long term follow-up in Canada. Orthomolecular Psychiatry, 9(2), 107-113. http://psycnet.apa.org/psycinfo/1981-13316-001
33. Hoffer, A., Osmond, H., Callbeck, M. J., & Kahan, I. (1957). Treatment of schizophrenia with nicotinic acid and nicotinamide. Journal of Clinical and Experimental Psychopathology, 18(2), 131-157. http://www.ncbi.nlm.nih.gov/pubmed/13439009
34. Tung-Yep, T. (1981). The use of orthomolecular therapy in the control of schizophrenia-a study preview. The Australian Journal of Clinical Hypnotherapy, 2(2), 111-116. http://schizophreniabulletin.oxfordjournals.org/content/12/1/141.full.pdf
35. Verzosa, P. L. (1976). A report on a twelve-month period of treating metabolic diseases using mainly vitamins and minerals on the schizophrenias. Orthomolecular Psychiatry, 5(4), 253-260. http://www.orthomolecular.org/library/jom/1976/pdf/1976-v05n04-p253.pdf
36. Gilmer, T. P., Dolder, C. R., Lacro, J. P., Folsom, D. P., Lindamer, L., Garcia, P., & Jeste, D. V. (2004). Adherence to treatment with antipsychotic medication and health care costs among Medicaid beneficiaries with schizophrenia. American Journal of Psychiatry, 161(4), 692-699. http://www.ncbi.nlm.nih.gov/pubmed/15056516
37. McGrath, J., Saha, S., Chant, D., & Welham, J. (2008). Schizophrenia: A concise overview of incidence, prevalence, and mortality. Epidemiologic Reviews, 30, 67-76. http://www.ncbi.nlm.nih.gov/pubmed/18480098.
38. Saha, S., Chant, D., & McGrath, J. (2007). A systematic review of mortality in schizophrenia. Archives of General Psychiatry, 64(10), 1123-1131. http://www.ncbi.nlm.nih.gov/pubmed/17909124
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Healing the Kidneys with Sodium Bicarbonate (Baking Soda)
Posted by Dr Sircus on November 11, 2009 | Filed under Medicine, Sodium Bicarbonate (Baking Soda)
Sodium bicarbonate is not only an excellent agent for natural chemotherapy, bringing as it does higher O2 levels through increased alkalinity to the cells, it is also one of the most basic medicines we have for kidney disease. New research by British scientists at the Royal London Hospital shows that sodium bicarbonate can dramatically slow the progress of chronic kidney disease.[1] We don’t need a thousand years of tests to understand something as simple as water and it is quite the same with bicarbonate, which is always present in the best drinking waters. Bicarbonate acts to stimulate the ATPase by acting directly on it.[2] -The simple household product used for baking, cleaning, bee stings, treating asthma, cancer and acid indigestion is so effective in treating kidney disease that it prevents patients from having to be put on kidney machines. The findings have been published in the Journal of the American Society of Nephrology. Bicarbonate is a truly strong universal concentrated nutritional medicine that works effectively in many clinical situations that we would not normally think of. It is a prime emergency room and intensive care medicine that can save a person’s life in a heartbeat and it is also a supermarket item that you can take right off the shelf and use for more things than one can imagine – including diaper rash. -Dr. SK Hariachar, a nephrologist who oversees the Renal Hypertension Unit in Tampa Florida stated, upon seeing the research on bicarbonate and kidney disease, ”I am glad to see confirmation of what we have known for so long. I have been treating my patients with bicarbonate for many years in attempts to delay the need for dialysis, and now we finally have a legitimate study to back us up. Not only that, we have the added information that some people already on dialysis can reverse their condition with the use of sodium bicarbonate”. -John, a dialysis technician at the same center as Dr. Hariachar, who used to be on dialysis himself for 2 years as a result of kidney failure, had his kidneys miraculously start functioning to the point where dialysis was no longer needed. He states that he was prescribed oral doses of sodium bicarbonate throughout his treatment, and still takes it daily to prevent recurrences of kidney failure. Dr. Hariachar maintains though, that not everyone will be helped by taking bicarbonate. He says that those patients who have difficulty excreting acids, even with dialysis using a bicarbonate dialysate bath, that, “oral bicarbonate makes all the difference.”
Kidneys Produce Bicarbonate
The exocrine section of the pancreas has been greatly ignored in the treatment of diabetes even though its impairment is a well documented condition. The pancreas is primarily responsible for the production of enzymes and bicarbonate necessary for normal digestion of food. Bicarbonate is so important for protecting the kidneys that even the kidneys get into the act of producing bicarbonate and now we know the common denominator between diabetes and kidney disease. When the body is hit with reductions in bicarbonate output by these two organs,’ acid conditions build and then entire body physiology begins to go south. Likewise when acid buildup outstrips these organs normal bicarbonate capacity cellular deterioration begins.-The kidneys alone produce about two hundred and fifty grams (about half a pound) of bicarbonate per day in an attempt to neutralize acid in the body. -The kidneys monitor and control the acidity or “acid-base” (pH) balance of the blood. If the blood is too acidic, the kidney makes bicarbonate to restore the bloods pH balance. If the blood is too alkaline, then the kidney excretes bicarbonate into the urine to restore the balance. Acid-base balance is the net result of two processes, first, the removal of bicarbonate subsequent to hydrogen ion production from the metabolism of dietary constituents; second, the synthesis of “new” bicarbonate by the kidney.[3] -It is considered that normal adults eating ordinary Western diets have chronic, low-grade acidosis which increases with age. This excess acid, or acidosis, is considered to contribute to many diseases and to contribute to the aging process. Acidosis occurs often when the body cannot produce enough bicarbonate ions (or other alkaline compounds) to neutralize the acids in the body formed from metabolism and drinking highly acid drinks like Coke, Pepsi and we are even seeing reports on bottled mineral water being way too acidic.-Acid-buffering by means of base supplementation is one of the major roles of dialysis. Bicarbonate concentration in the dialysate (solution containing water and chemicals (electrolytes) that passes through the artificial kidney to remove excess fluids and wastes from the blood, also called “bath.”) should be personalized in order to reach a midweek pre-dialysis serum bicarbonate concentration of 22 mmol/l.[4] Use of sodium bicarbonate in dialysate has been shown in studies to better control some metabolic aspects and to improve both treatment tolerance and patients’ life quality. Bicarbonate dialysis, unlike acetate-free biofiltration, triggers mediators of inflammation and apoptosis.[5]-One of the main reasons we become acid is from over-consumption of protein. Eating meat and dairy products may increase the risk of prostate cancer, research suggests.[6] We would find the same for breast and other cancers as well. Conversely mineral deficiencies are another reason and when you combine high protein intake with decreasing intake of minerals you have a disease in the making through lowering of pH into highly acidic conditions. When protein breaks down in our bodies they break into strong acids.-Unless a treatment actually removes acid toxins from the body and increases oxygen, water, and nutrients most medical interventions come to naught.-These acids must be excreted by the kidneys because they contain sulfur, phosphorus or nitrogen which cannot break down into water and carbon dioxide to be eliminated as the weak acids are. In their passage through the kidneys these strong acids must take a basic mineral with them because in this way they are converted into their neutral salts and don’t burn the kidneys on their way out. This would happen if these acids were excreted in their free acid form.-Substituting a sodium bicarbonate solution for saline infusion prior to administration of radiocontrast material seems to reduce the incidence of nephropathy.[7] – Dr. Thomas P. Kennedy
American Medical Association
Bicarbonate ions neutralize the acid conditions required for chronic inflammatory reactions. Hence, sodium bicarbonate is of benefit in the treatment of a range of chronic inflammatory and autoimmune diseases. Sodium bicarbonate is a well studied and used medicine with known effects. Sodium bicarbonate is effective in treating poisonings or overdoses from many chemicals and pharmaceutical drugs by negating their cardiotoxic and neurotoxic effects.[8] It is the main reason it is used by orthodox oncology – to mitigate the highly toxic effects of chemotherapy.-Sodium bicarbonate possesses the property of absorbing heavy metals, dioxins and furans. Comparison of cancer tissue with healthy tissue from the same person shows that the cancer tissue has a much higher concentration of toxic chemicals, pesticides, etc.-Sodium bicarbonate injection is indicated in the treatment of metabolic acidosis, which may occur in severe renal disease, uncontrolled diabetes, and circulatory insufficiency due to shock or severe dehydration, extracorporeal circulation of blood, cardiac arrest and severe primary lactic acidosis. The acid/alkaline balance is one of the most overlooked aspects of medicine. In general, the American public is heavily acid, excepting vegetarians, and even their bodies have to face increasing levels of toxic exposure, which help turn the body to acidic pH conditions.-For more detailed information feel free to consult my book Sodium Bicarbonate E-Book that’s with a reasonable price, or for a more personal approach check my Consultations page.
[1] http://www.nelm.nhs.uk/en/NeLM-Area/News/2009—July/20/Bicarbonate-supplementation-may-slow-renal-decline-in-chronic-kidney-disease/
[2] Origin of the Bicarbonate Stimulation of Torpedo Electric Organ Synaptic Vesicle ATPase. Joan E. Rothlein 1 Stanley M. Parsons. Department of Chemistry and the Marine Science Institute, University of California, Santa Barbara, Santa Barbara, California, U.S.A.
[3] Levine DZ, Jacobson HR: The regulation of renal acid secretion: New observations from studies of distal nephron segments. Kidney Int 29:1099–1109, 1986
[4] http://www.uptodate.com/patients/content/abstract.do?topicKey=~G/p55S8w8sQDwqG&refNum=28
[5] http://www.ncbi.nlm.nih.gov/pubmed/16523427
[6] news.bbc.co.uk/2/hi/health/7655405.stm
[7] JAMA 2004;291:2328-2334,2376-2377.
http://www.urotoday.com/56/browse_categories/renal_transplantation_vascular_disease/ sodium_bicarbonate_may_prevent_radiocontrastinduced_renal_injury.html
[8] These include, Benzotropines (valium) cyclic antidepressants (amytriptayine), organophosphates, methanol (Methyl alcohol is a cheap and potent adulterant of illicit liquors) Diphenhydramine (Benedryl), Beta blockers (propanalol) Barbiturates, and Salicylates (Aspirin). Poisoning by drugs that block voltage-gated sodium channels produces intraventricular conduction defects, myocardial depression, bradycardia, and ventricular arrhythmias. Human and animal reports suggest that hypertonic sodium bicarbonate may be effective therapy for numerous agents possessing sodium channel blocking properties, including cocaine, quinidine, procainamide, flecainide, mexiletine, bupivacaine, and others.
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Effects of poor eating habits persist even after diet is improvedEK
Date-November 3, 2014
Source-Federation of American Societies for Experimental Biology
Almost everyone knows that improving your eating habits will most likely improve your health. What most people may not know, however, is that the effects of poor eating habits persist long after dietary habits are improved. In a new report appearing in the November 2014 issue of the Journal of Leukocyte Biology, scientists use mice to show that even after successful treatment of atherosclerosis (including lowering of blood cholesterol and a change in dietary habits) the effects of an unhealthy lifestyle still affect the way the immune system functions. This change in function occurs largely because poor eating habits alter the way genes express themselves, including genes related to immunity. This change in gene expression (epigenetics) ultimately keeps the risk of cardiovascular disorders higher than it would be had there been no exposure to unhealthy foods in the first place.–“I hope that this study demonstrates the importance of diet-induced changes in the epigenome and encourages further research into the interaction between dietary patterns, DNA methylation and disease,” said Erik van Kampen, a researcher involved in the work from the Division of Biopharmaceutics at the Leiden Academic Centre for Drug Research at Leiden University in Leiden, The Netherlands.–To make their discovery, scientists used two groups of mice that had an altered gene making them more susceptible to developing high blood cholesterol and atherosclerosis. These mice were either fed a high-fat, high-cholesterol diet (Western-type diet, WTD) or a normal diet (chow). After a long period of feeding, bone marrow was isolated from the mice and transplanted into mice with a similar genetic background that had their own bone marrow destroyed. The recipient mice were left on chow diet for several months, after which the development of atherosclerosis in the heart was measured. The number and status of immune cells throughout the body and epigenetic markings on the DNA in the bone marrow also were examined. They found that DNA methylation, an epigenetic signature, in the bone marrow was different in mice that received bone marrow from the WTD-fed donors compared to the mice receiving bone marrow from chow-fed donors. Furthermore, these mice had large differences in their immune system and increased atherosclerosis.–“We’ve long known that lifestyle and nutrition could affect immune system function,” said John Wherry, Ph.D., Deputy Editor of the Journal of Leukocyte Biology. “The ability of nutritional history to have durable affects on immune cells demonstrated in this new report could have profound implications for treatment of diseases with immune underpinnings. The length of such effects will be critical to determine and it will be interesting to examine the effects of drugs that can modify epigenetics.”–Story Source-The above story is based on materials provided by Federation of American Societies for Experimental Biology. Note: Materials may be edited for content and length.—Journal Reference-E. van Kampen, A. Jaminon, T. J. C. van Berkel, M. Van Eck. Diet-induced (epigenetic) changes in bone marrow augment atherosclerosis. Journal of Leukocyte Biology, 2014; 96 (5): 833 DOI: 10.1189/jlb.1A0114-017R
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Alzheimer’s Disease and Parkinson’s Disease. A Dietary Connection
By Fred Kummerow, Ph.D.
For the past 70 years I have been researching lipids (fats) and their relationship to heart disease. I found that patients who ate an overabundance of deep fat fried foods and too much polyunsaturated fatty acids (PUFAs) produced a chemical change in the composition of their arteries. –When I analyzed the blood of these patients I found that their arteries had an increase of calcification. If these patients continue to eat these oxidized fats, the calcification will completely block their arteries. Heart disease can be prevented if these foods are not consumed. —-The oils generally used in deep fat frying, like soybean oil (and other vegetable oils) are readily oxidized because they contain linoleic and linolenic acids. These acids are easily oxidized. Prolonged exposure to air causes them to pick up oxygen and become oxidized. Repeated use just creates more oxidation.—In my laboratory we have fed weanling rats oils that had been heated at various temperatures. The rats that were fed the high temperature fats (365°F / 180°C) had lower growth rates than the rats that were fed lower temperature fats. Any foods that have been deep fried should be avoided, including potato chips and fried food from fast-food restaurants. Oils that are high in linoleic acid and linolenic acid should be avoided. —-The current research is on Alzheimer’s disease (AD) and Parkinson’s disease (PD.—AD is the most common cause of dementia. During the course of the disease, the chemistry and structure of the brain changes, leading to the death of brain cells. The challenges in AD research today include discovering methods to diagnose patients in an earlier stage and to find new treatments to prevent or cure the disease.–The brain is 81% lipids and over half of these lipids are phospholipids (fatlike, phosphorus-containing substances). PUFAs, which are easily oxidized (combined with oxygen), attach to the phospholipid molecule creating oxidative stress. The damaging consequences of oxidative stress have been implicated in a variety of very different human disorders including arteriosclerosis and diseases of the nervous system. Oxidative stress is an important pathogenic factor in AD. –I believe, just like heart disease patients, people with AD are eating too many polyunsaturated fatty acids (PUFAs) and deep fried foods. The American Heart Association and the National Institute of Health have recommended increasing PUFA consumption and decreasing saturated fat intake. Doing this increases free radicals when it is not offset with enough antioxidant rich fruits and vegetables. —Free radical damage accumulates with age. They may cause cells to function poorly or even die. When free radicals overwhelm the body’s ability to regulate them, oxidative stress occurs. An excess of oxidative stress can lead to the oxidation of lipids and proteins.
The research on preventing heart disease can also be used to prevent brain diseases. Tissue from the brain of someone who had AD is receptive to dyes that do not stain normal tissue suggesting that a chemical change occurred. –I suspect this chemical change occurs during oxidation of PUFAs. Discoverying that PUFAs are easily oxidized in the arterial cells and this could also be a factor in brain cells. The fact that AD is steadily increasing is alerting to the fact that –there is something wrong in the diet of these patients. –The Idea that AD and PD can be alleviated by monitoring the diets of patients with these diseases. A recent study at UCLA has shown that cognitive decline can be reversed by controlling the diet.–Patients eliminated simple carbohydrates and processed food from their diets. They increased their consumption of vegetables and fruits and limited their consumption of fish to non-farmed. The patients increased their sleep to almost 8 hours nightly, exercised 4-5 times per week and reduced their stress with meditation and relaxation.[F3] These patients also fasted three hours between meals and 12 hours between dinner and breakfast[F4]. The personalized therapeutic program was used based on the underlying pathogenesis of AD. Nine out of ten showed improvement and improvements have been sustained after two and one half years. This shows that more extensive therapeutic trials are needed. –The aim of my research is to find a way to prevent AD by analyzing the lipid plasma for two oxysterols. These two oxysterols were present in the plasma of the patients who needed bypass operations and are present in the food supply as frying fats and powdered egg yolk. My hypothesis is based on my studies of preventing calcification of the coronary arteries. I want to show that these two components are in the blood of patients with AD. — Controlling the amount of oxidation and consuming a healthy balanced diet the body can rid itself of the oxidized polyunsaturated fat. If this is the cause of Alzheimer’s disease, proper nutrition will end this terrible disease.[F5]–The diet plan that I would suggest would be to eat three balanced meals a day. Including 3 serving of protein, 5 -8 servings of fruits and vegetables, 3 servings of whole dairy products, at least one egg daily and eliminating simple carbohydrates and processed foods. Adequate amounts of sleep and exercise would also be encouraged. I then hope to continue this research with Parkinson’s disease patients. –.
Fred A. Kummerow, Ph.D.
Adjunct professor in biochemistry at the University of Illinois
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Biological fat with a sugar attached essential to maintaining brain’s supply of stem cells
Date-November 3, 2014
Source-Medical College of Georgia at Georgia Regents University
Dr. Robert Yu, MCG neuroscientist and corresponding author of the study in The Journal of Neuroscience and Dr. Jing Wang, MCG postdoctoral fellow and the study’s first author.
Fat and sugar aren’t usually considered healthy staples, but scientists have found that a biological fat with a sugar attached is essential for maintaining the brain’s store of stem cells.–Neural stem cells help the brain develop initially, then repopulate brain cells lost to usual cell turnover as well as to a trauma or malady, such as a head injury or stroke.–While the cell population and activity decrease as a natural part of aging, scientists at the Medical College of Georgia at Georgia Regents University are studying how neural stem cells are normally maintained with the long-term goal of helping the supply stay robust despite aging as well as infirmity.–They have discovered that in mice missing the sugar containing lipid ganglioside GD3, neural stem cells have a dramatically impaired ability to self-renew, said Dr. Robert K. Yu, MCG neuroscientist and corresponding author of the study in The Journal of Neuroscience.–The scientists focused on brain areas with typically the largest supply of neural stem cells: an area just below several midbrain cavities filled with cerebrospinal fluid, called the subventricular zone, as well as the hippocampus, a major center for learning and memory.–Mice missing ganglioside GD3 on the membranes of neural stem cells had much smaller supplies of the cells in these key areas throughout life and expressed signs of lost hope with behaviors such as not actively seeking dry land when placed in water, Yu said. Additionally, the mice had impaired maintenance of the area of the brain involved in the sense of smell as well as the portion of the hippocampus that enables formation of new memories.–The changes, which correlate with aging or illness, were corrected when GD3 was restored.–“If GD3 is missing, we found these neural stem cells cannot be maintained throughout life; they are reduced by a big percentage even in a one-month-old mouse,” said Dr. Jing Wang, MCG postdoctoral fellow and the study’s first author. In fact, by one month of life, there was about a 60 percent reduction in the supply and by six months, which is considered aged in a mouse, there were only a handful of neural stem cells remaining, Wang said.–The scientists note that in healthy young mice, GD3 is abundant but seems to naturally decrease with age.–A Yu and Wang paper published in the journal PNAS in 2013 showed that GD3 is the predominant ganglioside in mouse neural stem cells where it interacts with epidermal growth factor receptors, also found on the cell surface. GD3 plays an important role in growth factor signaling, which, in turn, tells neural stem cells to proliferate or die.–“In a normal situation, that growth factor enables the neural stem cells to reproduce more stem cells,” Wang said. “This gives us a better idea about how our neural stem cell population is maintained over our life. Our long-term goal is to use endogenous neural stem cells for repair of brain or spinal cord damage, so we need to learn how they proliferate, how to keep them inside the brain.”–The two are optimistic that one day manipulating levels of growth factors and sugar-containing lipids will enable a more steadfast supply of neural stem cells throughout life, although getting the substances into the brain is a challenge. It’s already known that, at least in rats, exercise can also help.–Neural stem cells are able to self-renew, in theory at least, forever. Their ability to maintain a steady supply of themselves and to differentiate into different types of brain cells are their most important properties, Yu said.–Next steps include examining the role of other growth factors and gangliosides.–Yu is the Georgia Research Alliance Eminent Scholar Chair in Molecular and Cellular Neurobiology. The studies were funded by the National Institutes of Health and the Veterans Administration.-Story Source-The above story is based on materials provided by Medical College of Georgia at Georgia Regents University. Note: Materials may be edited for content and length.–Journal Reference-J. Wang, A. Cheng, C. Wakade, R. K. Yu. Ganglioside GD3 Is Required for Neurogenesis and Long-Term Maintenance of Neural Stem Cells in the Postnatal Mouse Brain. Journal of Neuroscience, 2014; 34 (41): 13790 DOI: 10.1523/JNEUROSCI.2275-14.2014
Suggestions to consider—MCT Oils- Glycerol—Octacosanol—ATP—Ribose—Saturated Fats—these are components that activate the body on several fronts and support immune functions—regeneration—immune protecting—
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Show of the Month November 15 2014
This Drug Has Sickened Thousands of Animals – Will It Be At Your Holiday Feast?
Startling decline in European birds- Majority of losses from most common species
Ignoring This will cost You
37 Million Bees Found Dead In Ontario, Canada After Planting Large GMO Corn Field
Glyphosate-based herbicides are toxic and endocrine disruptors in human cell lines- Glyphosate-based herbicides toxicity
Time- and dose-dependent effects of roundup on human embryonic and placental cells – Glyphosate inhibits beneficial gut bacteria
HOW WELL DO FLU VACCINES WORK
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This Drug Has Sickened Thousands of Animals – Will It Be At Your Holiday Feast?
I have been to countless holiday meals when I had no control over the ingredients. Of course, I ate what was offered and was polite but knowing what I know now about what’s really in food – it’s hard for me to just shut up and take it. The more we shut up and take it, the more disgusting things like what I am about to share with you continue to happen. That’s why I am sharing these important facts about how to avoid drugged up turkeys this holiday season.
I know it’s tempting this time of year when you get coupons from the grocery store offering a whole turkey for FREE in exchange for shopping in their store. These “FREE” store-brand turkeys generally aren’t free of antibiotics and are raised on a diet of GMOs. Most conventionally raised (non-organic) turkeys are pumped full of antibiotics, and this overuse of antibiotics is creating a major human health issue.. There is another drug that is permitted to be fed to turkeys in the U.S. that is banned in dozens of countries due to health issues. You won’t find it on the label, it’s been shown to leave residues in the meat, and the meat companies are not required to tell you whether they use it.—–I’m talking about Topmax (otherwise known as Ractopamine).-Ractopamine is a growth enhancing drug that’s fed to some turkeys to increase their muscle mass. Basically, it’s used to make big turkeys look perfect for a big Holiday feast. We’ve been conditioned to think that “bigger is better” – but when it comes to turkey, its not! This drug has been shown to cause horrible health problems (and even the death of) animals, as can be witnessed by it’s rampant use on pigs during the last decade. As reported by NBC News, “Since it was introduced, ractopamine had sickened or killed more than 218,000 pigs as of March 2011, more than any other animal drug on the market, a review of FDA veterinary records shows. Pigs suffered from hyperactivity, trembling, broken limbs, inability to walk and death, according to FDA reports released under a Freedom of Information Act request.”–It’s fed to some conventional turkeys, and we might be eating it too.-Residues of ractopamine have been found in meat samples tested by the USDA and Consumer Reports. This is because there’s no mandatory withdrawal period for the drug, which can be fed to turkeys right up until the day they are slaughtered. The FDA established some “safe maximum residue limits” (MRLs) for ractopamine residue, so they are allowing some of this residue to remain in the meat sold at the store. Most meat is never tested for ractopamine residues, so it’s anyone’s guess how much we are really eating. That’s frightening, considering that ractopamine carries a bold warning label that states:
“NOT FOR HUMAN USE”
Label for TopmaxWhy is this permitted?
The FDA has allowed widespread use of ractopamine in turkey feed since its approval in 2008. This led the Animal Legal Defense Fund and the Center For Food Safety to file a legal petition with FDA demanding that they conduct comprehensive scientific studies that document the risks of ractopamine to human and animal health – because clearly more needed to be done before it gained FDA approval. The FDA approved ractopamine based on safety studies submitted by the company that makes it (Elanco), which is standard for most food and drugs on the market, and have reportedly refused to share their records. To date, ractopamine is still allowed to be fed to turkeys, cows, and pigs (up to 80% of pigs eat ractopamine-laced feed).
Other countries don’t take the use of ractopamine so lightly. For instance, China and Taiwan prohibit any traces of ractopamine residue in meat, and have rejected some U.S. exports. Also any meat exported to the European Union needs to be certified as ractopamine-free or it will be rejected.
Jennie-O’s customer service agent told us that it’s not routinely used and only used on a limited basis if necessary — whatever that means, because ractopamine is not a “necessary” drug used to treat disease. Jennie-O indicated that there would be no way of knowing at the store if their turkeys were fed ractopamine because it’s not labeled or otherwise indicated.
According to Safeway Grocery Stores – “Ractopamine is a growth promotant that can be feed to turkeys so our Safeway Farms turkey may or may not have the promotant in their feed. To guarantee that growth promotant was not part of the diet, please choose our Open Nature or O Organics brands which do not allow growth promotants.”
As these companies aren’t required to disclose whether ractopamine is used, and their claims are not third-party certified, it’s difficult to confirm its use. Even turkeys that are labeled “No Hormones Added” or “Raised Without Hormones” may have still been fed ractopamine to promote growth (because it is not a hormone), so don’t be fooled by this label. Growth hormones aren’t allowed to be used in raising poultry, so this label is meaningless and used as a marketing trick when labeled on turkeys (such as Butterball).
BREAKING NEWS UPDATE!
I just found out that two lawsuits were filed against the FDA yesterday (11/6/14), as reported in the Wall Street Journal, “In two different lawsuits filed on Thursday…groups including the Center for Food Safety, the Humane Society of the United States and United Farm Workers of America argue that in approving drugs like Topmax, a medicated feed additive used to produce lean muscle instead of fat, the FDA failed to adequately consider the drugs’ collective effects on animal welfare, worker safety, wildlife and U.S. waterways”. Both of these lawsuits are asking the Court to set aside FDA’s unlawful approval of these drugs until the FDA issues a more thorough environmental analyses. You can read these Complaints here and here.
From Humane Society, et al:
“FDA approved Ractopamine for use in pigs in 1999 under the brand name Paylean, and subsequently approved Ractopamine for cattle and turkeys under the brand names Optaflexx and Topmax, respectively. Since its initial approval as Paylean, Ractopamine use has increased significantly in the pork, beef, and turkey industries”–“Today, Ractopamine is fed to approximately 60% to 80% of pigs, cattle, and turkeys raised in the United States”–“The FDA also apparently failed to provide for any public or expert comment on its NEPA analysis for Topmax”.
From The Center for Food Safety, et al:
“FDA does not require any withdrawal period for ractopamine before slaughter. A 2006 scientific study concluded “there is a possibility that adulteration of feed with ractopamine could result in residues in animal tissues and lead to human poisoning.” A 2013 Consumer Reports test of 240 U.S. pork products found that about one in five tested positive for ractopamine residues”
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Startling decline in European birds- Majority of losses from most common species
Date:
November 2, 2014 Source:University of Exeter
Around 90 percent of these losses were from the 36 most common and widespread species, including house sparrows, skylarks, grey partridges and starlings.–Bird populations across Europe have experienced sharp declines over the past 30 years, with the majority of losses from the most common species, say the University of Exeter, the RSPB and the Pan-European Common Bird Monitoring Scheme (PECBMS) in a new study. However numbers of some less common birds have risen.-The study, published today in the journal Ecology Letters, reveals a decrease of 421 million individual birds over 30 years. Around 90 percent of these losses were from the 36 most common and widespread species, including house sparrows, skylarks, grey partridges and starlings, highlighting the need for greater efforts to halt the continent-wide declines of our most familiar countryside birds.–Richard Inger from the University of Exeter said: “It is very worrying that the most common species of bird are declining rapidly because it is this group of birds that people benefit from the most.”–“It is becoming increasingly clear that interaction with the natural world and wildlife is central to human wellbeing and significant loss of common birds could be quite detrimental to human society.”–Birds provide multiple benefits to society. They help to control agricultural pests, are important dispersers of seeds, and scavenging species play a key role in the removal of carcasses from the environment. In addition, for many people birds are the primary way in which they interact with wildlife, through listening to bird song, enjoying the sight of birds in their local environment, feeding garden birds and through the hobby of bird watching.–The majority of the declines can be attributed to considerable losses from relatively few common birds, but not all common species are declining. Numbers of great tits, robins, blue tits and blackbirds were all shown to be increasing. Populations of rarer species, including marsh harriers, ravens, buzzards and stone curlews have also shown increases in recent years: this is likely to be the result of direct conservation action and legal protection in Europe.–Head of Species Monitoring and Research at the RSPB’s Centre for Conservation Science Richard Gregory said: “The rarer birds in this study, whose populations are increasing, have benefited from protection across Europe. For example, white storks and marsh harriers receive among the highest level of protection in the EU — this is why their numbers have increased. The conservation and legal protection of all birds and their habitats in tandem are essential to reverse declines.–“This is a warning from birds throughout Europe. It is clear that the way we are managing the environment is unsustainable for many of our most familiar species.”–Petr Vorisek from the PECBMS said: “The study brings a very important message to conservation practice in Europe. This would not have been possible without thousands of skilled volunteer fieldworkers who count birds according to high scientific standards and contribute their data to the national monitoring schemes.”–Conservation efforts tend to be focused on rarer species but the research suggests that conservationists should also address issues affecting common birds, for example those traditionally associated with farmland. The decline in bird populations can be linked to modern farming methods, deterioration of the quality of the environment and habitat fragmentation, although the relative importance of these pressures remains unclear.–The study brought together data on 144 species of European bird from many thousands of individual surveys in 25 different countries, highlighting the value of the different national monitoring schemes increasingly working together. The researchers suggest that greater conservation funding and effort should be directed to wider scale environmental improvement programmes. These could include urban green space projects, and effective agri-environment schemes, which, informed by lessons learned from past schemes, should aim to deliver real outcomes for declining bird species whether they are rare or common.–Story Source-The above story is based on materials provided by University of Exeter.-Journal Reference-Richard Inger, Richard Gregory, James P. Duffy, Iain Stott, Petr Voříšek, Kevin J. Gaston. Common European birds are declining rapidly while less abundant species’ numbers are rising. Ecology Letters, 2014; DOI: 10.1111/ele.12387
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Ignoring This will cost You
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37 Million Bees Found Dead In Ontario, Canada After Planting Large GMO Corn Field
Millions of bees dropped dead after GMO corn was planted few weeks ago in Ontario, Canada. The local bee keeper, Dave Schuit who produces honey in Elmwood lost about 37 million bees which are about 600 hives.–“Once the corn started to get planted our bees died by the millions,” Schuit said. While many bee keepers blame neonicotinoids, or “neonics.” for colony collapse of bees and many countries in EU have banned neonicotinoid class of pesticides, the US Department of Agriculture fails to ban insecticides known as neonicotinoids, manufactured by Bayer CropScience Inc.–Two of Bayer’s best-selling pesticides, Imidacloprid and Clothianidin, are known to get into pollen and nectar, and can damage beneficial insects such as bees. The marketing of these drugs also coincided with the occurrence of large-scale bee deaths in many European countries and the United States.–Nathan Carey another local farmer says that this spring he noticed that there were not enough bees on his farm and he believes that there is a strong correlation between the disappearance of bees and insecticide use.–In the past, many scientists have struggled to find the exact cause of the massive die-offs, a phenomenon they refer to as “colony collapse disorder” (CCD). In the United States, for seven consecutive years, honeybees are in terminal decline.–US scientists have found 121 different pesticides in samples of bees, wax and pollen, lending credence to the notion that pesticides are a key problem. “We believe that some subtle interactions between nutrition, pesticide exposure and other stressors are converging to kill colonies,” said Jeffery Pettis, of the ARS’s bee research laboratory.-The collapse in the global honeybee population is a major threat to crops. It is estimated that a third of everything we eat depends upon honeybee pollination, which means that bees contribute over 30 billion to the global economy.–A new study published in the Journal Proceedings of the National Academy of Sciences revealed that neonicotinoid pesticides kill honeybees by damaging their immune system and making them unable to fight diseases and bacteria.–After reporting large losses of bees after exposure to Imidacloprid, banned it for use on corn and sunflowers, despite protests by Bayer. In another smart move, France also rejected Bayer’s application for Clothianidin, and other countries, such as Italy, have banned certain neonicotinoids as well.–After record-breaking honeybee deaths in the UK, the European Union has banned multiple pesticides, including neonicotinoid pesticides.
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Glyphosate-based herbicides are toxic and endocrine disruptors in human cell lines
Glyphosate-based herbicides are the most widely used across the world; they are commercialized in different formulations. Their residues are frequent pollutants in the environment. In addition, these herbicides are spread on most eaten transgenic plants, modified to tolerate high levels of these compounds in their cells. Up to 400 ppm of their residues are accepted in some feed. We exposed human liver HepG2 cells, a well-known model to study xenobiotic toxicity, to four different formulations and to glyphosate, which is usually tested alone in chronic in vivo regulatory studies. We measured cytotoxicity with three assays (Alamar Blue®, MTT, ToxiLight®), plus genotoxicity (comet assay), anti-estrogenic (on ERα, ERβ) and anti-androgenic effects (on AR) using gene reporter tests. We also checked androgen to estrogen conversion by aromatase activity and mRNA. All parameters were disrupted at sub-agricultural doses with all formulations within 24 h. These effects were more dependent on the formulation than on the glyphosate concentration. First, we observed a human cell endocrine disruption from 0.5 ppm on the androgen receptor [F6]in MDA-MB453-kb2 cells for the most active formulation (R400), then from 2 ppm the transcriptional activities on both estrogen receptors were also inhibited on HepG2[F7]. Aromatase transcription and activity were disrupted from 10 ppm. Cytotoxic effects started at 10 ppm with Alamar Blue assay (the most sensitive), and DNA damages at 5 ppm. A real cell impact of glyphosate-based herbicides residues in food, feed or in the environment has thus to be considered, and their classifications as carcinogens/mutagens/reprotoxics is discussed.
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Glyphosate-based herbicides toxicity
Roundup (R) was highly toxic on human cells, from 10-20 ppm, far below agricultural dilutions. This occurred on hepatic (HepG2, Hep3B and embryonic (HEK293) as well on placental (JEG3) cell lines, but also on human placental extracts, primary umbilical cord cells (HUVEC) and freshly isolated testicular cells (Richard et al. 2005; Benachour et al. 2007; Benachour & Seralini 2009; Gasnier et al. 2010; Clair et al. 2012). All formulations cause total cell death within 24 h, through an inhibition of the mitochondrial succinate dehydrogenase activity, and necrosis, through the release of cytosolic adenylate kinase measuring membrane damage. They also induced apoptosis through the activation of enzymatic caspases 3 / 7 activities. Most importantly, the R commercialized formulation is always more toxic than the active principle alone, the glyphosate (G). These effects were more dependent on the formulation and thus adjuvants content than on the G concentration. We recently measured compositions and effects of 9 Gbased formulations and identified ethoxylated adjuvants (commonly called POEA) asthe active principle of cytotoxicity (Messnage et al. 2012a). However, these are considered as inert diluents in international regulations and are not taken into account for chronic effects which are insufficiently tested, and only with G in pre-commercial testing. We previously underlined this loophole (Mesnage 2010). Long term feeding and reproductive trials with pesticides are the only tests long enough to reveal a potential endocrine disruption which was consequently never studied for R until recently (Seralini et al. 2012), however it was for G by itself. We investigated it by measuring androgen to estrogen conversion by aromatase activity and mRNA on placental human cells and showed that G interacts with the active site of the purifed enzyme (Richard et al. 2005). Both parameters were disrupted at subagricultural doses within 24 h. We also observed a human cell endocrine disruption from 0.5 ppm on the androgen receptor in transfected cells, and then from 2 ppm the transcriptional activities on both estrogen receptors which were also inhibited (Gasnier et al. 2009). Aromatase transcription and activity were disrupted from 10 ppm on
HepG2. On freshly isolated rat testicular cells, low non-toxic concentrations of R and G (1 ppm) induced a testosterone decrease by 35 % (Clair et al. 2012). This is expected to occur in human cells which are fitted with the same steroidogenic equipment. G-based formulations are claimed to have been extensively studied by industry and regulatory agencies and are considered as one of the safest pesticides (Williams et al.2000). This allowed the establishment of high maximum residue limits (MRL) for GM food / feed (up to 400 ppm). For instance, 20 ppm of G are authorized in GM soy and this MRL is in the range of concentrations typically found in a GM soy harvest. In the light of our results, the safety of these thresholds is clearly challenged.
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Time- and dose-dependent effects of roundup on human embryonic and placental cells.
Benachour N1, Sipahutar H, Moslemi S, Gasnier C, Travert C, Séralini GE.
Author information
Abstract
Roundup is the major herbicide used worldwide, in particular on genetically modified plants that have been designed to tolerate it. We have tested the toxicity and endocrine disruption potential of Roundup (Bioforce on human embryonic 293 and placental-derived JEG3 cells, but also on normal human placenta and equine testis. The cell lines have proven to be suitable to estimate hormonal activity and toxicity of pollutants. The median lethal dose (LD(50)) of Roundup with embryonic cells is 0.3% within 1 h in serum-free medium, and it decreases to reach 0.06% (containing among other compounds 1.27 mM glyphosate) after 72 h in the presence of serum. In these conditions, the embryonic cells appear to be 2-4 times more sensitive than the placental ones. In all instances, Roundup (generally used in agriculture at 1-2%, i.e., with 21-42 mM glyphosate) is more efficient than its active ingredient, glyphosate, suggesting a synergistic effect provoked by the adjuvants present in Roundup. We demonstrated that serum-free cultures, even on a short-term basis (1 h), reveal the xenobiotic impacts that are visible 1-2 days later in serum. We also document at lower non-overtly toxic doses, from 0.01% (with 210 microM glyphosate) in 24 h, that Roundup is an aromatase disruptor. The direct inhibition is temperature-dependent and is confirmed in different tissues and species (cell lines from placenta or embryonic kidney, equine testicular, or human fresh placental extracts). Furthermore, glyphosate acts directly as a partial inactivator on microsomal aromatase, independently of its acidity, and in a dose-dependent manner. The cytotoxic, and potentially endocrine-disrupting effects of Roundup are thus amplified with time. Taken together, these data suggest that Roundup exposure may affect human reproduction and fetal development in case of contamination. Chemical mixtures in formulations appear to be underestimated regarding their toxic or hormonal impact.
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Glyphosate inhibits beneficial gut bacteria
Tuesday, Jan. 8, 2013 – A new study published in the journal Current Microbiology describes the harmful effect of glyphosate on intestinal bacteria in poultry. The evidence is that glyphosate is toxic to beneficial bacteria such as Enterococcus faecalis, Enterococcus faecium, Bacillus badius, Bifidobacterium adolescentis and Lactobacillus spp, while pathogenic bacteria such as Salmonella Entritidis, Salmonella Gallinarum, Salmonella Typhimurium, Clostridium perfringens and Clostridium botulinum are highly resistant to glyphosate.–A reduction of beneficial bacteria in the gastrointestinal tract disturbs the normal gut bacterial community and allows salmonella and clostridia species to grow unchecked thus increasing the incidence of these two diseases.–The researchers pointed out that glyphosate also has the potential to induce genetic mutations within bacteria, making it possible for a new level of pathogenicity to emerge following chronic exposure to this chemical.- Oral bioavailability of glyphosate: studies using two intestinal cell lines.
Vasiluk L1, Pinto LJ, Moore MM.–Author information –Abstract
Glyphosate is a commonly used nonselective herbicide that inhibits plant growth through interference with the production of essential aromatic amino acids. In vivo studies in mammals with radiolabeled glyphosate have shown that 34% of radioactivity was associated with intestinal tissue 2 h after oral administration. The aim of our research was to investigate the transport, binding, and toxicity of glyphosate to the cultured human intestinal epithelial cell line, Caco-2, and the rat small intestinal crypt-derived cell line, ileum epithelial cells-18 (IEC-18). An in vitro analysis of the transport kinetics of [14C]-glyphosate showed that 4 h after exposure, approximately 8% of radiolabeled glyphosate moved through the Caco-2 monolayer in a dose-dependent manner. Binding of glyphosate to cells was saturable and approximately 4 x 10(11) binding sites/cell were estimated from bound [14C]. Exposure of Caco-2 cells to > or =10 mg/ml glyphosate reduced transmembrane electrical resistance (TEER) by 82 to 96% and increased permeability to [3H]-mannitol, indicating that paracellular permeability increased in glyphosate-treated cells. At 10-mg/ml glyphosate, both IEC-18 and Caco-2 cells showed disruption in the actin cytoskeleton. In Caco-2 cells, significant lactate dehydrogenase leakage was observed when cells were exposed to 15 mg/ml of glyphosate. These data indicate that at doses >10 mg/ml, glyphosate significantly disrupts the barrier properties of cultured intestinal cells
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HOW WELL DO FLU VACCINES WORK? FALL CAMPAIGN IS IN FULLSWING
One easily gets the impression that the answer is very well indeed. Get your shot and you will be protected. Flu vaccination has become mandatory in many health care institutions. No shot and either wear a mask or quit. One would expect that most would be protected. The efficacy (relative risk reduction in controlled trials) is typically 50-60 % and can go higher, especially for children. Vaccine Manufacturers and promoters would of course like it close to 100% which would justify the claim if one gets their shot, they won’t get the flu. If one took an exit poll was taken from a vaccination clinic at a local mall, probably a surprising number would say just that. Thus it is of interest to look at two recent meta-analyses and examine the other side of the coin, the absolute benefits, a taboo subject in this field. International Health News November 2014 Page 7 –Recently, Ossterholm et al16 examined the efficacy of influenza vaccination as indicated by studies that were randomized, placebo controlled and where the cases were laboratory verified as viral influenza. It was required that vaccine efficacy be reported for all circulating influenza strains. Meta analyses of qualifying trials were conducted separately for adults and children or just adults A second recent study by Tricco et al17 compared the efficacy of influenza vaccines depending on whether or not they were matched to at least one of the strains circulating that year. Both matched and unmatched randomized controlled trials involving either trivalent inactivated vaccine (TIV) or nasal spray containing live attenuated influenza vaccine (LAIV) were analyzed. All the meta analyses had a mixture of studies involving children and adults in varying proportions, but more than half of the studies using LAIV involved children. The results of these two studies are given in the table below. Both papers provided enough information to calculate absolute results, actually by two methods which gave very close to identical results. The published papers ignored absolute results.
VACCINE EFFICACY IN RECENT META -ANALYSES
Study STUDIES Age NNT RRR No Benefit Vaccine
Osterholm16 8 18-64 64 60% 98.4% TIV
Osterholm 16 7 0.5-7 8 84% 87.3% LAIV
Trico17 12 A&C 93 62% 98.9% TIV-Matched
Tricco17 11 A&C 204 51% 99.5% TIV-Mismatched
Tricco17 15 A&C 18 77% 94.4% LAIV-Matched
Tricco17 15 A&C 48 60% 97.9% LAIV-Mismatched
TIV—Trivalent inactivated vaccine. LAIV—Live attenuated influenza vaccine.
NNT—Number needed to treat. RRR—Relative risk reduction. A&C—adults and children. Note that most of the relative risk reductions (RRR) are impressive. Those who do not understand relative risk reduction will assume that for example, a RRR of 60% means that 60% of those vaccinated will not get the flu. However, only 1.6% will actually benefit whereas 98.4 will not. The magnitude of the relativemrisk reduction is related to the absolute risk reduction divided by the absolute risk in the control group, and thus can be very large for small absolute benefits in the case of disorders or diseases that have a low population incidence, which is the case with the flu in adults. Children have a higher untreated population risk, but it is still only generally only a few percentage points. Risk reductions are generally adjusted for confounding, and but these can be used to calculate the adjusted absolute risk reduction and number needed to treat. Note also that the RRR correlate rather poorly with the NNT, something at the very heart of the problem of using the RRR. The above table suggests that independent of the type of the vaccine or how well it matches the strains during a given year, most vaccinated individuals do not benefit but must simply hope they are lucky. For TIV, a very common vaccine, mismatching does not seem to make much difference. However, the benefit for children from the LAIV is quite strong, as seen in the analysis involving LAIV by Osterholm et al and in the two by Tricco et al involving both LAIV which had heavy representation of children in the studies included, since it is the popular vaccine type for children. While numbers needed to treat of 8 are not common in clinical trials or their pooled analyses, it is unfortunately still true, as shown in the table, that even with such a low number, most do not benefit. There is very little data for those over 65 of age. The analysis by Osterholm et al prompted a number of comments in the literature. It is interesting in these comments that the focus was universally on relative risk reduction, never on the percentage treated that do or do not benefit, i.e. the absolute results. This appears to be a taboo point of view. Commentators worried that the “modest” relative risk reductions in the 50% range would be used by critics to discourage vaccination, but if this is the case, the more realistic view based on absolute benefit would rightly terrify proponents of this popular public health intervention and the related desire to develop herd immunity. Furthermore, there is always the worrisome problem that adverse effects have been suppressed by the industry, certainly far from an unheard of approach to doing business; therefore one cannot do a risk/benefit analysis.-The above results are a nice example of how a given set of trial results can be presented in different ways (another term is spin) that either accentuate the positive or provide a more realistic view. For those who find this hard to believe, an appendix at the end of this issue is included which gives a sample calculation. The potential for creating unrealistic expectations is obviously great and an almost universally used approach. It seems worth mentioning in passing that pregnant women, if they decide to get a flu shots, should demand the mercury free one which generally comes in a single dose vial not a septum capped little bottle. Live attenuated influenza vaccine which is delivered as a nasal spray, in generally mercury free. However, given that the vaccine preparation may have other dangers to the fetus aside from mercury toxicity which may be unknown or suppressed, perhaps the dismal percentage of adults benefiting should be given considerable weight by this special group. What should one do? There do not appear to be studies that have provided strong evidence concerning actions found to dramatically reduce the risk of the flu. Mainstream medicine regards the problem solved with vaccination. While maintaining a vitamin D status that is sufficient or more than just sufficient can be justified from a number of studies and is easy and inexpensive to accomplish and justified for a large number of other reasons, definitive studies have yet to appear. The subject of maintaining a high level of immune response will have to wait for a future issue of IHN.
CDC REPORTS INFLUENZA OUTBREAK IN A VACCINATED POPULATION
On October 24, 2014 the Centers for Disease Cont rol in its Morbidity and Mortality Report described a flu outbreak among the crew of a navy ship moored in San Diego. In February of 2014, 25 cases of influenza, of which 20 were influenza A, occurred over a short period among a crew of 102. Ninety-nine percent of the crew had been vaccinated with a vaccine very well matched with the flu viruses circulating in 2013-14. The fact that it was influenza was documented by laboratory tests. The headline in the New England Journal of Medicine’s daily online Journal Watch of October 24 read as follows: Flu Outbreak Aboard Navy Ship Highlights Possibility of Illness in Vaccinated Populations. The interesting word is “possibility.” Reference to the above table indicates that 94.4% to 98.9% of vaccinated populations are not protected with a matched vaccine, depending on the type of vaccine, and the 94.4% is due in part to heavy weighting from children. These results apply to large pooled populations and studies covered a number of years. Of the 25 flu cases, 16 received the TIV form, 8 the LAIV and one was unvaccinated. Using the term “possibly” seems rather an understatement. According to the CDC report, Tamiflu was given to the crew to “reduce the impact and spread of the disease.” This is the same antiviral that has been discredited and found virtually useless after huge amounts of government funds throughout the world were spend stockpiling it. See the February 2013 issue of IHN for the full story of the shocking Tamiflu saga.
Reference List
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2. Cullmann M, Hilding A, Ostenson CG. Alcohol consumption and risk of pre-diabetes and type 2 diabetes
development in a Swedish population. Diabet Med. 2012;29:441-452.
3. Marfella R, Cacciapuoti F, Siniscalchi M et al. Effect of moderate red wine intake on cardiac prognosis after
recent acute myocardial infarction of subjects with Type 2 diabetes mellitus. Diabet Med. 2006;23:974-981.
4. Knoops KT, de Groot LC, Kromhout D et al. Mediterranean diet, lifestyle factors, and 10-year mortality in
elderly European men and women: the HALE project. JAMA. 2004;292:1433-1439.
5. Blomster JI, Zoungas S, Chalmers J et al. The relationship between alcohol consumption and vascular
complications and mortality in individuals with type 2 diabetes. Diabetes Care. 2014;37:1353-1359.
6. Karatzi K, Karatzis E, Papamichael C, Lekakis J, Zampelas A. Effects of red wine on endothelial function:
postprandial studies vs clinical trials. Nutr Metab Cardiovasc Dis. 2009;19:744-750.
7. Karatzi K, Papamichael C, Karatzis E et al. Postprandial improvement of endothelial function by red wine and
olive oil antioxidants: a synergistic effect of components of the Mediterranean diet. J Am Coll Nutr.
2008;27:448-453.
8. Natella F, Macone A, Ramberti A et al. Red wine prevents the postprandial increase in plasma cholesterol
oxidation products: a pilot study. Br J Nutr. 2011;105:1718-1723.
9. Natella F, Ghiselli A, Guidi A, Ursini F, Scaccini C. Red wine mitigates the postprandial increase of LDL
susceptibility to oxidation. Free Radic Biol Med. 2001;30:1036-1044.
10. Wu Y, Ding Y, Tanaka Y, Zhang W. Risk Factors Contributing to Type 2 Diabetes and Recent Advances in the
Treatment and Prevention. Int J Med Sci. 2014;11:1185-1200.
11. Li G, Zhang P, Wang J et al. The long-term effect of lifestyle interventions to prevent diabetes in the China Da
Qing Diabetes Prevention Study: a 20-year follow-up study. Lancet. 2008;371:1783-1789.
12. Wilson PW, Meigs JB, Sullivan L, Fox CS, Nathan DM, D’Agostino RB, Sr. Prediction of incident diabetes
mellitus in middle-aged adults: the Framingham Offspring Study. Arch Intern Med. 2007;167:1068-1074.
13. Taylor R. Type 2 diabetes: etiology and reversibility. Diabetes Care. 2013;36:1047-1055.
14. Lim EL, Hollingsworth KG, Aribisala BS, Chen MJ, Mathers JC, Taylor R. Reversal of type 2 diabetes:
normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol.
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systematic review and meta-analysis. Lancet Infect Dis. 2012;12:36-44.
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strains: a systematic review and meta-analysis. BMC Med. 2013;11:153.
APPENDIX
Pooled data from 8 studies, adults 18-64 years of age, given trivalent inactivated influenza vaccine compared to unvaccinated controls. Cases laboratory -validated as viral influenza. Taken from Figure 2.16
THE RAW DATA
Vaccinated Control
Cases of flu 221 357
Total in group 18,797 13,095
CALCULATIONS
Flu Case %: (221/18,797) X 100 = 1.118%, No Flu % (357/13,095) X 100 = 2.730%,
Percentage who benefited: 2.730% — 1.118% = 1.55% or 1.55 per 100
Percentage with no benefit: 100% – 1.55% = 98.4%
The absolute risk reduction produced by vaccination was the percentage that benefited, 1.55% is the difference between the flu rates in the two groups, expressed as a percentage rather than probability, i.e. 0.0155. If 1.55/100 had benefit, how many must be vaccinated for one to benefit? It is calculated from 1.55/100 = 1/x and thus x = 64. This number needed to treat for one individual to benefit, i.e. not get the viral flu, and is the NNT. Put another way, it is the reciprocal of the absolute risk reduction expresses as a probability (range 1.0 to 0), not a percentage, i.e. NNT = 1/0.0155. The time interval is approximately the flu season. The unadjusted risk ratio 0.4 is obtained from the ratio 1.118/ 2.730 = 0.4 and the relative risk reduction (RRR) was 1 — 0.4 = 0.60 or as a percentage 60%. Why is this true? Details. Risk ratio = (case % in treated group)/(case % in untreated group) = T/U. But 1 = (T/U) = (U – T)/U = RRR, the relative risk reduction obtained comparing the % of cases prevented to the case % in the untreated (control) group. The same calculation can be done without expressing the numbers as percentages, since the 100 cancels out. Thus the four numbers, i.e. the cases and size of the groups, constitute the input data that produce these various final results used to express how well the treatment works. The 60% RRR looks great, the number who do not benefit looks terrible. Same data, just different presentations, both correct. Some think that by getting the vaccination they will not get the flu, some think that their risk is reduced by 60%, but interpret this by thinking that if a group of 100 are vaccinated, 60 will not get the flu. In fact, if 100 are vaccinated, between 1 and 2 individuals will be protected and 98% to 99% will not be protected. This is what the critics of the use of relative risk reductions are talking about, but no one is listening. Why spoil a nice picture based on a perfectly valid calculation. It is also noteworthy that when a disease or disorder has a very small population prevalence reflected by the percentage of cases in the control group, this forces the NNT and the percentage that do not benefit into the range seen in this example. This is the consequence of treating a group where the vast majority will not become cases, treatment or no treatment. One can argue that treatment is still desirable, but one must not have unrealistic expectations, and now the risk of adverse side effects becomes a major issue. Small absolute benefits and large NNT should stimulate research to find something better. Instead the RRR becomes a powerful marketing and public health tool.
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Show of the Month November 22 2014
Synthetic biology- First functional ‘designer’ chromosome in yeast synthesized by scientists–
Scientists ‘boot up’ a bacterial cell with a synthetic genome
Repeated Oral AdministrationHistopathological and ultra structural effects of nanoparticles on rat testis following 90 days
High-fat diet postpones brain aging in mice
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Synthetic biology– ‘Telomerator’ reshapes synthetic yeast chromosome into more flexible, realistic form, redefining what geneticists can build
Date:
November 3, 2014
Source:
NYU Langone Medical Center / New York University School of Medicine
The telomerator can reformat the “clockface” of a synthetic yeast chromosome into 12 unique linear “timelines,” or chromosomes of equal length.
Credit: Courtesy of NYU Langone.–NYU Langone yeast geneticists report they have developed a novel tool — dubbed “the telomerator” — that could redefine the limits of synthetic biology and advance how successfully living things can be engineered or constructed in the laboratory based on an organism’s genetic, chemical base-pair structure.–Synthetic biologists aim to use such “designer” microorganisms to produce novel medicines, nutrients, and biofuels[F8].–In a report in the Proceedings of the National Academy of Sciences online Nov. 3, NYU Langone scientists say the telomerator should also improve study of yeast genetics, the model microorganism for human genetics, and help researchers determine how genes, as well as the chromosomes housing them, interact with each other.–The research team, led by Jef Boeke, PhD, a professor and director of NYU Langone’s Institute for Systems Genetics, built the telomerator to convert circular chromosomes into linear ones. Boeke says this better resembles the natural structure of more complex organisms, including humans. Comprising about 1,500 chemical base pairs linked together, the human-made piece of telomerator code can be inserted as a single unit at any position on circular DNA and almost anywhere among a chromosome’s other genes, whose base pairs can number into the hundreds of thousands.—“Our new telomerator resolves a serious and practical issue facing biologists everywhere by helping us experiment with synthetic genes in ways that are more realistic and more closely aligned to the biology of higher organisms, such as humans,” says Boeke. “Until now, we’ve relied on synthesizing functional and stable yeast chromosomes in a circular format — with their telomeres cut off — so they can be uniformly reproduced for easy experimentation within bacteria, whose chromosomes are circular in shape,” he says.–What makes the telomerator particularly effective, researchers say, is its precise capacity to add buffering chromosome endings, or telomeres, to newly linearized yeast chromosomes.–Moreover, the telomerator, which took Boeke and lead study investigator Leslie Mitchell, PhD, two years to construct and test, allows researchers to study how a gene’s position or placement on a chromosome affects the gene’s function.–The key components of the telomerator are its telomere seed sequences, which are exposed when the telomerator “cassette” — its packaged components — is activated.–To test the device, Mitchell inserted a telomerator cassette at 54 different locations on a circular synthetic yeast chromosome of about 90,000 base pairs and tested whether the chromosome could be segmented and straightened at each position. Researchers compared the process to a clock dial, in which they could insert the telomerator at any “hour” on the clock face to break the circle and yield 12 different timelines, but all of equal length. Colonies grew for 51 of the linear yeast chromosomes, failing only in chromosomes where essential genes were placed too close to the telomere ends.–Additional testing confirmed that the modified yeast chromosomes were in a linear format and of the precise length predicted by researchers.–Boeke’s research is part of an international effort to manufacture all the yeast chromosomes, threadlike structures that carry genes in the nucleus of all plant and animal cells, and move genetic research one step closer to constructing the organism’s entire functioning genome. Earlier this year, Boeke’s team reported building the first of the 16 yeast chromosomes, which they call synIII, and successfully incorporating it into brewer’s yeast, known scientifically as Saccharomyces cerevisiae.–Story Source-The above story is based on materials provided by NYU Langone Medical Center / New York University School of Medicine. Note: Materials may be edited for content and length.[F9]
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First functional ‘designer’ chromosome in yeast synthesized by scientists
Date-March 27, 2014 Source-NYU Langone Medical Center
Researchers have synthesized the first functional chromosome in yeast, an important step in the emerging field of synthetic biology, designing microorganisms to produce novel medicines, raw materials for food, and biofuels.–An international team of scientists led by Jef Boeke, PhD, director of NYU Langone Medical Center’s Institute for Systems Genetics, has synthesized the first functional chromosome in yeast, an important step in the emerging field of synthetic biology, designing microorganisms to produce novel medicines, raw materials for food, and biofuels.–Over the last five years, scientists have built bacterial chromosomes and viral DNA, but this is the first report of an entire eukaryotic chromosome, the threadlike structure that carries genes in the nucleus of all plant and animal cells, built from scratch. Researchers say their team’s global effort also marks one of the most significant advances in yeast genetics since 1996, when scientists initially mapped out yeast’s entire DNA code, or genetic blueprint.–“Our research moves the needle in synthetic biology from theory to reality,” says Dr. Boeke, a pioneer in synthetic biology who recently joined NYU Langone from Johns Hopkins University.–“This work represents the biggest step yet in an international effort to construct the full genome of synthetic yeast,” says Dr. Boeke. “It is the most extensively altered chromosome ever built. But the milestone that really counts is integrating it into a living yeast cell. We have shown that yeast cells carrying this synthetic chromosome are remarkably normal[F10]. They behave almost identically to wild yeast cells, only they now possess new capabilities and can do things that wild yeast cannot.”-In this week’s issue of Science online March 27, the team reports how, using computer-aided design, they built a fully functioning chromosome, which they call synIII, and successfully incorporated it into brewer’s yeast, known scientifically as Saccharomyces cerevisiae.–The seven-year effort to construct synIII tied together some 273, 871 base pairs of DNA, shorter than its native yeast counterpart, which has 316,667 base pairs. Dr. Boeke and his team made more than 500 alterations to its genetic base, removing repeating sections of some 47,841 DNA base pairs, deemed unnecessary to chromosome reproduction and growth. Also removed was what is popularly termed junk DNA, including base pairs known not to encode for any particular proteins, and “jumping gene” segments known to randomly move around and introduce mutations. Other sets of base pairs were added or altered to enable researchers to tag DNA as synthetic or native, and to delete or move genes on synIII.–“When you change the genome you’re gambling. One wrong change can kill the cell,” says Dr. Boeke. “We have made over 50,000 changes to the DNA code in the chromosome and our yeast still live. That is remarkable. It shows that our synthetic chromosome is hardy, and it endows the yeast with new properties[F11].”–The Herculean effort was aided by some 60 undergraduate students enrolled in the “Build a Genome” project, founded by Dr. Boeke at Johns Hopkins. The students pieced together short snippets of the synthetic DNA into stretches of 750 to 1,000 base pairs or more, an effort led by Srinivasan Chandrasegaran, PhD, a professor at Johns Hopkins. Chandrasegaran is also the senior investigator of the team’s studies on synIII.–Student participation kicked off what has become an international effort, called Sc2.0 for short, in which several academic researchers have partnered to reconstruct the entire yeast genome, including collaborators at universities in China, Australia, Singapore, the United Kingdom, and elsewhere in the U.S.-Yeast chromosome III was selected for synthesis because it is among the smallest of the 16 yeast chromosomes and controls how yeast cells mate and undergo genetic change. DNA comprises four letter-designated base macromolecules strung together in matching sets, or base pairs, in a pattern of repeating letters. “A” stands for adenine, paired with “T” for thymine; and “C” represents cysteine, paired with “G” for guanine. When stacked, these base pairs form a helical structure of DNA resembling a twisted ladder.–Yeast shares roughly a third of its 6,000 genes — functional units of chromosomal DNA for encoding proteins — with humans. The team was able to manipulate large sections of yeast DNA without compromising chromosomal viability and function using a so-called scrambling technique that allowed the scientists to shuffle genes like a deck of cards, where each gene is a card. “We can pull together any group of cards, shuffle the order and make millions and millions of different decks, all in one small tube of yeast,” Dr. Boeke says. “Now that we can shuffle the genomic deck, it will allow us to ask, can we make a deck of cards with a better hand for making yeast survive under any of a multitude of conditions, such as tolerating higher alcohol levels.”–Using the scrambling technique, researchers say they will be able to more quickly develop synthetic strains of yeast that could be used in the manufacture of rare medicines, such as artemisinin for malaria, or in the production of certain vaccines, including the vaccine for hepatitis B, which is derived from yeast. Synthetic yeast, they say, could also be used to bolster development of more efficient biofuels, such as alcohol, butanol, and biodiesel[F12].–The study will also likely spur laboratory investigations into specific gene function and interactions between genes, adds Dr. Boeke, in an effort to understand how whole networks of genes specify individual biological behaviors.–Their initial success rebuilding a functioning chromosome will likely lead to the construction of other yeast chromosomes (yeast has a total of 16 chromosomes, compared to humans’ 23 pairs), and move genetic research one step closer to constructing the organism’s entire functioning genome, says Dr. Boeke.–Dr. Boeke says the international team’s next steps involve synthesizing larger yeast chromosomes, faster and cheaper. His team, with further support from Build a Genome students, is already working on assembling base pairs in chunks of more than 10,000 base pairs. They also plan studies of synIII where they scramble the chromosome, removing, duplicating, or changing gene order.–Detailing the Landmark Research Process–Before testing the scrambling technique, researchers first assessed synIII’s reproductive fitness, comparing its growth and viability in its unscrambled from — from a single cell to a colony of many cells — with that of native yeast III. Yeast proliferation was gauged under 19 different environmental conditions, including changes in temperature, acidity, and hydrogen peroxide, a DNA-damaging chemical. Growth rates remained the same for all but one condition.–Further tests of unscrambled synIII, involving some 30 different colonies after 125 cell divisions, showed that its genetic structure remained intact as it reproduced. According to Dr. Boeke, individual chromosome loss of one in a million cell divisions is normal as cells divide. Chromosome loss rates for synIII were only marginally higher than for native yeast III.–To test the scrambling technique, researchers successfully converted a non-mating cell with synIII to a cell that could mate by eliminating the gene that prevented it from mating.–Story Source-The above story is based on materials provided by NYU Langone Medical Center. Note: Materials may be edited for content and length.-Journal Reference-N. Annaluru, H. Muller, L. A. Mitchell, S. Ramalingam, G. Stracquadanio, S. M. Richardson, J. S. Dymond, Z. Kuang, L. Z. Scheifele, E. M. Cooper, Y. Cai, K. Zeller, N. Agmon, J. S. Han, M. Hadjithomas, J. Tullman, K. Caravelli, K. Cirelli, Z. Guo, V. London, A. Yeluru, S. Murugan, K. Kandavelou, N. Agier, G. Fischer, K. Yang, J. A. Martin, M. Bilgel, P. Bohutski, K. M. Boulier, B. J. Capaldo, J. Chang, K. Charoen, W. J. Choi, P. Deng, J. E. DiCarlo, J. Doong, J. Dunn, J. I. Feinberg, C. Fernandez, C. E. Floria, D. Gladowski, P. Hadidi, I. Ishizuka, J. Jabbari, C. Y. L. Lau, P. A. Lee, S. Li, D. Lin, M. E. Linder, J. Ling, J. Liu, J. Liu, M. London, H. Ma, J. Mao, J. E. McDade, A. McMillan, A. M. Moore, W. C. Oh, Y. Ouyang, R. Patel, M. Paul, L. C. Paulsen, J. Qiu, A. Rhee, M. G. Rubashkin, I. Y. Soh, N. E. Sotuyo, V. Srinivas, A. Suarez, A. Wong, R. Wong, W. R. Xie, Y. Xu, A. T. Yu, R. Koszul, J. S. Bader, J. D. Boeke, S. Chandrasegaran. Total Synthesis of a Functional Designer Eukaryotic Chromosome. Science, 2014; DOI: 10.1126/science.1249252
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Scientists ‘boot up’ a bacterial cell with a synthetic genome
Date-May 20, 2010-Source-American Association for the Advancement of Science
Scanning electron micrographs of M. mycoides JCVI-syn1. Samples were post-fixed in osmium tetroxide, dehydrated and critical point dried with CO2 , then visualized using a Hitachi SU6600 scanning electron microscope at 2.0 keV.
Credit: Electron micrographs were provided by Tom Deerinck and Mark Ellisman of the National Center for Microscopy and Imaging Research at the University of California at San Diego–Scientists have developed the first cell controlled by a synthetic genome. They now hope to use this method to probe the basic machinery of life and to engineer bacteria specially designed to solve environmental or energy problems[F13].–The study will be published online by the journal Science, at the Science Express website, on May 20.–The research team, led by Craig Venter of the J. Craig Venter Institute, has already chemically synthesized a bacterial genome, and it has transplanted the genome of one bacterium to another.[F14] Now, the scientists have put both methods together, to create what they call a “synthetic cell,” although only its genome is synthetic.–“This is the first synthetic cell that’s been made, and we call it synthetic because the cell is totally derived from a synthetic chromosome, made with four bottles of chemicals on a chemical synthesizer, starting with information in a computer,” said Venter.–“This becomes a very powerful tool for trying to design what we want biology to do. We have a wide range of applications [in mind],” he said.–For example, the researchers are planning to design algae that can capture carbon dioxide and make new hydrocarbons that could go into refineries. They are also working on ways to speed up vaccine production. [F15]Making new chemicals or food ingredients and cleaning up water are other possible benefits, according to Venter.–In the Science study, the researchers synthesized the genome of the bacterium M. mycoides and added DNA sequences that “watermark” the genome to distinguish it from a natural one.–Because current machines can only assemble relatively short strings of DNA letters at a time, the researchers inserted the shorter sequences into yeast, whose DNA-repair enzymes linked the strings together. They then transferred the medium-sized strings into E. coli and back into yeast. After three rounds of assembly, the researchers had produced a genome over a million base pairs long.–The scientists then transplanted the synthetic M. mycoides genome into another type of bacteria, Mycoplasm capricolum.[F16] The new genome “booted up” the recipient cells. Although fourteen genes were deleted or disrupted in the transplant bacteria, they still looked like normal [F17]M. mycoides bacteria and produced only M. mycoides proteins, the authors report.–“This is an important step we think, both scientifically and philosophically. It’s certainly changed my views of the definitions of life and how life works,” Venter said.–Acknowledging the ethical discussion about synthetic biology research, Venter explained that his team asked for a bioethical review in the late 1990s and has participated in variety of discussions on the topic.–“I think this is the first incidence in science where the extensive bioethical review took place before the experiments were done. It’s part of an ongoing process that we’ve been driving, trying to make sure that the science proceeds in an ethical fashion, that we’re being thoughtful about what we do and looking forward to the implications to the future,” he said.–This research was funded by Synthetic Genomics, Inc. Three of the authors and the J. Craig Venter Institute hold Synthetic Genomics, Inc. stock. The J. Craig Venter Institute has filed patent applications on some of the techniques described in this paper.–More information can be found on the J. Craig Venter Institute web site at: http://www.jcvi.org/cms/research/projects/first-self-replicating-synthetic-bacterial-cell/—Story Source–The above story is based on materials provided by American Association for the Advancement of Science. Note: Materials may be edited for content and length.–Journal Reference–Daniel G. Gibson, John I. Glass, Carole Lartigue, Vladimir N. Noskov, Ray-Yuan Chuang, Mikkel A. Algire, Gwynedd A. Benders, Michael G. Montague, Li Ma, Monzia M. Moodie, Chuck Merryman, Sanjay Vashee, Radha Krishnakumar, Nacyra Assad-Garcia, Cynthia Andrews-Pfannkoch, Evgeniya A. Denisova, Lei Young, Zhi-Qing Qi, Thomas H. Segall-Shapiro, Christopher H. Calvey, Prashanth P. Parmar, Clyde A. Hutchison III, Hamilton O. Smith, and J. Craig Venter. Creation of a Bacterial Cell Controlled by a Chemically Synthesized Genome. Science, May 20, 2010 DOI: 10.1126/science.1190719
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Repeated Oral AdministrationHistopathological and ultra structural effects of nanoparticles on rat testis following 90 days (Chronic study)
Mansee Thakur, Himanshu Gupta, Dipty Singh, Ipseeta R Mohanty, Ujjwala Maheswari, Geeta Vangae, Arvind Joshi
[Hide abstract]
ABSTRACT: Background Nanoparticles (Ag NPs)[F18] have recently received much attention for their possible applications in biotechnology and biomedical. However, little is known about the toxicity in reproductive organs of animal model following exposure to Nanoparticles.Objective This study therefore, tried to examine the effects of Nanoparticles with a mean diameter of 5-20 nm range on the histology of the testis of wistar rats and correlate it with Transmission Electron Microscopy results.Materials and methods Sixteen wistar rats were randomly divided into two groups of 8 rats each. Each group received the following via gavage technique for 90 days: Control Group (Group-1)-tap water; Experimental group (Group 2) – Nanoparticles (20ug/kg/day). After ninety days (chronic study), rats were sacrificed and testis tissues was processed for histology and transmission electron microscopic study. There was significant difference between the observations of group-1 and group 2. The changes observed in the testis were disarray of the spermatogenic cells and disorientation of the testis. These changes were observed to have been disappearing from normal histological features. Detailed structural damages were observed with TEM analysis, such as depletion of germ cells, germinal cells necrosis, especially in spermatogonia and Leydig cells had an abnormal fibroblast-like appearance, abnormal space between neighboring sertoli cells, mitochondria, lost cristae and vacuolated (none energized) with those animals exposed to nanoparticles.Conclusion It seems that nanoparticles have acute and significant effects on spermatogenesis and number of spermatogenic cells. More experimental investigations are necessary to elucidate better conclusion regarding the safety of nanoparticles on male reproduction system.
Journal of nanobiotechnology. 10/2014; 12(1):42.
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High-fat diet postpones brain aging in mice
Date:
November 5, 2014
Source:
University of Copenhagen – The Faculty of Health and Medical Sciences
Coconut oil and fresh coconut The researchers see a particular positive effect when the mice are given the so-called medium chain fatty acids — e.g., from coconut oil.—New Danish-led research suggests that signs of brain aging can be postponed in mice if placed on a high-fat diet. In the long term, this opens the possibility of treatment of children suffering from premature aging and patients with Alzheimer’s and Parkinson’s disease. The research project is headed by the Center for Healthy Aging, University of Copenhagen and the National Institute of Health.–When we get older, defects begin to develop in our nervous system, our brain loses some of its intellectual capacity, and the risk of developing diseases such as Parkinson’s and Alzheimer’s increases. Alzheimer’s disease is currently the fastest-growing age-related disease.–Throughout our lives, it is important that our cells — to the extent possible — keep our DNA undamaged, and, therefore, the cells have a system that repairs the damage that occurs all the time. Humans age when the repair system ceases to function. In diseases such as Alzheimer’s, the researchers also see damage to the DNA–A new research project headed by the Center for Healthy Aging, University of Copenhagen and the National Institute of Health has studied mice having a defect in their DNA repair system. In humans, this defect causes the disorder Cockayne syndrome, where patients prematurely age as children and die at an age of 10-12 years. The study shows that placing a mouse model of Cockayne syndrome on a high-fat diet will postpone aging processes such as impaired hearing and weight loss.
Fat putting a stop to premature aging–“The study is good news for children with Cockayne syndrome, because we do not currently have an effective treatment. Our study suggests that a high-fat diet can postpone aging processes. A diet high in fat also seems to postpone the aging of the brain. The findings therefore potentially imply that patients with Alzheimer’s and Parkinson’s disease in the long term may benefit from the new knowledge,” says Professor Vilhelm Bohr from the Center for Healthy Aging, University of Copenhagen and the National Institute of Health, who has headed the study.–Our brain has a constant need for fuel in the form of either sugar or so-called ketones. Ketones are the brain’s fuel reserve, and, in particular, play an important role in periods of low blood sugar levels, e.g. if you are fasting[F19]. This is because the body breaks down fat if it needs sugar, and during this process it produces ketones. The researchers see a particular positive effect when the mice are given the so-called medium chain fatty acids — e.g. from coconut oil.[F20]
Brain cells need extra fuel
“In cells from children with Cockayne syndrome, we have previously demonstrated that aging is a result of the cell repair mechanism being constantly active. It eats into the resources and causes the cell to age very quickly. We therefore hope that a diet with a high content of coconut oil or similar fats will have a beneficial effect, because the brain cells are given extra fuel and thus the strength to repair the damage,” says postdoc Morten Scheibye-Knudsen from the National Institute of Health.–The study has just been published in the scientific journal Cell Metabolism.–Story Source-The above story is based on materials provided by University of Copenhagen – The Faculty of Health and Medical Sciences. Note: Materials may be edited for content and length.–Journal Reference-Morten Scheibye-Knudsen, Sarah J. Mitchell, Evandro F. Fang, Teruaki Iyama, Theresa Ward, James Wang, Christopher A. Dunn, Nagendra Singh, Sebastian Veith, Md Mahdi Hasan-Olive, Aswin Mangerich, Mark A. Wilson, Mark P. Mattson, Linda H. Bergersen, Victoria C. Cogger, Alessandra Warren, David G. Le Couteur, Ruin Moaddel, David M. Wilson, Deborah L. Croteau, Rafael de Cabo, Vilhelm A. Bohr. A High-Fat Diet and NAD Activate Sirt1 to Rescue Premature Aging in Cockayne Syndrome. Cell Metabolism, 2014; 20 (5): 840 DOI: 10.1016/j.cmet.2014.10.005EK
[F1]In other words the results will be reflective back the individual who is using the methods—proof is in the results
[F2]In other words —the glory was in the practice rather then the results
[F3]A process to alleviate and reverse the decline require habits and chemistry
[F4]Key point here —allowing the body to utilize and rest –so not to overload and over consume
[F5]At this point it is theoretical but anyone who makes the right changes to what they consume and eliminate things that cause organ or tissue failure or eliminate cellular damage will slow down or reverse negative implication causing health to become dysfunctional or debilitated
[F6]Male Hormone–
[F7]Female Hormones
[F8]This is utilizing things on a nanoscale—we are dealing here with creation with no restrictions—and with nanogenetics there is a real danger and a significant concern on what these things will assimilate with—what they can alter—disrupt or incorporate into there matrix or be incorporated—and it’s effect on NORMAL biological life and if once incorporated can it be removed and the original DNA or GENE be restored to it’s original design
[F9]This is a form of weaponizing the genes as a bionano weapon —which may have been already releases through chemtrails and other bioagents in the water supply and food chain—with this technology you could insert this sequence target a specific gene or gene type and activate or deactivate the signals or program that the gene des —disrupting any biology in the system —anything from heart rate to sugar regulation to immune response or non response—this is the real implication to this —another form of weaponizing ones own body against itself through genetic manipulation
[F10]Normal!!!— only they now possess new capabilities and can do things that wild yeast cannot—and this is called NORMAL
[F11]Now the question remains what are those new properties—what do they do —how do they work—what function do they fulfil
[F12]Will never happen unless the oil industry controls this technology—whenthey mention the benfits they forget to mention who will have this technology to produce these wonderful developments as well—when you are talking progress and development things like this are utilized more for war and control then benefit
[F13]That could be classified as anything—from human populations to environmental
[F14]Genetic Engineering–
[F15]Bio Manipulation and incorporating this with a nano delivery method—you will have genetic alterations with this in anything you inject this into–
[F16]Disease Creation??—pestilence—even an accidental release of this could wipe out –populations and set back people in evolution
[F17]But the alterations caused a different effect—what was that effect
[F18]Silver Nano Particles
[F19]palm kernel oil and coconut oil. Sources of MCT’s as well as horse fat–
[F20]
From a nutritional standpoint, saturated triglycerides with a medium (6 to 12) carbon chain length (MCT) have traditionally been regarded as biologically inert substances, merely serving as a source of fuel calories that is relatively easily accessible for metabolic breakdown compared with long chain triglycerides (LCT). This quality of MCT has been shown to offer both benefits and risks depending on the clinical situation, with potential positive effects on protein metabolism in some studies on one side, and an increased risk for ketogenesis and metabolic acidosis on the other. At another level, studies regarding lipid effects of MCT on the immune system, as with LCT, so far have yielded equivocal results, although there is a recent experimental evidence to suggest that MCT posses immune modulating properties and should in fact be regarded as bioactive mediators. Most of this information comes from studies where effects of MCT have been compared with those of LCT in lipid emulsions, as part of parenteral (intravenous) nutrition formulations. Unfortunately, the relevance of these observations for clinical practice remains largely unclear because adequately powered trials that clearly point out the position of MCT in relation to structurally different lipids have not been performed. In the present paper we review the experimental and clinical evidence for cellular and physiological effects of nutritional MCT. In addition, studies describing possible mechanisms behind the observed effects
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Show of the Month November 29 2014
Industrial pollution turning Canadian lakes into ‘jelly’
Improved neuroprotective effects by combining Bacopa monnieri and Rosmarinus officinalis supercritical CO2 extracts
Derivative of vitamin B3 prevents liver cancer in mice
Energizing sick mitochondria with vitamin B3: Effective treatment for mitochondrial disease
Copper on the brain at rest
Copper can protect against Alzheimer’s disease
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Industrial pollution turning Canadian lakes into ‘jelly’
Published time: November 20, 2014 01:03
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Reuters / NASA / Handout
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Canada, Ecology, Science
The Canadian lakes are slowly but steadily turning into jelly since the industrial pollution has given jelly-clad organisms an edge over their calcium-protected competitors, researchers say, warning about potential impact on drinking water systems.—A battle between competing planktons in the delicate Ontario Lakes ecosystems is being won by “jelly-clad organism” called Holopedium that’s got an advantage over the planktonic Daphnia – all thanks to industrial pollution and acid rain – says new research by Cambridge University scientists published in Proceedings of the Royal Society B[F1]. The population of Holopedium – which has a “jelly” coat that gives them more protection from water predators – have doubled since the 1980s in many of the lakes, scientists behind the study say. [F2]— Eric Cai (@chemstateric) November 19, 2014 ———The dramatic decline in the water calcium levels has left Daphnia without crucial component to develop their exoskeleton defending them from predators. Thus Daphnia populations are declining, leaving more algae for other organisms to feed on, such as jelly-protected Holopedium. [F3]-“Lakes across eastern Canada have seen Holopedium populations explode in the last thirty years; particularly in lakes in the province of Ontario that have seen a recent Eurasian invasion of the spiny water flea – which also favours hunting Daphnia, affording Holopedium even more room in these ecosystems to expand,” Cambridge said in a press release. –Scientists warn that the “jellification” of Canada’s lakes will further prevent vital nutrients in the food chain flow and may eventually clog filtration and drinking water systems, as in Ontario, some 20 percent of drinking water comes from lakes with depleted calcium concentrations. [F4]–“As calcium declines, the increasing concentrations of jelly in the middle of these lakes will reduce energy and nutrient transport right across the food chain, and will likely impede the withdrawal of lake water for residential, municipal and industrial uses,” said study co-author Dr Andrew Tanentzap, from the University of Cambridge’s Department of Plant Sciences. [F5]
‘Daphnia Family’ by Karl Gaff, winner 2014 UCD Images of Research Competition @UCD_Research @ucdscience @UCDSciEx pic.twitter.com/4zhaGSSZnu —— UCD Innovation (@UCDinnovation) September 26, 2014 –Tanentzap says that industrialization in northern hemisphere deposited a lot of acid that displaced calcium from soil that feed these lakes. —-“Pollution control may have stopped acid deposits in the landscape, but it’s only now that we are discovering the damage wasn’t entirely reversed,” he says. –Besides Calcium loss, scientists also suggest that climate change is causing depletion of oxygen in the lakes that could lead to increasing populations of “larval midges – the main predator of Daphnia.” –“It may take thousands of years to return to historic lake water calcium concentrations solely from natural weathering of surrounding watersheds,” Tanentzap warned. “In the meanwhile, while we’ve stopped acid rain and improved the pH of many of these lakes, we cannot claim complete recovery from acidification. Instead, we many have pushed these lakes into an entirely new ecological state.” —
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Improved neuroprotective effects by combining Bacopa monnieri and Rosmarinus officinalis supercritical CO2 extracts.
J Evid Based Complementary Altern Med. 2014 Apr;19(2):119-27
Authors: Ramachandran C, Quirin KW, Escalon E, Melnick SJ
Abstract
Ethnobotanical evidence suggests that herbs such as brahmi (Bacopa monnieri) and rosemary (Rosmarinus officinalis) may possess antioxidant and neuroprotective properties. We compared the antioxidant and neuroprotective effects of supercritical extract of Bacopa monnieri and rosemary antioxidant extract obtained from Rosmarinus officinalis as well as their combination to examine the effects on human glial (U-87 MG) and embryonic mouse hypothalamus cells. Bacopa monnieri extract, rosemary antioxidant extract, and their combination (1:1) are not cytotoxic in both glial and embryonic mouse hypothalamus cell lines up to 200 μg/mL concentration. The combination of extracts of Bacopa monnieri + rosemary antioxidant has better antioxidant potential and antilipid peroxidation activity than either agent alone[F6]. Although the extract of Bacopa monnieri + rosemary antioxidant showed almost similar inhibition of phospho tau expression as Bacopa monnieri or rosemary antioxidant extract alone, the combination has better inhibitory effect on amyloid precursor protein synthesis and higher brain-derived neurotrophic factor production in hypothalamus cells than single agents. These results suggest that the extract of Bacopa monnieri + rosemary antioxidant is more neuroprotective than Bacopa monnieri or rosemary antioxidant extract. –PMID: 24647092 [PubMed – indexed for MEDLINE]
Recipe—make either a tea or extract of these and make them separate as extracts—then when done—combine —as a tea take equal portions of each Boil together and drink as a tea—may see other benefits as well other then brain support —may see analgesic effects as well as heart –eye—and liver support
If you have powdered rosemary and bacopa then sprinkle on eggs and othee fats to increase protection of lipid issues and use as a brain tonic since all foods here mentioned are brain support
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Derivative of vitamin B3 prevents liver cancer in mice
Date-November 20, 2014–Source-Centro Nacional de Investigaciones Oncologicas (CNIO)
Liver cancer is one of the most frequent cancers in the world, and with the worst prognosis; according to the World Health Organisation (WHO), in 2012, 745,000 deaths were registered worldwide due to this cause, a figure only surpassed by lung cancer. The most aggressive and frequent form of liver cancer is hepato-cellular carcinoma (HCC); little is known about it and there are relatively few treatment options.–Researchers from the Spanish National Cancer Research Centre (CNIO), have produced the first mouse model that faithfully reproduces the steps of human HCC development, from the appearance of the first lesions in the liver to the development of metastasis. The results, published in the journal Cancer Cell, indicate that diets rich in nicotinamide riboside, a derivative of vitamin B3, protect these mice from developing HCC in its most initial stage, when genotoxic stress is damaging cellular DNA. [F7]They also show a curative effect of the diet in those mice that had previously developed the disease.
A MOUSE MODEL FOR HUMAN HEPATIC CANCER
One obstacle to the study of human HCC is the absence of mouse models that replicate the disease, which could be used to investigate molecular pathways or new therapies. Given that human HCC is associated to alterations in hepatocytes survival, and that the URI oncogene plays a role in this process, the researchers genetically engineered mice that contained high levels of URI only in the liver, in a controlled manner over time.-At 30 weeks, the mice with high levels of URI generated sporadic tumours in the liver and even metastasis when the induction lasted longer. The study details how deficiency in nicotinamide adenine dinucleotide (NAD+), a universal compound found in living organisms that is needed to burn calories via cell metabolism, orchestrates the development of the disease.[F8]–“An increase in URI reduces cellular NAD+ and as a consequence produces genotoxic stress and DNA damage,” says Nabil Djouder, leader of the study and Head of the Growth Factors, Nutrients and Cancer Group in the BBVA Foundation-CNIO Cancer Cell Biology Programme. “It is still not totally clear, however, why the deficit in NAD+ causes these lesions,” he adds.
ENERGY METABOLISM AND CANCER
The appearance of DNA damage is the first link in the chain of events that activate the carcinogenic process in the liver, even before apoptosis or cell death, as has been described in the literature. “We normally say that oncogenes induce DNA damage. Now we may be able to say, more appropriately, that oncogenes induce NAD+ depletion [or deficits in NAD+] which causes DNA damage,” says Djouder–The inverse relationship between NAD+ and cancer awakened the curiosity of the researchers: could an increase in NAD+ have beneficial effects on the disease? When the scientists supplemented the diet in genetically modified mice with nicotinamide riboside, a derivative of vitamin B3 that increases intracellular levels of NAD+, they did not observe tumour development. Surprisingly, when they gave this diet to mice that had already developed the disease, the size of the tumours was reduced and they eventually disappeared.–The results have been reproduced in other types of cancer such as pancreatic cancer. “We observed the same results in mice with pancreatic adenocarcinoma with regards to DNA damage[F9], so we could conclude that this treatment is effective on tumours caused by oncogene[F10]-induced DNA damage and thus, deficit in NAD+,” says Krishna Tummala, first author of the study.–In addition to working with the mouse model, the authors have collated the results of nearly a hundred human samples. “Those from patients with HCC contain URI levels that double those of healthy samples,” according to the article. The data, which also associates URI with a worse prognosis or evolution of the illness, suggests that the gene could be a possible new HCC marker, and nicotinamide riboside boosting NAD+ levels may have a human relevance.
FUTURE RESEARCH——–Several epidemiological studies coincide in associating diets low in tryptophan [a NAD+ precursor] with an increased incidence of certain types of cancer[F11]. It has also been observed that daily supplements of vitamin B3 in populations with chronic nutritional deficiencies, reduces the incidence of some cancers including esophageal cancer.–Despite the results, the researchers underline that the efficiency of NAD+ enhancing nutritional supplements to protect healthy cells from chemotoxic stress as a combined therapy in oncology still needs to be demonstrated. Djouder’s team is collaborating with the CNIO Clinical Research Programme, lead by the oncologist Manuel Hidalgo to broaden these studies in mice and evaluate the possibility of carrying out clinical trials in humans in the future.
Story Source–The above story is based on materials provided by Centro Nacional de Investigaciones Oncologicas (CNIO). Note: Materials may be edited for content and length.–Journal Reference-Krishna S. Tummala, Ana L. Gomes, Mahmut Yilmaz, Osvaldo Graña, Latifa Bakiri, Isabel Ruppen, Pilar Ximénez-Embún, Vinayata Sheshappanavar, Manuel Rodriguez- Justo, David G. Pisano, Erwin F. Wagner & Nabil Djouder. Inhibition of De Novo NAD Synthesis by Oncogenic URI Causes Liver Tumorigenesis through DNA Damage. Cancer Cell, November 2014 DOI: 10.1016/j.ccell.2014.10.002
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Energizing sick mitochondria with vitamin B3- Effective treatment for mitochondrial disease
Date-April 7, 2014
Source-Helsingin yliopisto (University of Helsinki)
The researchers of the University of Helsinki, Finland, and École Polytechnique Fédérale de Lausanne, Switzerland, have shown that vitamin B3 form nicotinamide riboside can slow down the progression of mitochondrial disease, suggesting its potential as a novel therapy approach to adult-onset mitochondrial muscle diseases.-Vitamins B have recently been turned out to be potent modifiers of energy metabolism, especially the function of mitochondria. Vitamin B3, (niacin) has been found to delay the signs of aging in animal models.–An international collaboration between the University of Helsinki and École Polytechnique Fédérale de Lausanne reported today in the journal Embo Molecular Medicine that vitamin B3 form, nicotinamide riboside, can slow down the progression of mitochondrial disease, suggesting its potential as a novel therapy approach to adult-onset mitochondrial muscle diseases.–Mitochondria power up all cells in our bodies, by generating fuel, ATP, for all cellular functions. Dysfunction of these cellular engines can cause mitochondrial disorders, which are the most common cause of inherited metabolic diseases in adults and children. Mitochondrial myopathy is the most frequent form of adult mitochondrial disorder. The typical symptoms in the patients are muscle weakness, pain and cramps. Despite the progressive nature of these diseases, no curative treatment is available.–In their current publication, Dr Nahid Khan in Prof Anu Suomalainen Wartiovaara’s group showed that feeding mice with food supplemented with B3 form, nicotinamide riboside, delayed their mitochondrial myopathy[F12]. The treatment increased mitochondrial mass and function, and cured the structural abnormalities. These results clearly showed the potential of this vitamin B form, a natural constituent of milk, to activate dysfunctional mitochondrial metabolism.–“These results are a breakthrough for understanding the mechanisms of human mitochondrial muscle diseases and for exploring the efficient treatment options for these progressive disorders of adults. They also highlight the potent role of niacin in guiding mitochondrial energy metabolism,” Professor Anu Suomalainen Wartiovaara states.-Story Source-The above story is based on materials provided by Helsingin yliopisto (University of Helsinki). Note: Materials may be edited for content and length.-Journal Reference-Nahid A Khan, Mari Auranen, Ilse Paetau, Eija Pirinen, Liliya Euro, Saara Forsström, Lotta Pasila, Vidya Velagapudi, Christopher J Carroll, Johan Auwerx and Anu Suomalainen. Effective treatment of mitochondrial myopathy by nicotinamide riboside, a vitamin B3. EMBO Molecular Medicine, April 2014 DOI: 10.1002/emmm.201403943
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Copper on the brain at rest
Date:November 26, 2014
Source:DOE/Lawrence Berkeley National Laboratory
Two-photon imaging of CF3 shows that the addition of acute BCS dosages also reduces labile copper pools in retinal neurons.
In recent years it has been established that copper plays an essential role in the health of the human brain. Improper copper oxidation has been linked to several neurological disorders including Alzheimer’s, Parkinson’s, Menkes’ and Wilson’s. Copper has also been identified as a critical ingredient in the enzymes that activate the brain’s neurotransmitters in response to stimuli. Now a new study by researchers with the U.S. Department of Energy (DOE)’s Lawrence Berkeley National Laboratory (Berkeley Lab) has shown that proper copper levels are also essential to the health of the brain at rest.-“Using new molecular imaging techniques, we’ve identified copper as a dynamic modulator of spontaneous activity of developing neural circuits, which is the baseline activity of neurons without active stimuli, kind of like when you sleep or daydream, that allows circuits to rest and adapt,” says Chris Chang, a faculty chemist with Berkeley Lab’s Chemical Sciences Division who led this study. “Traditionally, copper has been regarded as a static metabolic cofactor that must be buried within enzymes to protect against the generation of reactive oxygen species and subsequent free radical damage. We’ve shown that dynamic and loosely bound pools of copper can also modulate neural activity and are essential for the normal development of synapses and circuits.”–Chang , who also holds appointments with the University of California (UC) Berkeley’s Chemistry Department and the Howard Hughes Medical Institute (HHMI), is the corresponding author of a paper that describes this study in the Proceedings of the National Academy of Sciences (PNAS). The paper is titled “Copper is an endogenous modulator of neural circuit spontaneous activity.” Co-authors are Sheel Dodani, Alana Firl, Jefferson Chan, Christine Nam, Allegra Aron, Carl Onak, Karla Ramos-Torres, Jaeho Paek, Corey Webster and Marla Feller.–Although the human brain accounts for only two-percent of total body mass, it consumes 20-percent of the oxygen taken in through respiration. This high demand for oxygen and oxidative metabolism has resulted in the brain harboring the body’s highest levels of copper, as well as iron and zinc. Over the past few years, Chang and his research group at UC Berkeley have developed a series of fluorescent probes for molecular imaging of copper in the brain.–“A lack of methods for monitoring dynamic changes in copper in whole living organisms has made it difficult to determine the complex relationships between copper status and various stages of health and disease,” Chang said. “We’ve been designing fluorescent probes that can map the movement of copper in live cells, tissue or even model organisms, such as mice and zebra fish.”
For this latest study, Chang and his group developed a fluorescent probe called Copper Fluor-3 (CF3) that can be used for one- and two-photon imaging of copper ions. This new probe allowed them to explore the potential contributions to cell signaling of loosely bound forms of copper in hippocampal neurons and retinal tissue.–“CF3 is a more hydrophilic probe compared to others we have made, so it gives more even staining and is suitable for both cells and tissue,” Chang says. “It allows us to utilize both confocal and two-photon imaging methods when we use it along with a matching control dye (Ctrl-CF3) that lacks sensitivity to copper.”–With the combination of CF3 and Ctrl-CF3, Chang and his group showed that neurons and neural tissue maintain stores of loosely bound copper that can be attenuated by chelation to create what is called a “labile copper pool.” Targeted disruption of these labile copper pools by acute chelation or genetic knockdown of the copper ion channel known as CTR1 (for copper transporter 1) alters spontaneous neural activity in developing hippocampal and retinal circuits.[F13]- “We demonstrated that the addition of the copper chelator bathocuproine disulfonate (BCS) modulates copper signaling which translates into modulation of neural activity,” Chang says. “Acute copper chelation as a result of additional BCS in dissociated hippocampal cultures and intact developing retinal tissue removed the copper which resulted in too much spontaneous activity.”–The results of this study suggest that the mismanagement of copper in the brain that has been linked to Wilson’s, Alzheimer’s and other neurological disorders can also contribute to misregulation of signaling in cell−to-cell communications.–“Our results hold therapeutic implications in that whether a patient needs copper supplements or copper chelators depends on how much copper is present and where in the brain it is located,” Chang says. “These findings also highlight the continuing need to develop molecular imaging probes as pilot screening tools to help uncover unique and unexplored metal biology in living systems.”–Story Source-The above story is based on materials provided by DOE/Lawrence Berkeley National Laboratory. The original article was written by Lynn Yarris. Note: Materials may be edited for content and length.–Journal Reference-Sheel C. Dodani, Alana Firl, Jefferson Chan, Christine I. Nam, Allegra T. Aron, Carl S. Onak, Karla M. Ramos-Torres, Jaeho Paek, Corey M. Webster, Marla B. Feller, Christopher J. Chang. Copper is an endogenous modulator of neural circuit spontaneous activity. Proceedings of the National Academy of Sciences, 2014; 111 (46): 16280 DOI: 10.1073/pnas.1409796111
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Copper can protect against Alzheimer’s disease
Date:February 17, 2013
Source: Keele University
Researchers in The Birchall Centre at Keele University, Staffordshire, UK, have provided unequivocal evidence that under conditions which are approximately similar to those found in the brain, copper can only protect against beta amyloid forming beta sheets and as such it is highly unlikely that copper is directly involved in the formation of senile plaques in Alzheimer’s disease.–The research, published by Nature’s online journal Scientific Reports, may also imply that lower levels of copper in the brain may promote the mechanisms whereby beta amyloid is deposited as senile plaques in Alzheimer’s disease.–This research addressed the on-going question as to whether copper in the brain contributes to the formation of the senile plaques in Alzheimer’s disease. While previous research at Keele’s Birchall Centre pointed towards copper being potentially protective in preventing the protein beta amyloid from aggregating as beta sheets and forming senile plaques it had remained a controversial issue for some.–Story Source–The above story is based on materials provided by Keele University. Note: Materials may be edited for content and length.–Journal Reference–Matthew Mold, Larissa Ouro-Gnao, Beata M Wieckowski, Christopher Exley. Copper prevents amyloid-β1–42 from forming amyloid fibrils under near-physiological conditions in vitro. Scientific Reports, 2013; 3 DOI: 10.1038/srep01256
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[F1]Chemtrail Fallout would be more the reality—them dumping tons of nanoparticles and nanometals have accumulated over time and now the water table is being poisoned—in a military exercise this would be considered as “poisoning the wells” where by the water would not be fir for consumption or irrigation and anything it would be exposed to —spread pathogens –in this case nanopoisoning
[F2]Polymers can ba a lipid or protein mix to create a “Jelly like effect”
[F3]Glyphosates in the region would case this as well –since glyphosates strip out minerals allowing pathogenic materials to become more predomnant
[F4]This sounds fishy—with the amount of GE chemicals such as glyphosates leeching into the water table this would be more credible as the cause and as a result this will now be in the drinking water which will further strip out of people vitals
[F5]Almost sounds like there is another reason to reduce the consumer usage—possible water rationing!!!
[F6]Protects Fat From Breaking down and going bad
[F7]B3 –used ot be used by medicicne to reduce cholesterol in the liver
[F8]And a lot have a B3 deficiency one way to tell is Sleep and rest depeleton—which without B3 you cannot regulate trytophan
[F9]Huge –info here –pancreatic and lung cancers are some of the hardest cancers to reverse—so this canbe effective as well
[F10]oncogene, genetic material that carries the ability to induce cancer. An oncogene is a sequence of deoxyribonucleic acid (DNA) that has been altered or mutated from its original form, the proto-oncogene
[F11]Foods with Tryptophan
(mg of Tryptophan per 100 grams)
Algae: Spirulina 929
Animal-Derived Supplements:
Velvet Deer Antler
Dairy Products: Cottage Cheese Milk
Yogurt Cheese (cheddar) 340
Swiss Cheese 401 Parmesan Cheese 482
Edam Cheese 352 Gouda Cheese 352
Gruyere Cheese 421 Cheddar Cheese 320
Blue Cheese 312
Eggs: Whole Eggs 210
Fish Crab 330 Tuna (canned) 300
Fruit: Bananas 12 Dates
Pineapple
Beef 400 Turkey 400
Chicken 400 Pork 400
Nuts: Peanuts 340 Brazil Nuts 185
Cashew Nuts 287 Pistachio Nuts 273
Processed Foods: Chocolate Cocoa
Sea Vegetables:
Kelp 48
Seeds: Sunflower Seeds 350 Pumpkin Seeds 560
Sesame Seeds 388 Mustard Seeds 526
Fenugreek Seeds 391 Poppy Seeds 255
Fennel Seeds 253
Vegetables: Carrots Broccoli
Potato Spinach
Fennel Garlic
Pumpkin 578
[F12]In medicine, a myopathy is a muscular disease in which the muscle fibers do not function for any one of many reasons, resulting in muscular weakness.
[F13]Glyphosate poisoning removes from the body copper—iron and zinc—and when combo’d with sulphur appears to take away the floaters as well zince zinc+ copper make SOD—which is located in lung –highest –Eyes second highestEK
Glyphosate-Endocrine Disrupting
“First of all, we need to understand what we mean by the word safe. Actually, in terms of the academic literature, “safe” refers to “an acceptable level of risk.” It doesn’t refer to situations where there is no risk. Most of us drive in cars all the time and consider it to be safe even though we know that people are killed and injured in automobiles frequently. We have to understand that safe equals acceptable risk.
Glyphosate Poses Risk to Female Reproductive Health
Although there are only a handful of studies on the safety of GE soybeans, there is considerable evidence that glyphosate? especially in conjunction with the other ingredients in Roundup? wreaks havoc with the endocrine and reproductive systems.
Glyphosate throws off the delicate hormonal balance that governs the whole reproductive cycle. It interferes with aromatase, which produces estrogen, and it’s also highly toxic to the placenta in pregnant women. In a 2009 French study, scientists discovered that glyphosate can kill the cells in the outer layer of the human placenta (the trophoblast membrane), which in turn can kill the placenta. A mere 1/500th the amount needed to kill weeds was able to kill these cells! The amount is so small, according to the study’s authors, that the “residual levels to be expected, especially in food and feed derived from Roundup formulation-treated crops” could be enough to “cause cell damage and even [cell] death.” If the endocrine function of the placenta is destroyed, then ovarian and endometrial function may also suffer, and the end result could be a miscarriage. It’s important to remember that glyphosate can accumulate in your body, allowing its toxic effects to grow worse with repeated consumption of foods containing these Roundup Ready crops. Clearly, this may become a serious concern for the next generation, as most young children girls and boys alike growing up today are fed processed foods containing GE ingredients on a daily basis, year after year…—
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Monsanto Roundup: The Impacts of Glyphosate Herbicide on Human Health. Pathways to Modern Diseases
Glyphosate’s Suppression of Cytochrome P450 Enzymes and Amino Acid Biosynthesis by the Gut Microbiome: Pathways to Modern Diseases
By Global Research News
Global Research, January 02, 2014
Entropy and Global Research 12 July 2013
Theme: Biotechnology and GMO, Science and Medicine
by Anthony Samsel and Stephanie Seneff
Glyphosate, the active ingredient in Roundup®, is the most popular herbicide used worldwide[F1]. The industry asserts it is minimally toxic to humans, but here we argue otherwise. Residues are found in the main foods of the Western diet, comprised primarily of sugar, corn, soy and wheat. Glyphosate’s inhibition of cytochrome P450 (CYP) enzymes is an overlooked component of its toxicity to mammals. CYP enzymes play crucial roles in biology, one of which is to detoxify xenobiotics. Thus, glyphosate enhances the damaging effects of other food borne chemical residues and environmental toxins. Negative impact on the body is insidious and manifests slowly over time as inflammation damages cellular systems throughout the body. Here, we show how interference with CYP enzymes acts synergistically with disruption of the biosynthesis of aromatic amino acids by gut bacteria, as well as impairment in serum sulfate transport. Consequences are most of the diseases and conditions associated with a Western diet, which include gastrointestinal disorders, obesity, diabetes, heart disease, depression, autism, infertility, cancer and Alzheimer’s disease. We explain the documented effects of glyphosate and its ability to induce disease, and we show that glyphosate is the “textbook example” of exogenous semiotic entropy[F2]: the disruption of homeostasis by environmental toxins.
Introduction
The foodstuffs of the Western diet, primarily grown by industrial agriculture, are increasingly being produced using a two-part system of engineered plant seeds and toxic chemical application.[F3]–Novel bacterial genes are incorporated through genetic engineering, and toxic chemical residues are readily taken up by the engineered plants[F4]. Research indicates that the new bacterial RNA and DNA present in genetically engineered plants, providing chemical herbicide resistance and other traits, have not yet fully understood biological effects. This paper however, will only examine the effects of the chemical glyphosate, the most dangerous Bio Agent on the planet.——–Glyphosate (N-phosphonomethylglycine), the active ingredient in the herbicide Roundup®, is the main herbicide in use today in the United States, and increasingly throughout the World, in agriculture and in lawn maintenance, especially now that the patent has expired. 80% of genetically modified crops, particularly corn, soy, canola, cotton, sugar beets and most recently alfalfa, are specifically targeted towards the introduction of genes resistant to glyphosate, the so-called “Roundup Ready® feature” In humans, only small amounts (~2%) of ingested glyphosate are metabolized to aminomethylphosphonic acid (AMPA), and the rest enters the blood stream and is eventually eliminated through the urine [1].
Studies have shown sharp increases in glyphosate contamination in streams in the Midwestern United States following the mid 1990s, pointing to its increasing role as the herbicide of choice in agriculture [2]. A now common practice of crop desiccation through herbicide administration shortly before the harvest assures an increased glyphosate presence in food sources as well [3–5]. The industry asserts that glyphosate is nearly nontoxic to mammals [6,7], and therefore it is not a problem if glyphosate is ingested in food sources. Acutely, it is claimed to be less toxic than aspirin [1,6]. As a consequence, measurement of its presence in food is practically nonexistent. A vocal minority of experts believes that glyphosate may instead be much more toxic than is claimed, although the effects are only apparent after a considerable time lapse.
Thus, while short-term studies in rodents have shown no apparent toxicity [8], studies involving life-long exposure in rodents have demonstrated liver and kidney dysfunction and a greatly increased risk of cancer, with shortened lifespan [9].
Glyphosate’s claimed mechanism of action in plants is the disruption of the shikimate pathway, which is involved with the synthesis of the essential aromatic amino acids, phenylalanine, tyrosine, and tryptophan [10].
The currently accepted dogma is that glyphosate is not harmful to humans or to any mammals because the shikimate pathway is absent in all animals. However, this pathway is present in gut bacteria, which play an important and heretofore largely overlooked role in human physiology [11–14] through an integrated biosemiotic relationship with the human host. In addition to aiding digestion, the gut microbiota synthesize vitamins, detoxify xenobiotics, and participitate in immune system homeostasis and gastrointestinal tract permeability [14]. Furthermore, dietary factors modulate the microbial composition of the gut [15].[F5]—-The incidence of inflammatory bowel diseases such as juvenile onset Crohn’s disease has increased substantially in the last decade in Western Europe [16] and the Entropy 2013, 15 1418 United States [17]. It is reasonable to suspect that glyphosate’s impact on gut bacteria may be contributing to these diseases and conditions.—-However, the fact that female rats are highly susceptible to mammary tumors following chronic exposure to glyphosate [9] suggests that there may be something else going on. Our systematic search of the literature has led us to the realization that many of the health problems that appear to be associated with a Western diet could be explained by biological disruptions that have already been attributed to glyphosate. These include digestive issues, obesity, autism, Alzheimer’s disease, depression, Parkinson’s disease, liver diseases, and cancer, among others. While many other environmental toxins obviously also contribute to these diseases and conditions, we believe that glyphosate may be the most significant environmental toxin, mainly because it is pervasive and it is often handled carelessly due to its perceived nontoxicity.
In this paper, we will develop the argument that the recent alarming increase in all of these health issues can be traced back to a combination of gut dysbiosis, impaired sulfate transport, and suppression of the activity of the various members of the cytochrome P450 (CYP) family of enzymes. We have found clear evidence that glyphosate disrupts gut bacteria and suppresses the CYP enzyme class. The connection to sulfate transport is more indirect, but justifiable from basic principles of biophysics.
In the remainder of this paper, we will first provide evidence from the literature that explains some of the ways in which glyphosate adversely affects plants, microbes, amphibians and mammals.
Section 3 will discuss the role that gut dysbiosis, arguably resulting from glyphosate exposure, plays in inflammatory bowel disease and its relationship to autism.
Section 4 argues that the excess synthesis of phenolic compounds associated with glyphosate exposure represents a strategy to compensate for impairments in the transport of free sulfate.
Section 5 will provide evidence that glyphosate inhibits CYP enzymes. Section 6 explains how obesity can arise from depletion of serum tryptophan due to its sequestering by macrophages responding to inflammation. Section 7 shows how extreme tryptophan depletion can lead to impaired nutrient absorption and anorexia nervosa.
Section 8 provides a brief review of all the roles played by CYP enzymes in metabolism. Section 9 discusses a likely consequence to glyphosate’s disruption of the CYP-analog enzyme, endothelial nitric oxide synthase (eNOS). Section 10 shows how glyphosate’s effects could plausibly lead to brain-related disorders such as autism, dementia, depression, and Parkinson’s disease. Section 11 mentions several other health factors that can potentially be linked to glyphosate, including reproductive issues and cancer.
Section 12 discusses the available evidence that glyphosate is contaminating our food supplies, especially in recent years. Following a discussion section, we sum up our findings with a brief
Numerous laboratory studies have shown that glyphosate and the Roundup formulation can be genotoxic and endocrine disrupting. One study summarises these effects occurring at doses substantially lower than those used in agriculture, or permitted as residues: at 0.5 mg/kg (40 times lower than levels permitted in soybeans in the US) they were anti-androgenic; at 2 mg/kg they were anti-oestrogenic; at 1 mg/kg they disrupted the enzyme aromatase; at 5 mg/kg they damaged DNA, and at 10 mg/kg there were cytotoxic. These effects can result in crucial outcomes for sexual and other cell differentiation, bone metabolism, liver metabolism, reproduction, development and behaviour, and hormone dependent diseases such as breast and prostate cancer (Gasnier et al 2009).
Exposure to glyphosate-based herbicides, even at very low doses may result in reproductive and hormonal problems, miscarriages, low birth weights, birth defects, and various cancers—especially haematological cancers such as non-Hodgkin’s lymphoma, and hormonal cancers such as breast cancer. Several epidemiological studies have linked exposure to glyphosate with non-Hodgkin’s lymphoma, hairy cell leukaemia, multiple myeloma, DNA damage; and one study with spontaneous abortions and pre-term deliveries
GM pea protein caused lung damage in mice
Offspring of rats fed GM soy showed a five-fold increase in mortality, lower birth weights, and the inability to reproduce
GM potatoes may cause cancer in rats
Male mice fed GM soy had damaged young sperm cells
Bacteria in your gut can take up DNA from GM food
The embryo offspring of GM soy-fed mice had altered DNA functioning
GM foods lead to significant organ disruptions in rats and mice, specifically the kidney, liver, heart and spleen
Several US farmers reported sterility or fertility problems among pigs and cows fed on GM corn varieties
Bt corn caused a wide variety of immune responses in mice, commonly associated with diseases such as arthritis, Lou Gehrig’s disease, osteoporosis, and inflammatory bowel disease
Investigators in India have documented fertility problems, abortions, premature births, and other serious health issues, including deaths, among buffaloes fed GM cottonseed products
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Stick out your tongue- Tongue appearance and illness
Date-December 5, 2014
Source-Inderscience Publishers
Physicians often ask their patients to “Please stick out your tongue.” The tongue can betray signs of illness, which combined with other symptoms such as a cough, fever, presence of jaundice, headache or bowel habits, can help the physician offer a diagnosis. For people in remote areas who do not have ready access to a physician, a new diagnostic system is reported in the International Journal of Biomedical Engineering and Technology that works to combine the soft inputs of described symptoms with a digital analysis of an image of the patient’s tongue.–Karthik Ramamurthy of the Department of Information Technology, Rajalakshmi Engineering College, in Chennai, India, and colleagues, have trained a neural network that can take soft inputs such as standard questions about symptoms and a digitized image of the patient’s tongue and offer a likely diagnosis so that professional healthcare might then be sought if needed. The digitized images of the patient’s tongue reveal discoloration, engorgement, texture and other factors that might be linked to illness.–Smoothness and “beefiness” might reveal vitamin B12, iron, or folate deficiency, and anemia. Black discoloration could be indicative of fungal overgrowth in HIV patients or prolonged antibiotic use. Longitudinal furrows on the tongue are associated with syphilis. Ulcers may indicate the presence of Crohn’s disease or colitis and various other conditions. The team’s automated diagnostic, however, utilizes the condition of the tongue in combination with other symptoms to identify whether a patient has any of various illnesses: common cold, flu, bronchitis, streptococcal throat infection, sinusitis, allergies, asthma, pulmonary edema, food poisoning and diverticulitis.–The current system allows diagnosis of fourteen distinct conditions but the team adds that they will be able to add eye images and use those as an additional hard input for their neural network and so extend its repertoire significantly.–Story Source-The above story is based on materials provided by Inderscience Publishers. Note: Materials may be edited for content and length.–Journal Reference-Karthik, R., Menaka, R., Kulkarni, S. and Deshpande, R. Virtual doctor: an artificial medical diagnostic system based on hard and soft inputs. Int. J. Biomedical Engineering and Technology, Vol. 16, No. 4, pp.329-342
The two main characteristics of the tongue in TCM ZHENG diagnosis are the color and the coating. The color of the patient’s tongue color provides information about his/her health status. For example [13], dark red color can indicate inflammation or ulceration, while a white tongue indicates cold attack, mucus deposits, or a weakness in the blood leading to such conditions as anemia [12]. Moreover, a yellow tongue points out a disorder of the liver and gallbladder, and blue or purple implies stagnation of blood circulation and a serious weakening of the part of the digestive system that corresponds to the area of the tongue where the color appears.
Tongue Diagnosis: Color of the Tongue:
Progression of Color: When a body shows dis-ease the tongue color (underneath the coating) turns from pink to pale, to red and then to purple.
Purple tongues mean blood stasis.
Red dots on the tongue are called points and they have a meaning wherever they are. In Asian and African people these red dots can look brown.
Tongue Diagnosis: Coating of the Tongue: (Coating is related to Stomach function.)
A white coat corresponds to cold in the area of the body correlating to the tongue.
A yellow coat is related to heat.
A coating can be with “root” which means the coating cannot be scraped off and it looks like grass growing from the soil.
A coating without root looks like it has been sprinkled on and can be scraped off.
The thicker the coat, the more progressed the disease.
Lack of a coat means that the digestion is not working correctly.
The coating is slightly thicker on the back of the tongue.
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Antiproliferative activity and induction of apoptotic by ethanolic extract of Alpinia galanga rhizhome in human breast carcinoma cell line.
BMC Complement Altern Med. 2014;14:192
Authors: Samarghandian S, Hadjzadeh MA, Afshari JT, Hosseini M
Abstract
BACKGROUND: We investigated the potential of galangal rhizomes to induce cytotoxic and apoptotic effects in the cultured human breast carcinoma cell line, (MCF-7) in compare with the non-malignant (MRC-5) cells.-METHODS: Both cells were cultured in DMEM medium and treated with galangal rhizomes for three consecutive days. The percentage of apoptotic cells was determined by flow cytometry using Annexin-V fluorescein isothiocyanate.
RESULTS: The results showed that the ethanolic extract of galangal rhizomes decreased cell viability in the malignant cells as a concentration- and time- dependent manner. The IC50 values against MCF-7 were determined at 400.0 ± 11.7 and 170.0 ± 5.9 μg/ml after 48 and 72 h respectively. The morphology of MCF-7 cells treated with the ethanolic extract confirmed the cell proliferation assay results. Alpinia galanga induced apoptosis in MCF-7 cells, as determined by flow cytometry.–CONCLUSIONS: We concluded that the extract of Alpinia galanga exerts pro-apoptotic effects in a breast cancer-derived cell line and could be considered as a potential chemotherapeutic agent in breast cancer.–PMID: 24935101 [PubMed – indexed for MEDLINE]
Recipe—Make a tea out of this or even percolate this in a coffee percolator—this will also strengthen the heart and intestines
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A high whey protein–, leucine-, and vitamin D–enriched supplement preserves muscle mass during intentional weight loss in obese older adults: a double-blind randomized controlled trial1,2,3
Amely M Verreijen,
Sjors Verlaan,
Mariëlle F Engberink,
Sophie Swinkels,
Johan de Vogel-van den Bosch, and
Peter JM Weijs
+ Author Affiliations
1. 1From the Department of Nutrition and Dietetics, School of Sports and Nutrition, Amsterdam University of Applied Sciences, Amsterdam, The Netherlands (AMV, MFE, and PJMW), and Nutricia Research, Utrecht, The Netherlands (SV, SS, and JdV-vdB).
+ Author Notes
· ↵2 Supported by Nutricia Research, Nutricia Advanced Medical Nutrition.
· ↵3 Address correspondence to AM Verreijen, School of Sports and Nutrition, Amsterdam University of Applied Sciences, Dr. Meurerlaan 8, 1067 AM, Amsterdam, The Netherlands. E-mail: [email protected].
Abstract
Background: Intentional weight loss in obese older adults is a risk factor for muscle loss and sarcopenia.
Objective: The objective was to examine the effect of a high whey protein–, leucine-, and vitamin D–enriched supplement on muscle mass preservation during intentional weight loss in obese older adults.
Design: We included 80 obese older adults in a double-blind randomized controlled trial. During a 13-wk weight loss program, all subjects followed a hypocaloric diet (−600 kcal/d) and performed resistance training 3×/wk. Subjects were randomly allocated to a high whey protein–, leucine-, and vitamin D–enriched supplement including a mix of other macro- and micronutrients (150 kcal, 21 g protein; 10×/wk, intervention group) or an isocaloric control. Primary outcome was change in appendicular muscle mass. Secondary outcomes were body composition, handgrip strength, and physical performance. Data were analyzed by using ANCOVA and mixed linear models with sex and baseline value as covariates.
Results: At baseline, mean ± SD age was 63 ± 5.6 y, and body mass index (in kg/m2) was 33 ± 4.4. During the trial, protein intake was 1.11 ± 0.28 g [F6]· kg body weight–1 · d–1 in the intervention group compared with 0.85 ± 0.24 in the control group (P < 0.001). Both intervention and control groups decreased in body weight (−3.4 ± 3.6 kg and −2.8 ± 2.8 kg; both P < 0.001) and fat mass (−3.2 ± 3.1 kg and −2.5 ± 2.4 kg; both P < 0.001), with no differences between groups. The 13-wk change in appendicular muscle mass, however, was different in the intervention and control groups [+0.4 ± 1.2 kg and −0.5 ± 2.1 kg, respectively; β = 0.95 kg (95% CI: 0.09, 1.81); P = 0.03]. Muscle strength and function improved over time without significant differences between groups.
Conclusion: A high whey protein–, leucine-, and vitamin D–enriched supplement compared with isocaloric control preserves appendicular muscle mass in obese older adults during a hypocaloric diet and resistance exercise program and might therefore reduce the risk for sarcopenia. This trial was registered at the Dutch Trial Register (http://www.trialregister.nl) as NTR2751.
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Cottage Cheese Making
Method 1 of 3: Use Rennet
1
Heat the milk. Pour the milk into a small saucepan and place it over medium heat. Heat the milk slowly, making sure it doesn’t boil, until it reaches 85 degrees F. Use a candy thermometer to monitor the temperature. Turn off the heat when the milk is sufficiently warm.
2
Add the rennet. Place the drops of rennet directly in the milk. Use a spoon to stir the mixture for about 2 minutes.
3
Let the mixture stand. Cover the saucepan with a clean dish towel and let the rennet and milk sit untouched for about 4 hours. The rennet will start reacting with the milk to turn it into cheese.[1]
4
Slice the mixture. Remove the dish cloth and use a knife to make slices in the mixture and break up the curds. Slice several times in one direction, then make several slices in the opposite direction.
5
Cook the mixture. Add the salt to the saucepan. Turn the burner to medium low. Stir the mixture as it heats to help the curds separate from the whey. Stop as soon as the curds have separated and the whey looks slightly yellow. Don’t overcook the mixture, or the curds will be hard.
6
Strain the curds. Place a piece of cheesecloth or a fine-mesh strainer over a bowl Pour the curds and whey into the cheesecloth to strain the curds from the whey. Keeping the curds in the cheesecloth suspended over a bowl, cover the curds loosely with plastic wrap and place all of it in the refrigerator to let the whey continue to drain for a few hours. Stir it every once in awhile to help it along.
7
Serve the cottage cheese. Place the curds in a clean bowl and add the cream or half and half. Season with more salt to taste.
Method 2 of 3: Use Vinegar
1
Heat the milk. Place the milk in a saucepan and put it on the stove. Turn the burner to medium and let the milk heat to 120 degrees. Use a candy thermometer to monitor the milk’s temperature. Remove it from heat once it is sufficiently warmed.
2
Add the vinegar. Pour the vinegar into the saucepan and stir the mixture slowly for 2 minutes. Cover the pan with a dish cloth and let the mixture rest for 30 minutes.
3
Strain the curds from the whey. Pour the mixture into a colander lined with cheesecloth or a thin dish cloth. Let the whey drain for about five minutes.[2]
4
Rinse the curds. Gather the edges of the cloth and hold the curds under a stream of cold water. Squeeze the curds and move them around until they are all rinsed and cooled.
5
Finish the cottage cheese. Place the curds in a bowl. Add the salt and the cream or half and half. Store in the refrigerator or serve immediately.
Method 3 of 3: Use Lemon Juice
1
Heat the milk. Place it in a saucepan and heat it until it begins to steam, but does not come to a boil. Remove the milk from heat.
2
Add the lemon juice. Pour the lemon juice into the warm milk and stir it slowly for several minutes.
3
Let the mixture rest. Cover the saucepan with a dish cloth and let the curds separate from the whey for about an hour.
4
Strain the curds from the whey. Place a piece of cheesecloth over a bowl and pour the curds and whey into the cheesecloth. Let the curds drain for about 5 minutes.
5
Rinse the curds. Gather the ends of the cheesecloth and hold it under cool water to rinse the curds. Continue until they are completely cooled, then squeeze the cloth to get the curds as dry as possible.
6
Finish the cottage cheese. Place the curds in a bowl and add the salt and cream or half and half.
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Doubling saturated fat in diet does not increase saturated fat in blood
Date:
November 21, 2014
Source:
Ohio State University
This is a sampling of foods provided to research participants during the three weeks that they were eating a very-low-carb diet. Doubling or even nearly tripling saturated fat in the diet does not drive up total levels of saturated fat in the blood, according to a controlled diet study.–However, increasing levels of carbohydrates in the diet during the study promoted a steady increase in the blood of a fatty acid linked to an elevated risk for diabetes and heart disease. The finding “challenges the conventional wisdom that has demonized saturated fat and extends our knowledge of why dietary saturated fat doesn’t correlate with disease,” said senior author Jeff Volek, a professor of human sciences at The Ohio State University. In the study, participants were fed six three-week diets that progressively increased carbs while simultaneously reducing total fat and saturated fat, keeping calories and protein the same. The researchers found that total saturated fat in the blood did not increase — and went down in most people — despite being increased in the diet when carbs were reduced. Palmitoleic acid, a fatty acid associated with unhealthy metabolism of carbohydrates that can promote disease, went down with low-carb intake and gradually increased as carbs were re-introduced to the study diet. “It’s unusual for a marker to track so closely with carbohydrate intake, making this a unique and clinically significant finding. As you increase carbs, this marker predictably goes up,” Volek said. When that marker increases, he said, it is a signal that an increasing proportion of carbs are being converted to fat instead of being burned as fuel. Reducing carbs and adding fat to the diet in a well-formulated way, on the other hand, ensures the body will promptly burn the saturated fat as fuel — so it won’t be stored. “When you consume a very low-carb diet your body preferentially burns saturated fat,” Volek said. “We had people eat 2 times more saturated fat than they had been eating before entering the study, yet when we measured saturated fat in their blood, it went down in the majority of people. Other traditional risk markers improved, as well.” The research is published in the Nov. 21, 2014, issue of the journal PLOS ONE. Volek and colleagues recruited 16 adults for the study, all of whom had metabolic syndrome, defined as the presence of at least three of five factors that increase the risk for heart disease and diabetes (excess belly fat, elevated blood pressure, low “good” cholesterol, insulin resistance or glucose intolerance, and high triglycerides). After getting them to a baseline reduced-carb diet for three weeks, researchers fed the participants the exact same diets, which changed every three weeks, for 18 weeks. The diets started with 47 grams of carbs and 84 grams of saturated fat each day, and ended with 346 carb grams per day and 32 grams daily of saturated fat. Each day’s meals added up to 2,500 calories and included about 130 grams of protein. The highest-carb level represented 55 percent of daily calories, which roughly matches the estimated daily percentage of energy provided by carbs in the American diet.
Compared to baseline, there were significant improvements in blood glucose, insulin and blood pressure that were similar across diets. Participants, on average, lost almost 22 pounds by the end of the trial. When looking at palmitoleic acid, however, the scientists found that it consistently decreased on the high-fat/low-carb diet in all participants. The fatty acid then showed a step-wise increase in concentration in the blood as carbs were progressively added to the diet. Elevated levels of palmitoleic acid in the blood have been linked to obesity and higher risk for inflammation, insulin resistance, impaired glucose tolerance, metabolic syndrome, type-2 diabetes, heart disease and prostate cancer. The study does not address what happens to palmitoleic acid levels when high carbs are combined with a diet high in saturated fat. Instead, Volek hoped to identify the carb-intake point at which participants began to store fat. “That turned out to be highly variable,” he said. “Everyone showed increased palmitoleic acid levels as carbs increased, but values varied widely between individuals, especially at the highest carb intake. This is consistent with the idea that people vary widely in their tolerance to carbohydrates.” Participants’ existing health risks were not a factor in the study because everyone ate the exact same diet for 18 weeks. Their bodies’ responses to the food were the focus of the work. “There is widespread misunderstanding about saturated fat. In population studies, there’s clearly no association of dietary saturated fat and heart disease, yet dietary guidelines continue to advocate restriction of saturated fat. That’s not scientific and not smart,” Volek said. “But studies measuring saturated fat in the blood and risk for heart disease show there is an association. Having a lot of saturated fat in your body is not a good thing. The question is, what causes people to store more saturated fat in their blood, or membranes, or tissues? “People believe ‘you are what you eat,’ but in reality, you are what you save from what you eat,” he said. “The point is you don’t necessarily save the saturated fat that you eat. And the primary regulator of what you save in terms of fat is the carbohydrate in your diet. Since more than half of Americans show some signs of carb intolerance, it makes more sense to focus on carb restriction than fat restriction.[F7]” Volek sees this palmitoleic acid as a potential biomarker to signal when the body is converting carbs to fat, an early event that contributes to what he calls “metabolic mayhem.””There is no magical carb level, no cookie-cutter approach to diet, that works for everyone,” he said. “There’s a lot of interest in personalized nutrition, and using a dynamically changing biomarker could provide some index as to how the body is processing carbohydrates.”-Story Source-The above story is based on materials provided by Ohio State University. The original article was written by Emily Caldwell. Note: Materials may be edited for content and length.-Journal Reference-Brittanie M. Volk, Laura J. Kunces, Daniel J. Freidenreich, Brian R. Kupchak, Catherine Saenz, Juan C. Artistizabal, Maria Luz Fernandez, Richard S. Bruno, Carl M. Maresh, William J. Kraemer, Stephen D. Phinney, Jeff S. Volek. Effects of Step-Wise Increases in Dietary Carbohydrate on Circulating Saturated Fatty Acids and Palmitoleic Acid in Adults with Metabolic Syndrome. PLoS ONE, 2014; 9 (11): e113605 DOI: 10.1371/journal.pone.0113605
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[F1]Most powerful Bioagent that is the most destructive mix ever to be released on humanity
[F2]Signs of death or complete termination or destructive effects
[F3]Binary Effect—a dual method of attacking the body
[F4]Delivery method to impact the consumer—entering in a epigenetic venue and then to more readily take up more chemicals
[F5]With out these key aminos —everything from serotonin-dopamaine thyroid-hypothalmus-pituatary are completely disabled
[F6]This would mean taking your body weight divide by 2.2 to get the kilo conversion and then multiply the weight by the amount of protein in milligrams to grams
180 lb person / 2.2- 81 kg then multiply by the amount of protein intake so a 180 lb person taking 1.1 gram per Kg = 90 grams of protein the equivalent of 2 -3 oz pieces of meat or approximately a scoop of 30 gram of protein powder 3 times a day
[F7]The carbs as well that people would be intolerant to would be the ones that would be genetically engineered—processed or loaded with glyphosates that would have a huge impact on normal bodily functions
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Show of the Month December 2014
Glyphosate-Endocrine Disrupting
Stick out your tongue- Tongue appearance and illness
Antiproliferative activity and induction of apoptotic by ethanolic extract of Alpinia galanga rhizhome in human breast carcinoma cell line
A high whey protein–, leucine-, and vitamin D–enriched supplement preserves muscle mass during intentional weight loss
Cottage Cheese Making
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“First of all, we need to understand what we mean by the word safe. Actually, in terms of the academic literature, “safe” refers to “an acceptable level of risk.” It doesn’t refer to situations where there is no risk. Most of us drive in cars all the time and consider it to be safe even though we know that people are killed and injured in automobiles frequently. We have to understand that safe equals acceptable risk.
Glyphosate Poses Risk to Female Reproductive Health
Although there are only a handful of studies on the safety of GE soybeans, there is considerable evidence that glyphosate? especially in conjunction with the other ingredients in Roundup? wreaks havoc with the endocrine and reproductive systems.
Glyphosate throws off the delicate hormonal balance that governs the whole reproductive cycle. It interferes with aromatase, which produces estrogen, and it’s also highly toxic to the placenta in pregnant women. In a 2009 French study, scientists discovered that glyphosate can kill the cells in the outer layer of the human placenta (the trophoblast membrane), which in turn can kill the placenta. A mere 1/500th the amount needed to kill weeds was able to kill these cells! The amount is so small, according to the study’s authors, that the “residual levels to be expected, especially in food and feed derived from Roundup formulation-treated crops” could be enough to “cause cell damage and even [cell] death.” If the endocrine function of the placenta is destroyed, then ovarian and endometrial function may also suffer, and the end result could be a miscarriage. It’s important to remember that glyphosate can accumulate in your body, allowing its toxic effects to grow worse with repeated consumption of foods containing these Roundup Ready crops. Clearly, this may become a serious concern for the next generation, as most young children girls and boys alike growing up today are fed processed foods containing GE ingredients on a daily basis, year after year…—
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Monsanto Roundup: The Impacts of Glyphosate Herbicide on Human Health. Pathways to Modern Diseases
Glyphosate’s Suppression of Cytochrome P450 Enzymes and Amino Acid Biosynthesis by the Gut Microbiome: Pathways to Modern Diseases
By Global Research News
Global Research, January 02, 2014
Entropy and Global Research 12 July 2013
Theme: Biotechnology and GMO, Science and Medicine
by Anthony Samsel and Stephanie Seneff
Glyphosate, the active ingredient in Roundup®, is the most popular herbicide used worldwide[F1]. The industry asserts it is minimally toxic to humans, but here we argue otherwise. Residues are found in the main foods of the Western diet, comprised primarily of sugar, corn, soy and wheat. Glyphosate’s inhibition of cytochrome P450 (CYP) enzymes is an overlooked component of its toxicity to mammals. CYP enzymes play crucial roles in biology, one of which is to detoxify xenobiotics. Thus, glyphosate enhances the damaging effects of other food borne chemical residues and environmental toxins. Negative impact on the body is insidious and manifests slowly over time as inflammation damages cellular systems throughout the body. Here, we show how interference with CYP enzymes acts synergistically with disruption of the biosynthesis of aromatic amino acids by gut bacteria, as well as impairment in serum sulfate transport. Consequences are most of the diseases and conditions associated with a Western diet, which include gastrointestinal disorders, obesity, diabetes, heart disease, depression, autism, infertility, cancer and Alzheimer’s disease. We explain the documented effects of glyphosate and its ability to induce disease, and we show that glyphosate is the “textbook example” of exogenous semiotic entropy[F2]: the disruption of homeostasis by environmental toxins.
Introduction
The foodstuffs of the Western diet, primarily grown by industrial agriculture, are increasingly being produced using a two-part system of engineered plant seeds and toxic chemical application.[F3]–Novel bacterial genes are incorporated through genetic engineering, and toxic chemical residues are readily taken up by the engineered plants[F4]. Research indicates that the new bacterial RNA and DNA present in genetically engineered plants, providing chemical herbicide resistance and other traits, have not yet fully understood biological effects. This paper however, will only examine the effects of the chemical glyphosate, the most dangerous Bio Agent on the planet.——–Glyphosate (N-phosphonomethylglycine), the active ingredient in the herbicide Roundup®, is the main herbicide in use today in the United States, and increasingly throughout the World, in agriculture and in lawn maintenance, especially now that the patent has expired. 80% of genetically modified crops, particularly corn, soy, canola, cotton, sugar beets and most recently alfalfa, are specifically targeted towards the introduction of genes resistant to glyphosate, the so-called “Roundup Ready® feature” In humans, only small amounts (~2%) of ingested glyphosate are metabolized to aminomethylphosphonic acid (AMPA), and the rest enters the blood stream and is eventually eliminated through the urine [1].
Studies have shown sharp increases in glyphosate contamination in streams in the Midwestern United States following the mid 1990s, pointing to its increasing role as the herbicide of choice in agriculture [2]. A now common practice of crop desiccation through herbicide administration shortly before the harvest assures an increased glyphosate presence in food sources as well [3–5]. The industry asserts that glyphosate is nearly nontoxic to mammals [6,7], and therefore it is not a problem if glyphosate is ingested in food sources. Acutely, it is claimed to be less toxic than aspirin [1,6]. As a consequence, measurement of its presence in food is practically nonexistent. A vocal minority of experts believes that glyphosate may instead be much more toxic than is claimed, although the effects are only apparent after a considerable time lapse.
Thus, while short-term studies in rodents have shown no apparent toxicity [8], studies involving life-long exposure in rodents have demonstrated liver and kidney dysfunction and a greatly increased risk of cancer, with shortened lifespan [9].
Glyphosate’s claimed mechanism of action in plants is the disruption of the shikimate pathway, which is involved with the synthesis of the essential aromatic amino acids, phenylalanine, tyrosine, and tryptophan [10].
The currently accepted dogma is that glyphosate is not harmful to humans or to any mammals because the shikimate pathway is absent in all animals. However, this pathway is present in gut bacteria, which play an important and heretofore largely overlooked role in human physiology [11–14] through an integrated biosemiotic relationship with the human host. In addition to aiding digestion, the gut microbiota synthesize vitamins, detoxify xenobiotics, and participitate in immune system homeostasis and gastrointestinal tract permeability [14]. Furthermore, dietary factors modulate the microbial composition of the gut [15].[F5]—-The incidence of inflammatory bowel diseases such as juvenile onset Crohn’s disease has increased substantially in the last decade in Western Europe [16] and the Entropy 2013, 15 1418 United States [17]. It is reasonable to suspect that glyphosate’s impact on gut bacteria may be contributing to these diseases and conditions.—-However, the fact that female rats are highly susceptible to mammary tumors following chronic exposure to glyphosate [9] suggests that there may be something else going on. Our systematic search of the literature has led us to the realization that many of the health problems that appear to be associated with a Western diet could be explained by biological disruptions that have already been attributed to glyphosate. These include digestive issues, obesity, autism, Alzheimer’s disease, depression, Parkinson’s disease, liver diseases, and cancer, among others. While many other environmental toxins obviously also contribute to these diseases and conditions, we believe that glyphosate may be the most significant environmental toxin, mainly because it is pervasive and it is often handled carelessly due to its perceived nontoxicity.
In this paper, we will develop the argument that the recent alarming increase in all of these health issues can be traced back to a combination of gut dysbiosis, impaired sulfate transport, and suppression of the activity of the various members of the cytochrome P450 (CYP) family of enzymes. We have found clear evidence that glyphosate disrupts gut bacteria and suppresses the CYP enzyme class. The connection to sulfate transport is more indirect, but justifiable from basic principles of biophysics.
In the remainder of this paper, we will first provide evidence from the literature that explains some of the ways in which glyphosate adversely affects plants, microbes, amphibians and mammals.
Section 3 will discuss the role that gut dysbiosis, arguably resulting from glyphosate exposure, plays in inflammatory bowel disease and its relationship to autism.
Section 4 argues that the excess synthesis of phenolic compounds associated with glyphosate exposure represents a strategy to compensate for impairments in the transport of free sulfate.
Section 5 will provide evidence that glyphosate inhibits CYP enzymes. Section 6 explains how obesity can arise from depletion of serum tryptophan due to its sequestering by macrophages responding to inflammation. Section 7 shows how extreme tryptophan depletion can lead to impaired nutrient absorption and anorexia nervosa.
Section 8 provides a brief review of all the roles played by CYP enzymes in metabolism. Section 9 discusses a likely consequence to glyphosate’s disruption of the CYP-analog enzyme, endothelial nitric oxide synthase (eNOS). Section 10 shows how glyphosate’s effects could plausibly lead to brain-related disorders such as autism, dementia, depression, and Parkinson’s disease. Section 11 mentions several other health factors that can potentially be linked to glyphosate, including reproductive issues and cancer.
Section 12 discusses the available evidence that glyphosate is contaminating our food supplies, especially in recent years. Following a discussion section, we sum up our findings with a brief
Numerous laboratory studies have shown that glyphosate and the Roundup formulation can be genotoxic and endocrine disrupting. One study summarises these effects occurring at doses substantially lower than those used in agriculture, or permitted as residues: at 0.5 mg/kg (40 times lower than levels permitted in soybeans in the US) they were anti-androgenic; at 2 mg/kg they were anti-oestrogenic; at 1 mg/kg they disrupted the enzyme aromatase; at 5 mg/kg they damaged DNA, and at 10 mg/kg there were cytotoxic. These effects can result in crucial outcomes for sexual and other cell differentiation, bone metabolism, liver metabolism, reproduction, development and behaviour, and hormone dependent diseases such as breast and prostate cancer (Gasnier et al 2009).
Exposure to glyphosate-based herbicides, even at very low doses may result in reproductive and hormonal problems, miscarriages, low birth weights, birth defects, and various cancers—especially haematological cancers such as non-Hodgkin’s lymphoma, and hormonal cancers such as breast cancer. Several epidemiological studies have linked exposure to glyphosate with non-Hodgkin’s lymphoma, hairy cell leukaemia, multiple myeloma, DNA damage; and one study with spontaneous abortions and pre-term deliveries
GM pea protein caused lung damage in mice
Offspring of rats fed GM soy showed a five-fold increase in mortality, lower birth weights, and the inability to reproduce
GM potatoes may cause cancer in rats
Male mice fed GM soy had damaged young sperm cells
Bacteria in your gut can take up DNA from GM food
The embryo offspring of GM soy-fed mice had altered DNA functioning
GM foods lead to significant organ disruptions in rats and mice, specifically the kidney, liver, heart and spleen
Several US farmers reported sterility or fertility problems among pigs and cows fed on GM corn varieties
Bt corn caused a wide variety of immune responses in mice, commonly associated with diseases such as arthritis, Lou Gehrig’s disease, osteoporosis, and inflammatory bowel disease
Investigators in India have documented fertility problems, abortions, premature births, and other serious health issues, including deaths, among buffaloes fed GM cottonseed products
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Stick out your tongue- Tongue appearance and illness
Date-December 5, 2014
Source-Inderscience Publishers
Physicians often ask their patients to “Please stick out your tongue.” The tongue can betray signs of illness, which combined with other symptoms such as a cough, fever, presence of jaundice, headache or bowel habits, can help the physician offer a diagnosis. For people in remote areas who do not have ready access to a physician, a new diagnostic system is reported in the International Journal of Biomedical Engineering and Technology that works to combine the soft inputs of described symptoms with a digital analysis of an image of the patient’s tongue.–Karthik Ramamurthy of the Department of Information Technology, Rajalakshmi Engineering College, in Chennai, India, and colleagues, have trained a neural network that can take soft inputs such as standard questions about symptoms and a digitized image of the patient’s tongue and offer a likely diagnosis so that professional healthcare might then be sought if needed. The digitized images of the patient’s tongue reveal discoloration, engorgement, texture and other factors that might be linked to illness.–Smoothness and “beefiness” might reveal vitamin B12, iron, or folate deficiency, and anemia. Black discoloration could be indicative of fungal overgrowth in HIV patients or prolonged antibiotic use. Longitudinal furrows on the tongue are associated with syphilis. Ulcers may indicate the presence of Crohn’s disease or colitis and various other conditions. The team’s automated diagnostic, however, utilizes the condition of the tongue in combination with other symptoms to identify whether a patient has any of various illnesses: common cold, flu, bronchitis, streptococcal throat infection, sinusitis, allergies, asthma, pulmonary edema, food poisoning and diverticulitis.–The current system allows diagnosis of fourteen distinct conditions but the team adds that they will be able to add eye images and use those as an additional hard input for their neural network and so extend its repertoire significantly.–Story Source-The above story is based on materials provided by Inderscience Publishers. Note: Materials may be edited for content and length.–Journal Reference-Karthik, R., Menaka, R., Kulkarni, S. and Deshpande, R. Virtual doctor: an artificial medical diagnostic system based on hard and soft inputs. Int. J. Biomedical Engineering and Technology, Vol. 16, No. 4, pp.329-342
The two main characteristics of the tongue in TCM ZHENG diagnosis are the color and the coating. The color of the patient’s tongue color provides information about his/her health status. For example [13], dark red color can indicate inflammation or ulceration, while a white tongue indicates cold attack, mucus deposits, or a weakness in the blood leading to such conditions as anemia [12]. Moreover, a yellow tongue points out a disorder of the liver and gallbladder, and blue or purple implies stagnation of blood circulation and a serious weakening of the part of the digestive system that corresponds to the area of the tongue where the color appears.
Tongue Diagnosis: Color of the Tongue:
Progression of Color: When a body shows dis-ease the tongue color (underneath the coating) turns from pink to pale, to red and then to purple.
Purple tongues mean blood stasis.
Red dots on the tongue are called points and they have a meaning wherever they are. In Asian and African people these red dots can look brown.
Tongue Diagnosis: Coating of the Tongue: (Coating is related to Stomach function.)
A white coat corresponds to cold in the area of the body correlating to the tongue.
A yellow coat is related to heat.
A coating can be with “root” which means the coating cannot be scraped off and it looks like grass growing from the soil.
A coating without root looks like it has been sprinkled on and can be scraped off.
The thicker the coat, the more progressed the disease.
Lack of a coat means that the digestion is not working correctly.
The coating is slightly thicker on the back of the tongue.
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Antiproliferative activity and induction of apoptotic by ethanolic extract of Alpinia galanga rhizhome in human breast carcinoma cell line.
BMC Complement Altern Med. 2014;14:192
Authors: Samarghandian S, Hadjzadeh MA, Afshari JT, Hosseini M
Abstract
BACKGROUND: We investigated the potential of galangal rhizomes to induce cytotoxic and apoptotic effects in the cultured human breast carcinoma cell line, (MCF-7) in compare with the non-malignant (MRC-5) cells.-METHODS: Both cells were cultured in DMEM medium and treated with galangal rhizomes for three consecutive days. The percentage of apoptotic cells was determined by flow cytometry using Annexin-V fluorescein isothiocyanate.
RESULTS: The results showed that the ethanolic extract of galangal rhizomes decreased cell viability in the malignant cells as a concentration- and time- dependent manner. The IC50 values against MCF-7 were determined at 400.0 ± 11.7 and 170.0 ± 5.9 μg/ml after 48 and 72 h respectively. The morphology of MCF-7 cells treated with the ethanolic extract confirmed the cell proliferation assay results. Alpinia galanga induced apoptosis in MCF-7 cells, as determined by flow cytometry.–CONCLUSIONS: We concluded that the extract of Alpinia galanga exerts pro-apoptotic effects in a breast cancer-derived cell line and could be considered as a potential chemotherapeutic agent in breast cancer.–PMID: 24935101 [PubMed – indexed for MEDLINE]
Recipe—Make a tea out of this or even percolate this in a coffee percolator—this will also strengthen the heart and intestines
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A high whey protein–, leucine-, and vitamin D–enriched supplement preserves muscle mass during intentional weight loss in obese older adults: a double-blind randomized controlled trial1,2,3
Amely M Verreijen,
Sjors Verlaan,
Mariëlle F Engberink,
Sophie Swinkels,
Johan de Vogel-van den Bosch, and
Peter JM Weijs
+ Author Affiliations
1. 1From the Department of Nutrition and Dietetics, School of Sports and Nutrition, Amsterdam University of Applied Sciences, Amsterdam, The Netherlands (AMV, MFE, and PJMW), and Nutricia Research, Utrecht, The Netherlands (SV, SS, and JdV-vdB).
+ Author Notes
· ↵2 Supported by Nutricia Research, Nutricia Advanced Medical Nutrition.
· ↵3 Address correspondence to AM Verreijen, School of Sports and Nutrition, Amsterdam University of Applied Sciences, Dr. Meurerlaan 8, 1067 AM, Amsterdam, The Netherlands. E-mail: [email protected].
Abstract
Background: Intentional weight loss in obese older adults is a risk factor for muscle loss and sarcopenia.
Objective: The objective was to examine the effect of a high whey protein–, leucine-, and vitamin D–enriched supplement on muscle mass preservation during intentional weight loss in obese older adults.
Design: We included 80 obese older adults in a double-blind randomized controlled trial. During a 13-wk weight loss program, all subjects followed a hypocaloric diet (−600 kcal/d) and performed resistance training 3×/wk. Subjects were randomly allocated to a high whey protein–, leucine-, and vitamin D–enriched supplement including a mix of other macro- and micronutrients (150 kcal, 21 g protein; 10×/wk, intervention group) or an isocaloric control. Primary outcome was change in appendicular muscle mass. Secondary outcomes were body composition, handgrip strength, and physical performance. Data were analyzed by using ANCOVA and mixed linear models with sex and baseline value as covariates.
Results: At baseline, mean ± SD age was 63 ± 5.6 y, and body mass index (in kg/m2) was 33 ± 4.4. During the trial, protein intake was 1.11 ± 0.28 g [F6]· kg body weight–1 · d–1 in the intervention group compared with 0.85 ± 0.24 in the control group (P < 0.001). Both intervention and control groups decreased in body weight (−3.4 ± 3.6 kg and −2.8 ± 2.8 kg; both P < 0.001) and fat mass (−3.2 ± 3.1 kg and −2.5 ± 2.4 kg; both P < 0.001), with no differences between groups. The 13-wk change in appendicular muscle mass, however, was different in the intervention and control groups [+0.4 ± 1.2 kg and −0.5 ± 2.1 kg, respectively; β = 0.95 kg (95% CI: 0.09, 1.81); P = 0.03]. Muscle strength and function improved over time without significant differences between groups.
Conclusion: A high whey protein–, leucine-, and vitamin D–enriched supplement compared with isocaloric control preserves appendicular muscle mass in obese older adults during a hypocaloric diet and resistance exercise program and might therefore reduce the risk for sarcopenia. This trial was registered at the Dutch Trial Register (http://www.trialregister.nl) as NTR2751.
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Cottage Cheese Making
Method 1 of 3: Use Rennet
1
Heat the milk. Pour the milk into a small saucepan and place it over medium heat. Heat the milk slowly, making sure it doesn’t boil, until it reaches 85 degrees F. Use a candy thermometer to monitor the temperature. Turn off the heat when the milk is sufficiently warm.
2
Add the rennet. Place the drops of rennet directly in the milk. Use a spoon to stir the mixture for about 2 minutes.
3
Let the mixture stand. Cover the saucepan with a clean dish towel and let the rennet and milk sit untouched for about 4 hours. The rennet will start reacting with the milk to turn it into cheese.[1]
4
Slice the mixture. Remove the dish cloth and use a knife to make slices in the mixture and break up the curds. Slice several times in one direction, then make several slices in the opposite direction.
5
Cook the mixture. Add the salt to the saucepan. Turn the burner to medium low. Stir the mixture as it heats to help the curds separate from the whey. Stop as soon as the curds have separated and the whey looks slightly yellow. Don’t overcook the mixture, or the curds will be hard.
6
Strain the curds. Place a piece of cheesecloth or a fine-mesh strainer over a bowl Pour the curds and whey into the cheesecloth to strain the curds from the whey. Keeping the curds in the cheesecloth suspended over a bowl, cover the curds loosely with plastic wrap and place all of it in the refrigerator to let the whey continue to drain for a few hours. Stir it every once in awhile to help it along.
7
Serve the cottage cheese. Place the curds in a clean bowl and add the cream or half and half. Season with more salt to taste.
Method 2 of 3: Use Vinegar
1
Heat the milk. Place the milk in a saucepan and put it on the stove. Turn the burner to medium and let the milk heat to 120 degrees. Use a candy thermometer to monitor the milk’s temperature. Remove it from heat once it is sufficiently warmed.
2
Add the vinegar. Pour the vinegar into the saucepan and stir the mixture slowly for 2 minutes. Cover the pan with a dish cloth and let the mixture rest for 30 minutes.
3
Strain the curds from the whey. Pour the mixture into a colander lined with cheesecloth or a thin dish cloth. Let the whey drain for about five minutes.[2]
4
Rinse the curds. Gather the edges of the cloth and hold the curds under a stream of cold water. Squeeze the curds and move them around until they are all rinsed and cooled.
5
Finish the cottage cheese. Place the curds in a bowl. Add the salt and the cream or half and half. Store in the refrigerator or serve immediately.
Method 3 of 3: Use Lemon Juice
1
Heat the milk. Place it in a saucepan and heat it until it begins to steam, but does not come to a boil. Remove the milk from heat.
2
Add the lemon juice. Pour the lemon juice into the warm milk and stir it slowly for several minutes.
3
Let the mixture rest. Cover the saucepan with a dish cloth and let the curds separate from the whey for about an hour.
4
Strain the curds from the whey. Place a piece of cheesecloth over a bowl and pour the curds and whey into the cheesecloth. Let the curds drain for about 5 minutes.
5
Rinse the curds. Gather the ends of the cheesecloth and hold it under cool water to rinse the curds. Continue until they are completely cooled, then squeeze the cloth to get the curds as dry as possible.
6
Finish the cottage cheese. Place the curds in a bowl and add the salt and cream or half and half.
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Doubling saturated fat in diet does not increase saturated fat in blood
Date:
November 21, 2014
Source:
Ohio State UniversityEK
This is a sampling of foods provided to research participants during the three weeks that they were eating a very-low-carb diet. Doubling or even nearly tripling saturated fat in the diet does not drive up total levels of saturated fat in the blood, according to a controlled diet study.–However, increasing levels of carbohydrates in the diet during the study promoted a steady increase in the blood of a fatty acid linked to an elevated risk for diabetes and heart disease. The finding “challenges the conventional wisdom that has demonized saturated fat and extends our knowledge of why dietary saturated fat doesn’t correlate with disease,” said senior author Jeff Volek, a professor of human sciences at The Ohio State University. In the study, participants were fed six three-week diets that progressively increased carbs while simultaneously reducing total fat and saturated fat, keeping calories and protein the same. The researchers found that total saturated fat in the blood did not increase — and went down in most people — despite being increased in the diet when carbs were reduced. Palmitoleic acid, a fatty acid associated with unhealthy metabolism of carbohydrates that can promote disease, went down with low-carb intake and gradually increased as carbs were re-introduced to the study diet. “It’s unusual for a marker to track so closely with carbohydrate intake, making this a unique and clinically significant finding. As you increase carbs, this marker predictably goes up,” Volek said. When that marker increases, he said, it is a signal that an increasing proportion of carbs are being converted to fat instead of being burned as fuel. Reducing carbs and adding fat to the diet in a well-formulated way, on the other hand, ensures the body will promptly burn the saturated fat as fuel — so it won’t be stored. “When you consume a very low-carb diet your body preferentially burns saturated fat,” Volek said. “We had people eat 2 times more saturated fat than they had been eating before entering the study, yet when we measured saturated fat in their blood, it went down in the majority of people. Other traditional risk markers improved, as well.” The research is published in the Nov. 21, 2014, issue of the journal PLOS ONE. Volek and colleagues recruited 16 adults for the study, all of whom had metabolic syndrome, defined as the presence of at least three of five factors that increase the risk for heart disease and diabetes (excess belly fat, elevated blood pressure, low “good” cholesterol, insulin resistance or glucose intolerance, and high triglycerides). After getting them to a baseline reduced-carb diet for three weeks, researchers fed the participants the exact same diets, which changed every three weeks, for 18 weeks. The diets started with 47 grams of carbs and 84 grams of saturated fat each day, and ended with 346 carb grams per day and 32 grams daily of saturated fat. Each day’s meals added up to 2,500 calories and included about 130 grams of protein. The highest-carb level represented 55 percent of daily calories, which roughly matches the estimated daily percentage of energy provided by carbs in the American diet.
Compared to baseline, there were significant improvements in blood glucose, insulin and blood pressure that were similar across diets. Participants, on average, lost almost 22 pounds by the end of the trial. When looking at palmitoleic acid, however, the scientists found that it consistently decreased on the high-fat/low-carb diet in all participants. The fatty acid then showed a step-wise increase in concentration in the blood as carbs were progressively added to the diet. Elevated levels of palmitoleic acid in the blood have been linked to obesity and higher risk for inflammation, insulin resistance, impaired glucose tolerance, metabolic syndrome, type-2 diabetes, heart disease and prostate cancer. The study does not address what happens to palmitoleic acid levels when high carbs are combined with a diet high in saturated fat. Instead, Volek hoped to identify the carb-intake point at which participants began to store fat. “That turned out to be highly variable,” he said. “Everyone showed increased palmitoleic acid levels as carbs increased, but values varied widely between individuals, especially at the highest carb intake. This is consistent with the idea that people vary widely in their tolerance to carbohydrates.” Participants’ existing health risks were not a factor in the study because everyone ate the exact same diet for 18 weeks. Their bodies’ responses to the food were the focus of the work. “There is widespread misunderstanding about saturated fat. In population studies, there’s clearly no association of dietary saturated fat and heart disease, yet dietary guidelines continue to advocate restriction of saturated fat. That’s not scientific and not smart,” Volek said. “But studies measuring saturated fat in the blood and risk for heart disease show there is an association. Having a lot of saturated fat in your body is not a good thing. The question is, what causes people to store more saturated fat in their blood, or membranes, or tissues? “People believe ‘you are what you eat,’ but in reality, you are what you save from what you eat,” he said. “The point is you don’t necessarily save the saturated fat that you eat. And the primary regulator of what you save in terms of fat is the carbohydrate in your diet. Since more than half of Americans show some signs of carb intolerance, it makes more sense to focus on carb restriction than fat restriction.[F7]” Volek sees this palmitoleic acid as a potential biomarker to signal when the body is converting carbs to fat, an early event that contributes to what he calls “metabolic mayhem.””There is no magical carb level, no cookie-cutter approach to diet, that works for everyone,” he said. “There’s a lot of interest in personalized nutrition, and using a dynamically changing biomarker could provide some index as to how the body is processing carbohydrates.”-Story Source-The above story is based on materials provided by Ohio State University. The original article was written by Emily Caldwell. Note: Materials may be edited for content and length.-Journal Reference-Brittanie M. Volk, Laura J. Kunces, Daniel J. Freidenreich, Brian R. Kupchak, Catherine Saenz, Juan C. Artistizabal, Maria Luz Fernandez, Richard S. Bruno, Carl M. Maresh, William J. Kraemer, Stephen D. Phinney, Jeff S. Volek. Effects of Step-Wise Increases in Dietary Carbohydrate on Circulating Saturated Fatty Acids and Palmitoleic Acid in Adults with Metabolic Syndrome. PLoS ONE, 2014; 9 (11): e113605 DOI: 10.1371/journal.pone.0113605
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Show of the Month December 13 2014
Wake Forest research confirms controversial nitrite hypothesis
C-130 aircraft caught dropping massive ‘raindrop shaped fibers’ onto populace, lab tests confirm “metals”
AEROSPACE WORKER FIRED After Admitting– “I Installed Chemtrail Devices
Human exposure to metal cadmium may accelerate cellular aging
These Substances may help to Detoxify Cadmium
Bacterial biofilms are associated with colon cancer, imaging technique reveals
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Wake Forest research confirms controversial nitrite hypothesis[F8]
By Bonnie Davis, 336-758-5390, [email protected] Office of Communications and External Relations
Understanding how nitrite can improve conditions such as hypertension, heart attack and stroke has been the object of worldwide research studies. New research from Wake Forest University has potentially moved the science one step closer to this goal.–In a paper published online ahead of print in the February issue of the Journal of Biological Chemistry, senior co-author Daniel Kim-Shapiro, professor of physics at Wake Forest, and others show that deoxygenated hemoglobin is indeed responsible for triggering the conversion of nitrite to nitric oxide, a process that affects blood flow and clotting.—“We have shown that conversion of nitrite to nitric oxide by deoxygenated hemoglobin in red blood cells reduces platelet activation,” Kim-Shapiro said. “This action has implications in treatments to reduce clotting in pathological conditions including sickle cell disease and stroke.”–In 2003, Kim-Shapiro collaborated with Mark Gladwin, now at the University of Pittsburgh, who led a study that showed that nitrite (which is also used to cure processed meats), is not biologically inert as had been previously thought, but can be converted to the important signaling molecule nitric oxide (NO), and thereby increase blood flow[F9]. At that time, the researchers hypothesized that the conversion of nitrite to NO was due to a reaction with deoxygenated hemoglobin in red blood cells.–The main goal of the latest research, Kim-Shapiro said, was to determine how red blood cells perform these important signaling functions that lead to increased blood flow. The researchers used several biophysical techniques to measure NO production from nitrite and red blood cells and examined the mechanism of NO production.-“Importantly, this action was increased under conditions of low oxygen – so nitrite acts to increase blood flow in the body just when it is needed. What we’re showing with this research is what part of the red cell is doing this, and it’s consistent with our original hypothesis,” he said. “This speaks to the mechanisms and how they work – to how nitrite is dilating blood vessels and reducing clotting.”–As director of Wake Forest University’s Translational Science Center, Kim-Shapiro and others have conducted studies that look at how nitrite and its biological precursor, nitrate (found in beet root juice) can be utilized in treatments for a variety of conditions. In a 2010 study, they were the first to find a link between consumption of nitrate-rich beet juice and increased blood flow to the brain.—Kim-Shapiro said that next steps in the research include examining whether all red blood cells have this activation function and whether this function is diminished in red cell diseases like sickle cell disease, other blood diseases, or in the transfusion of older blood.–“Does this important function that we can now attribute to the hemoglobin in the red cells get compromised under certain conditions? And if so, how can we enhance it?” he said.
This work was supported by NIH grants HL058091, HL098032, and the Translational Science Center of Wake Forest University and Hypertension & Vascular Research Center of Wake Forest School of Medicine.–Lead co-authors include Chen Liu and Nadeem Wajih, of WFU department of physics. Contributing authors include Xiaohua Liu, Swati Basu, John Janes, Madison Marvel, Christian Keggi, Amber N. Lee, Andrea M. Belanger, Debra I. Diz, Paul J. Laurienti, and David L. Caudell, all of Wake Forest; Christine C. Helms, University of Richmond; and Jun Wang and Mark T. Gladwin, from the Lung, Blood and Vascular Medicine Institute at the University of Pittsburgh.
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C-130 aircraft caught dropping massive ‘raindrop shaped fibers’ onto populace, lab tests confirm “metals”
Independent lab tests point to mainstream cover-up of live biowarfare, geoengineering testing
By Shepard Ambellas
A C-130, tailed by two other aircraft, conducting biowarfare, geoengineering operations over Chino Valley, Arizona, Nov., 2014. –CHINO VALLEY, Ariz. (INTELLIHUB.COM) — Marie Snow and her friend Cori Gunnels knew they stumbled across something sinister, one November day, this year, when they saw what appeared to be 50 to 60-foot long “raindrops”, “solid” in nature, falling from the sky in clusters, after three military aircraft, including a C-130, flew overhead, minutes prior, at an altitude of an estimated 5,000-8,000 ft.–Using critical thinking skills, Snow and Gunnels, patriots and local residents, decided to collect samples of the fibrous material which was deployed from the three military planes earlier that day, saving the samples for testing. In fact, the fibers looked so ominous that Snow even opted not to touch them with her “bare hands” and collected them on “white pieces of paper”.–Visible fibers, 50 to 60 feet long, left after three military aircraft were flying at approx. 5,000-8,000 ft. altitude. –Soon after, Snow, determined to know the truth, contacted her local news station, KPHO, CBS 5, inviting them to investigate her fibrous discovery. —–Within days, CBS 5 took Snow up on her offer, sending reporter Greg Argos to investigate the fibrous samples she collected off of the natural terrain and nearby fence posts, also noting her eyewitness account to the 3 military aircraft which flew overhead that day. However, what happened after CBS 5 interviewed Snow may shock you.—According to Argos’ video piece, published Nov. 18, by CBS 5, samples of the unusual fibers, which are “thicker than a spider web and “very strong”, were taken to Grand Canyon University’s Forensic Science Lab for testing where a woman by the name of “Melissa Beddow” allegedly tested the samples under “40 times magnification”.–As reported in the Argos piece, Beddow stated that the fibrous samples were likely “biodegradable gauze” from “nearby cattle farms”, made up of “a mixture of wheat, gluten, flour and bacitracin, an antibiotic” in what the network touted as a “straight story”.–However, after the local news piece aired, Snow and others were skeptical of Argos’ findings. Snow was soon after urged by Al DiCicco, who appears in the documentary film “Shade the Motion Picture”, a film about covert and sinister bioweapons testing programs, to contact Intellihub News and get independent testing of the samples done by a reputable lab. And that’s just what Marie Snow did.—On Nov. 22, Snow reached out to me, [Intellihub’s Shepard Ambellas] to gather yet another opinion on how to proceed after something just didn’t feel right to Snow about KPHO, CBS 5′s report. –Once contacted by Snow, I, myself, recommended just what my friend Al DiCicco told her to do, “get some independent testing done”as we could than later do a “powerful article” if the results differed from KPHO, CBS 5′s findings.
And again, that’s just what Snow and Gunnels did, sending the samples to a credible lab, a testing facility located in Redding California to properly and scientifically carry out tests of several fibrous samples. –Days after, the actual results came back from the lab, and what was found may shock you.–The work orders, numbered “14K0279“, dated Dec. 4, 2014 and “14K0683“, dated Dec. 2, 2014, stated that “All analysis were performed under strict adherence to our established Quality Assurance Plan” and that “solid” “fibers” were submitted by “Marie Snow” for “general testing”.
Lab test “14K0683” dated Dec. 02, 2014. (Image Credit: Cori Gunnels)
Lab test “14K0683” dated Dec. 02, 2014. (Image Credit: Cori Gunnels)
Astonishingly, both tests concluded that both samples indeed tested positive for three metal analytes, “Aluminum”, “barium” and “strontium”, three substances commonly known by dedicated researchers to be found in persistent contrails, i.e. chemtrails and or geoengineering, terraforming operations as pointed out by investigative researcher, activist, Rosalind Peterson, Agriculture Defense Coalition, in Shade the Motion Picture.
Lab test “14K0729” dated Dec. 04, 2014. (Image Credit: Marie Snow)
Lab test “14K0729” dated Dec. 04, 2014. (Image Credit: Marie Snow)
Coupling the Redding lab’s scientific findings, with Marie Snow’s eyewitness account of the three military planes flying overhead, the fibrous material collected, and other breakthrough research noted in Shade the Motion Picture, we must now hold the mainstream news accountable for not reporting actual scientific evidence and findings pertaining to persistent contrails, chemtrails, geoengineering or the terraforming of our planetary atmosphere.—In fact scientists, likely not credible ones, Bill Gates and others are now claiming that geoengineering is needed to block solar radiation, to prevent “global warming”. –Although some like Dr. Matthew Watson, University of Bristol, say that Solar Radiation Management (SRM) could have “profoundly terrifying” consequences possibly causing extreme drought or severe rainfall, conflicting weather, in opposite regions of the globe not typical to the locality.–Mysterious fibers containing barium, strontium and aluminum found on power lines after military test, Chino Valley, AZ. (Photo Credit: Marie Snow)–“Some of the techniques could also damage the ozone layer, leaving people at risk of skin cancer, or potentially trigger conflicts amid tensions between those affected by their deployment, the scientists said.”, as reported by The Telegraph in the article Six radical ways to tackle global warming. —But maybe even more bothersome is the fact that theses biological, chemical, and in some cases radiological, tests have all been approved to be conducted on the general public, at any time, by the U.S. government or military, under a public law.—
Public Law 105–85 105th Congress
PUBLIC LAW 105-85- NOV. 18, 1997: USE OF HUMAN SUBJECTS FOR TESTING OF CHEMICAL OR BIOLOGICAL AGENTSSEC. 1078. RESTRICTIONS ON THE USE OF HUMAN SUBJECTS FOR TESTING OF CHEMICAL OR BIOLOGICAL AGENTS.(a) PROHIBITED ACTIVITIES. – The Secretary of Defense may not conduct (directly or by contract)(1) any test or experiment involving the use of a chemical agent or biological agent on a civilian population; or
(2) any other testing of a chemical agent or biological agent on human subjects.(b) EXCEPTIONS.- Subject to subsections (c), (d), and (e), the prohibition in subsection (a) does not apply to a test or experiment carried out for any of the following purposes:(1) Any peaceful purpose that is related to a medical, therapeutic, pharmaceutical, agricultural, industrial, or research activity.
(2) Any purpose that is directly related to protection against toxic chemicals or biological weapons and agents.
(3) Any law enforcement purpose, including any purpose related to riot control.
So section (a) prohibits these cruel and inhumane chemical and biological tests on humans.
Then section (b) says that the prohibitions in section (a) do not apply to tests carried out for virtually any purpose. So section (b) completely negates the prohibitions of section (a).
And don’t be fooled — testing is currently being conducted and is harming your health as pointed out by Luca Zanna and Al DiCicco in Shade the Motion Picture when lab work, i.e. official blood tests were revealed for the first time publicly, demonstrating that the very metals, “analyites” found in these chemtrail “raindrop” like fibers are also in the human bloodstream at alarmingly toxic levels.
Ladies and gentlemen we are being exterminated ever so slowly. Our eventual deaths brought on by the bi-product of geoengineering applications, now being sold to the American people as necessary. And yes, the U.S. government is aware of it and has prepared quite the secret budget, unseen to most, kept under the radar of the American people.
The secretive budget, that President Obama and other members of his administration don’t want you to know about, was first uncovered by myself [Shepard Ambellas] and Avalon, Intellihub.com, in March of 2011, published in an article titled “Exposed: Secret presidential chemtrail budget uncovered — Congress exceeds billions to spray populace like roaches” which garnered worldwide attention.
Focusing on exposing geoengineering, chemtrail, applications, the article called out the U.S. Global Change Research Program (USGCRP), which is composed of 13 federal member agencies, with FY budgets into the billions of dollars.
The USGCRP, working hand-and-hand with the University Corporation for Atmospheric Research (UCAR), the U.S. government, and other governments of the world are conducting sinister and experimental research on mother earth and all of its living inhabitants including humans, plants, animals and sea life.
Moreover, massive money-making schemes may also be partly to blame for modern weather manipulation, geoengineering, and terraforming operations as weather derivatives can now be traded on the Chicago Mercantile Exchange.
In fact the CME Group’s official website confirms the market for such operations, reading, “From heat waves to arctic cold outbreaks, weather often has a significant impact on business – accounting for $5.3 billion of the $16 trillion US GDP. CME Group’s temperature-based index futures and options provide the tools to help you manage weather-related risk.” All big business and opportunity for the wealthy, despite being downplayed by publications such as Fortune.
Snow’s personal encounter is described by her in the following memo sent to Intellihub News:
My friend Cori Gunnels, who lives eight miles south-west of me, called and told me to go outside to see a C-130 or KC-130, with two escorts flying over her home. I went outside and looked to the south-west and saw a 130 with two escorts to the rear of it heading west. The second (northern most) escort split off from the other two and was headed in my direction, (north-east).
When it began to fly directly over my house, (Cori was on the phone with me), I began seeing what looked like long rain drops, or extremely long cob-web type fibers (twenty to fifty feet long), falling from the direction of the aircraft. I did not see it falling directly from the aircraft, but it was an immediate action. The sun was in the perfect position for me to see this substance falling toward the ground, and on my head.
The substance also fell from the sky on my friend Cori at the time the aircraft were present and passing over her. Neither of us saw the substance fall directly from the aircraft, however, it was at the exact time the different aircraft passed over both of us. Cori lives at an altitude of approx. 5,400 ft., and Cori told me that the aircraft were almost at the same altitude as Granite Mountain, which is 7,629 ft. Cori’s friend was working in Chino Valley at that exact time and he also reports seeing the substance fall from the sky. I am not sure if he saw the aircraft.
I grabbed a white piece of paper and began collecting the unknown substance from mid-air. The fibers were so long that I had to wind the paper over and over for many minutes in order to collect it. I also collected the fibers from the cars, fences and plants. The telephone lines were covered in it. Not only was this substance found in my yard, but also all over of Chino Valley, the Yavapai College Campus in Chino Valley, Prescott, Williamson Valley, and there were reports in Phoenix as well.
I am very afraid that this substance may be harmful, as the fibers are very fine and I, along with anyone else that was outside at the time, breathed them in. Because it landed in my organic garden, I disposed of anything growing there.
I have many pictures of this substance, a picture of the three aircraft, and physical evidence we collected from the air, cars, fences and plants. The picture of the C130 seems to show the rear loading bay open on the back of the aircraft.
This matter is urgent and needs attention. I called Ernest Love Field in Prescott to inquire whether they had any knowledge of a C-130 with two escorts were in the area… they know nothing. I have contacted the EPA, who referred me to Arizona Dept. of Environmental Quality… who referred me back to the EPA. I also filed three complaints with the FAA, have emailed all ninety-four AZ State representatives, and only heard back from Judy Burgess, who requested that I notify her of the results of the lab tests. If none of these agencies are responsible for an unknown substance falling from an aircraft, why do they exist?
I contacted Luke AFB, and was told to contact Davis Monthan AFB. I spoke with an air force Lieutenant there, and they are investigating this event. I did a television interview with CBS on 11-12-14, they did not do an honest interview. When I left the interview they gathered their own samples and had them tested (Positive gauze, wheat gluten flour and bacitracin). I asked them to hold off on the story until we got our results back. We have sent two samples of the substance to different labs and as of 12-4-14, my results show highly positive for aluminum = 421mg (MDL = 156), Strontium = 70.8mg (MDL = 3.1), Cori’s results Aluminum 1020mg
(MDL = 164) Barium = 34.1 (MDL = 11.9).
Update, Nov. 19, 2014: Congressman Gosar has assigned the case to the EPA and I feel we are going to be heard finally.
Update Nov. 21, 2014: I have heard from the EPA… they are taking the case.
Update Dec. 02, 2014: We are searching for any labs: soil, air, rainwater, blood, fibers. Please help. Alerting alternative media to keep the truth alive.
Thank you,
Marie Snow
It’s also important to point out that Corri Gunnels, an admin on “Uniting for Our Planet, Redding CA’s” Facebook page, told Intellihub News in an interview Friday, that she “knew they [KPHO, CBS 5] were going to marginalize the story”, despite the fact that the station’s news editor, Scott Davis, told Gunnels that he had never been directed by corporate to skew a report.
Gunnels also wanted me to point out in this article that “three other eyewitnesses in Phoenix called CBS 5″, reporting the strange fibers days before Gunnel and Snow collected samples.
Gunnels believes that this information was withheld from the local news report, as “biodegradable bandages” wouldn’t be of any use in the city of Phoenix as limited livestock exists there, further demonstrating a potential cover-up of the actual story.
Other Sources:
‘Mysterious’ fibers in Chino Valley are biodegradable gauze — KPHO, CBS 5
Six radical ways to tackle global warming – The Telegraph
Recent U.S. snowstorms found to contain elements of entomological warfare being conducted on American populace – Intellihub.com
PUBLIC LAW 105–85—NOV. 18, 1997 — DOD.mil
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AEROSPACE WORKER FIRED After Admitting– “I Installed Chemtrail Devices”
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New World Order Plans To Destroy and Take Over!
In case you missed this relevant news mid-May, an ex-aerospace worker came forward and admitted that chemtrail devices are installed on airplanes (as he was one of the installers) and shares details about what they installed.–We need to be very concerned about this, as it is affecting the health of our loved ones, our children, ourselves, and society as a whole! It also has damaging catastrophic effects on the environment, our food supply, and much more.
In his words, from the included video footage below:
“We gutted the plane, mounted the tanks. Installed the cables and lines and spraying devices. I was a civilian worker supervised by the military. When we finished, we were told that this was a test conducted by the German Aeronautics and Space Administration. Meaning that the plane with the spraying devices goes ahead while a second plane with measuring devices flies behind and conducts measurements. Like, “we just want to find out how the particles do behave and propagate.–“So when we were finished with the installation, guys from the military came over and instructed us to wear full body protective clothing and breathing masks because they were now going to fill the tanks. And that the substances, like aluminum sulfides or barium oxides, would contain highly toxic nano particle sized polymers.–He then adds, “We are moving toward an ecological catastrophe! And those who don’t believe me, please come here and I will show you the proof!”
Aerospace Worker: “I Installed Chemtrails Devices” – ENGLISH SUBS
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Human exposure to metal cadmium may accelerate cellular aging
Date:
December 11, 2014
Source:
George Washington University Milken Institute School of Public Health
A new study led by a researcher at Milken Institute School of Public Health (Milken Institute SPH) at the George Washington University looks at the metal cadmium and finds that higher human exposure can lead to significantly shorter telomeres, bits of DNA at the ends of chromosomes that are associated with cardiovascular disease, diabetes and other diseases of old age[F10]. The study, which was published online in the American Journal of Epidemiology, is the largest-ever to look at cadmium exposure and telomeres.—“We looked at heavy metals in this study and found a strong association between exposure to low levels of cadmium and telomere shortening,” says Ami Zota, ScD, MS, an assistant professor of environmental and occupational health at Milken Institute SPH. “Our findings suggest that cadmium exposure can cause premature aging of cells.[F11] And they add to other evidence indicating this heavy metal can get into the bloodstream and trigger kidney disease and other health problems.”–The World Health Organization calls environmental exposure to cadmium a “major public health concern,” and notes this heavy metal has been associated with cardiovascular disease, respiratory problems, cancer and other serious diseases. People typically are exposed to small amounts of this toxic metal by inhaling tobacco smoke, eating fruits and vegetables grown in contaminated soil or living near an industrial site, according to Zota.—In this study, Zota and her colleagues looked at blood and urine samples taken from more than 6,700 adults who participated in the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2002, a nationally representative health survey of the U.S. population. The researchers obtained purified DNA from blood cells and then used a genetic technique known as polymerase chain reaction to measure the telomeres, the caps on the tips of chromosomes that help protect the genetic code[F12].–Then the researchers measured the concentration of cadmium in the blood and urine samples. They divided the participants up into fourths based on the concentrations of cadmium found in their bloodstream, finding that people in the highest group had telomeres that were about six percent shorter than those in the lowest group.–“People with the highest cadmium exposure had cells that looked on average 11 years older than their chronological age,” Zota said, adding that even people in the highest group of exposure still had very tiny amounts of metal in their bloodstream. “This study adds to evidence suggesting that no level of exposure to this metal is safe.”–Normal wear and tear on the telomeres leads to shortening as people get older. But other factors, including cadmium, may speed up that process. When the telomeres get too short, the cell can no longer divide and chronic diseases can be the result.–The findings of this study suggest that cadmium can elicit harmful effects on the human body at levels well below the current safety standards set by environmental and occupational safety agencies. Such findings suggest that public health officials may need to accelerate the efforts to reduce the contamination of the environment–so that people are protected from even trace amounts of this metal, Zota notes.–The World Health Organization says global efforts to reduce exposure to this metal are urgently needed in order to protect the public health. Because tobacco smoke releases cadmium into the air WHO recommends a ban on smoking in public places. The group also suggests that governments worldwide promote better ways of disposing batteries and other measures to prevent contamination of the environment. Interventions should be aimed at protecting the most vulnerable, such as minority or low-income populations, who are often disproportionately exposed.–For non-smokers, food is generally the largest source of cadmium exposure, Zota says. Cadmium levels in some foods can be increased due to the application of phosphate fertilizers [F13]or sludge that is applied to farm fields.–Many other studies have linked exposure to cadmium to a host of health problems but this is one of the first to suggest it can shorten telomeres and set people up for premature aging, Zota says. This study also looked at human exposure to the heavy metal lead but found no link between blood levels of lead and shorter telomeres, Zota says.–Still, she says the new study’s findings do not prove that exposure to cadmium actually causes telomeres to get shorter. Instead, this study finds an association between cadmium levels and shorter telomeres, a link that was strong and independent but must be proven with additional research.-Story Source–The above story is based on materials provided by George Washington University Milken Institute School of Public Health. Note: Materials may be edited for content and length.–Journal Reference-Ami R. Zota, Belinda L. Needham, Elizabeth H. Blackburn, Jue Lin, Sung Kyun Park, David H. Rehkopf, and Elissa S. Epel. Associations of Cadmium and Lead Exposure With Leukocyte Telomere Length: Findings From National Health and Nutrition Examination Survey, 1999–2002. American Journal of Epidemiology, December 2014 DOI: 10.1093/aje/kwu293
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These Substances may help to Detoxify Cadmium
Amino Acids
Cysteine may chelate Cadmium from the body: [more info]
-N-Acetyl-Cysteine (NAC) counteracts the toxic effects of Cadmium. references
Cystine may chelate Cadmium from the body. [more info]
Ethylene-Diamine-Tetra-Acetate (EDTA) – the synthetic Amino Acid used in Chelation Therapy – may chelate Cadmium from the body. references
Methionine may chelate Cadmium from the body. references
Taurine may facilitate the excretion of Cadmium and minimizes the toxic effects associated with Cadmium. references
Carbohydrates
Alginates may bind to Cadmium in the Digestive Tract, may reduce its absorption and may facilitate its excretion. references
Pectins may reduce the absorption of Cadmium in the digestive tract.
Hormones
Melatonin may counteract the ability of Cadmium to damage the Liver: references
Melatonin may inhibit the depletion of Glutathione in the Liver that is caused by Cadmium accumulation.
Minerals
Calcium may increase the elimination of Cadmium from the body by competing with Cadmium for absorption. [more info]
Copper may increase the elimination of Cadmium from the body. [more info]
Iron may facilitate the elimination of Cadmium from the body. references
Selenium may increase the elimination of Cadmium from the body and may inhibit Cadmium-induced stimulation of the Epithelium of the Prostate. references
Zinc may prevent the accumulation of Cadmium (by competing with it for absorption). references
Peptides
Glutathione (usually after incorporation into the Glutathione Peroxidase enzyme) may chelate Cadmium from the body. [more info]
Proteins
Metallothionein (an endogenous Protein) immobilizes Cadmium by binding to it, making it unavailable to the tissues and organs.
Sulfuric Compounds
DMSA may prevent the absorption of Cadmium from the Gastrointestinal Tract. references
Vitamins
Lipoic Acid may chelate (bind to and remove) accumulated Cadmium from the body and may help to prevent Liver damage caused by Cadmium. references
Vitamin C (500 – 1,000 mg per day) may assist in removing accumulated Cadmium and may reverse the symptoms of Cadmium toxicity. references
The Tocopherol Succinate form of Vitamin E may provide total protection to the body’s Cells from the toxic effects of Cadmium: references
Vitamin E may inhibit the ability of Cadmium to reduce the activity of 5′-Deiodinase (the enzyme that catalyzes the conversion of Thyroxine to Triiodothyronine).
Water
Hard Water may dissolve Cadmium that may be present in water pipes more easily than can Soft Water.
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Bacterial biofilms are associated with colon cancer, imaging technique reveals
Date:
December 12, 2014
Source:
Marine Biological Laboratory
Bacteria forming a mixed biofilm on colon cancer tissue.
Since the first “catalog” of the normal bacterial makeup of the human body was published in 2012, numerous connections between illness and disturbances in the human microbiota have been found. This week, scientists report yet another: Cancerous tumors in the ascending colon (the part nearest to the small intestine) are characterized by biofilms, which are dense clumps of bacterial cells encased in a self-produced matrix.—-“This is the first time that biofilms have been shown to be associated with colon cancer, to our knowledge,” says co-author Jessica Mark Welch, a scientist at the Marine Biological Laboratory (MBL) in Woods Hole, Mass.-The discovery, led by researchers at the Johns Hopkins Medical Institutions, draws on a novel way to “see” microbial community structure that was developed by Mark Welch and colleagues at the MBL. Called combinatorial imaging, it could potentially be used to clinically diagnose pre-cancerous and cancerous conditions in the ascending colon.–In healthy people, the colon is covered in a mucus layer (mucosa) that helps keep bacteria away from the colon’s “skin,” or epithelia. Remarkably, the team found that colon cancer patients who have tumor-associated biofilms also have biofilms on tumor-free areas of the nearby mucosa.-“This suggests that either the tumor allows the biofilm to form, or the biofilm is helping to cause the tumor,” says Mark Welch. “The breaching of the mucus layer could allow bacteria to come into contact with the host epithelial cells, and that is one thing that could lead to cancer.”–The team found that tumors in the descending colon (going to the rectum) do not have associated biofilms.–Mark Welch and MBL co-authors Gary Borisy (now at the Forsyth Institute) and Blair Rossetti are among a group of MBL scientists who invented the combinatorial imaging technique used in this research. Different colors of fluorescent probes (nine in this study) “light up” different species of bacteria in the biofilm, revealing the 3-D structure of its microbial community. They found that the biofilms associated with ascending colon tumors are composed of many species of bacteria; they are diverse (non-identical); and that the part of the biofilm that invades the mucosal layer contains a subset of all the bacterial strains in the biofilm, rather than just one invading strain[F14].
Story Source-The above story is based on materials provided by Marine Biological Laboratory. The original article was written by Diana Kenney. Note: Materials may be edited for content and length.–Journal Reference-Christine M. Dejea, Elizabeth C. Wick, Elizabeth M. Hechenbleikner, James R. White, Jessica L. Mark Welch, Blair J. Rossetti, Scott N. Peterson, Erik C. Snesrud, Gary G. Borisy, Mark Lazarev, Ellen Stein, Jamuna Vadivelu, April C. Roslani, Ausuma A. Malik, Jane W. Wanyiri, Khean L. Goh, Iyadorai Thevambiga, Kai Fu, Fengyi Wan, Nicolas Llosa, Franck Housseau, Katharine Romans, XinQun Wu, Florencia M. McAllister, Shaoguang Wu, Bert Vogelstein, Kenneth W. Kinzler, Drew M. Pardoll, Cynthia L. Sears. Microbiota organization is a distinct feature of proximal colorectal cancers. Proceedings of the National Academy of Sciences, 2014; 201406199 DOI: 10.1073/pnas.1406199111
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[F1]Most powerful Bioagent that is the most destructive mix ever to be released on humanity
[F2]Signs of death or complete termination or destructive effects
[F3]Binary Effect—a dual method of attacking the body
[F4]Delivery method to impact the consumer—entering in a epigenetic venue and then to more readily take up more chemicals
[F5]With out these key aminos —everything from serotonin-dopamaine thyroid-hypothalmus-pituatary are completely disabled
[F6]This would mean taking your body weight divide by 2.2 to get the kilo conversion and then multiply the weight by the amount of protein in milligrams to grams
180 lb person / 2.2- 81 kg then multiply by the amount of protein intake so a 180 lb person taking 1.1 gram per Kg = 90 grams of protein the equivalent of 2 -3 oz pieces of meat or approximately a scoop of 30 gram of protein powder 3 times a day
[F7]The carbs as well that people would be intolerant to would be the ones that would be genetically engineered—processed or loaded with glyphosates that would have a huge impact on normal bodily functions
[F8]Nitrite signaling likely occurs through its reduction to nitric oxide (NO). Several reports support a role of erythrocytes and hemoglobin in nitrite reduction, but this remains controversial and alternative reductive pathways have been proposed. In this work we determined whether the primary human erythrocytic nitrite reductase is hemoglobin as opposed to other erythrocytic proteins that have been suggested to be the major source of nitrite reduction. We employed several different assays to determine NO production from nitrite in erythrocytes including electron paramagnetic resonance detection of nitrosyl hemoglobin, chemiluminescent detection of NO, and inhibition of platelet activation and aggregation. Our studies show that NO is formed by red blood cells and inhibits platelet activation. Nitric oxide formation and signaling can be recapitulated with isolated deoxyhemoglobin. Importantly, there is limited NO production from erythrocytic xanthine oxidoreductase and nitric oxide synthase. Under certain conditions we find dorzolamide (an inhibitor of carbonic anhydrase) results in diminished nitrite bioactivation, but the role of carbonic anhydrase is abrogated when physiological concentrations of CO2 are present. Importantly, carbon monoxide, which inhibits hemoglobin function as a nitrite reductase, abolishes nitrite bioactivation. Overall our data suggest that deoxyhemoglobin is the primary erythrocytic nitrite reductase operating under physiological conditions and accounts for nitrite-mediated NO signaling in blood.
[F9]This is where it can be a an issue —if the meat it self has some kind of carcinogen in it—then the nitric oxide when converted from the nitrate or nitrite will also carry this throughout as well—the same effect found in cigarettes the nicotinic acid acts as a delivery mechanism to send throughout the body the poisons attached amplifying the effect
The nitrites would do the same—to offset this you would incorporate Vitamin C to negate the carcinogen—make the nitrite safe
[F10]Vitamin C can reverse the telomeres from the damge of cadmium and it can be bound with a sulphur as well to remove this
[F11]The have found higher then normal levels of cadmium in the northern part of Ontario where chemtrail activity has been
[F12]Protein enzyme that protect the telomeres
[F13]Glyphosates—these may even chealte or transport the metal more profoundly into the cells
[F14]Tuesday, Jan. 8, 2013 – A new study published in the journal Current Microbiology describes the harmful effect of glyphosate on intestinal bacteria in poultry. The evidence is that glyphosate is toxic to beneficial bacteria such as Enterococcus faecalis, Enterococcus faecium, Bacillus badius, Bifidobacterium adolescentis and Lactobacillus spp, while pathogenic bacteria such as Salmonella Entritidis, Salmonella Gallinarum, Salmonella Typhimurium, Clostridium perfringens and Clostridium botulinum are highly resistant to glyphosate.–A reduction of beneficial bacteria in the gastrointestinal tract disturbs the normal gut bacterial community and allows salmonella and clostridia species to grow unchecked thus increasing the incidence of these two diseases.–The researchers pointed out that glyphosate also has the potential to induce genetic mutations within bacteria, making it possible for a new level of pathogenicity to emerge following chronic exposure to this chemical.- Oral bioavailability of glyphosate: studies using two intestinal cell lines.
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Show of the Month December 27 2014
Polymorphism, bacteria inside us help dictate inflammation, antitumor activity
Terrestrosin D, a steroidal saponin from Tribulus terrestris L., inhibits growth and angiogenesis of human prostate cancer in vitro and in vivo
Steroidal saponins from Tribulus terrestris—Protective effect of Tribulus terrestris linn on liver and kidney in cadmium intoxicated rats
Wild blueberries (bilberries) can help tackle adverse effects of high-fat diet
Creation of ‘rocker’ protein opens way for new smart molecules in medicine, other fields
Bad air means bad news for seniors’ brainpower
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Polymorphism, bacteria inside us help dictate inflammation, antitumor activity
Date:
December 20, 2014
Source:
The Wistar Institute
A common polymorphism — a variation in a person’s DNA sequence that is found with regularity in the general population — can lead to a chain of events that dictates how a tumor will progress in certain types of cancer, including a form of breast cancer as well as ovarian cancer, according to new research from The Wistar Institute that was published online by the journal Cancer Cell.–The research reveals a more explicit role about the symbiotic relationship humans have with the various bacteria that inhabit our body and their role during tumor progression.–“Our research indicates that interactions between the helpful bacteria in our bodies and immune cells at places situated away from tumors influence systemic responses in the host that alter how these tumors are able to progress,” said José Conejo-Garcia, M.D., Ph.D., Associate Professor and Program Leader in the Tumor Microenvironment and Metastasis Program at The Wistar Institute and lead author of the study.–Humans are colonized with trillions of bacteria — known as commensal bacteria because there are benefits to having these bacteria in our bodies — that inhabit the gastrointestinal and respiratory tracts and our skin. [F1]These bacteria provide a first line of defense against infection. Recent research has found that interactions between these bacteria and the immune system are critical for providing important defenses against tumors occurring outside of the intestines.–[F2]In order for the immune system to recognize commensal as well as microscopic organisms that can cause disease — or pathogens — many of our cells are programmed to recognize pathogen-associated molecular patterns. At least 23% of the general public carries mutations in a group of pathogen recognition receptors called Toll-like receptor (TLR) genes. One of the most abundant polymorphisms, occurring in about 7.5% of the general population, or slightly more than one in fifteen people, which results in loss of function, is in TLR5. Although this polymorphism is found in completely healthy individuals, the people who do carry it are susceptible to illnesses such as Legionnaires disease, urinary tract infections, and bronchopulmonary dysplasia. Knowing that this variant could impact some immune responses, Wistar researchers set out to understand whether TLR5 signaling influences cancer.–The researchers found that TLR5 signaling influences certain types of cancer in different ways and is dependent upon the ability of the tumor to respond to interleukin 6 (IL-6), a small protein that can have both pro-inflammatory and anti-inflammatory properties. In individuals with functional TLR5 expression, commensal bacteria are able to stimulate IL-6 production, greater mobilization of myeloid-derived suppressor cells (MDSCs), which in turn transform gamma delta T cells, a T cell subset that possesses innate-like properties, to produce high amounts of galectin-1, a protein that suppresses antitumor immune activity and hastens tumor progression.—However, the researchers also showed that TLR5 signaling does not always mean that tumors will grow faster. TLR5-deficient mice with tumors that produce low levels of IL-6 have faster tumor progression. In this instance, IL-17, another interleukin closely associated with autoimmune diseases and inflammation, is consistently found in higher levels in TLR5-deficient mice that have tumors, but IL-17 only accelerates cancer when the tumors are unresponsive to IL-6.—Researchers observed these phenomena were dependent upon commensal bacteria. When commensal bacteria were removed with antibiotics, the differences in TLR5-mediated tumor progression were not observed. The researchers noted that the differences in inflammation and progression of tumors are recapitulated in TLR5-responsive and unresponsive patients with ovarian and luminal breast cancer. The researchers performed a survival analysis using data from The Cancer Genome Atlas (TCGA) on patients for whom data on their TLR5 status was known.—-“Although independent sets of data and higher numbers of patients are needed, our data suggest that ovarian cancer reflects the evolution of IL-6-dependent tumors, while luminal breast cancer appears to become more aggressive in carriers of the polymorphism that abrogates TLR5 signaling,” Conejo-Garcia said.—[F3]For ovarian cancer, which is associated with high levels of IL-6, researchers found a significantly higher number of TLR5-deficient patients alive six years after their initial diagnosis compared with patients with TLR5, indicating a correlation between the absence of TLR5 and improved survival. For luminal breast cancer, which is associated with low levels of IL-6, the long-term survival prospects were worse for patients without TLR5.—Story Source-The above story is based on materials provided by The Wistar Institute. Note: Materials may be edited for content and length.—Journal Reference-Melanie R. Rutkowski, Tom L. Stephen, Nikolaos Svoronos, Michael J. Allegrezza, Amelia J. Tesone, Alfredo Perales-Puchalt, Eva Brencicova, Ximena Escovar-Fadul, Jenny M. Nguyen, Mark G. Cadungog, Rugang Zhang, Mariana Salatino, Julia Tchou, Gabriel A. Rabinovich, Jose R. Conejo-Garcia. Microbially Driven TLR5-Dependent Signaling Governs Distal Malignant Progression through Tumor-Promoting Inflammation. Cancer Cell, 2014; DOI: 10.1016/j.ccell.2014.11.009
[F1]Glyphosates Destroy this bacteria opening everyone up to a variety or host of activity which can create all kinds of imbalances—with the added metals and biofilms as well from the chemtrails —you would be able to create a considerable overload and expedite the spread of anything to create the tumours-paracitical—viral—fungal and negative bacteria over load
[F2]This can refer to skin lesions as well
[F3]The reasons for different cancer activity in different regions what gets turned on and what gets turned off
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Terrestrosin D, a steroidal saponin from Tribulus terrestris L., inhibits growth and angiogenesis of human prostate cancer in vitro and in vivo.
Pathobiology. 2014;81(3):123-32
Authors: Wei S, Fukuhara H, Chen G, Kawada C, Kurabayashi A, Furihata M, Inoue K, Shuin T
Abstract
OBJECTIVE: The aim of this study was to investigate whether terrestrosin D (TED) inhibits the progression of castration-resistant prostate cancer and consider its mechanism.
METHODS: Cell cycle, mitochondrial membrane potential (ΔΨm) and apoptosis were determined by flow cytometry. Caspase-3 activity and vascular endothelial growth factor secretion were detected by a caspase-3 assay and human vascular endothelial growth factor kit, respectively. A PC-3 xenograft mouse model was used to evaluate the anticancer effect of TED in vivo.
RESULTS: In vitro, TED strongly suppressed the growth of prostate cancer cells and endothelial cells in a dose-dependent manner. TED induced cell cycle arrest and apoptosis in PC-3 cells and human umbilical vascular endothelial cells (HUVECs). TED-induced apoptosis did not involve the caspase pathway. TED also decreased ΔΨm in PC-3 cells and HUVECs. In vivo, TED significantly suppressed tumor growth in nude mice bearing PC-3 cells, without any overt toxicity. Immunohistochemical analysis showed TED induced apoptotic cell death and inhibited angiogenesis in xenograft tumor cells.
CONCLUSION: Cell cycle arrest and induction of apoptosis in cancer cells and endothelial cells might be plausible mechanisms of actions for the observed antitumor and antiangiogenic activities of TED.—PMID: 24642631 [PubMed – indexed for MEDLINE]
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Make a tea –with the herb—or a tincture —getting this herb in the spring may increase testosterone production which can fortify heart as well as muscle in the body—later in the harvest term the chemistry will not be same—which will be beneficial for kidney function as well
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Steroidal saponins from Tribulus terrestris.
Kang LP1, Wu KL2, Yu HS2, Pang X3, Liu J4, Han LF4, Zhang J3, Zhao Y3, Xiong CQ3, Song XB4, Liu C3, Cong YW3, Ma BP5.
Author information
Abstract
Sixteen steroidal saponins, including seven previously unreported compounds, were isolated from Tribulus terrestris. The structures of the saponins were established using 1D and 2D NMR spectroscopy, mass spectrometry, and chemical methods. They were identified as: 26-O-β-d-glucopyranosyl-(25R)-furost-4-en-2α,3β,22α,26-tetrol-12-one (terrestrinin C), 26-O-β-d-glucopyranosyl-(25R)-furost-4-en-22α,26-diol-3,12-dione (terrestrinin D), 26-O-β-d-glucopyranosyl-(25S)-furost-4-en-22α,26-diol-3,6,12-trione (terrestrinin E), 26-O-β-d-glucopyranosyl-(25R)-5α-furostan-3β,22α,26-triol-12-one (terrestrinin F), 26-O-β-d-glucopyranosyl-(25R)-furost-4-en-12β,22α,26-triol-3-one (terrestrinin G), 26-O-β-d-glucopyranosyl-(1→6)-β-d-glucopyranosyl-(25R)-furost-4-en-22α,26-diol-3,12-dione (terrestrinin H), and 24-O-β-d-glucopyranosyl-(25S)-5α-spirostan-3β,24β-diol-12-one-3-O-β-d-glucopyranosyl-(1→4)-β-d-galactopyranoside (terrestrinin I). The isolated compounds were evaluated for their platelet aggregation activities. Three of the known saponins exhibited strong effects on the induction of platelet aggregation
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Protective effect of Tribulus terrestris linn on liver and kidney in cadmium intoxicated rats.
Lakshmi GD1, Kumar PR, Bharavi K, Annapurna P, Rajendar B, Patel PT, Kumar CS, Rao GS.
Author information
Abstract
Administration of cadmium (Cd) significantly increased the peroxidation markers such as malondialdehyde and protein carbonyls along with significant decrease in antioxidant markers such as super oxide dismutase and reduced glutathione in liver and kidney tissues. Cadmium also caused a significant alteration in hepatic and renal functional markers in serum viz. total protein, albumin, alanine transaminase, blood urea nitrogen and creatinine. Prominent pathological changes observed in liver were severe vascular and sinusoidal congestion with diffuse degenerative changes and mononuclear infiltration into peripheral areas, while the kidney showed vascular and glomerular congestion, cloudy swelling of tubular epithelium. Coadministration of ethonolic extract of T. terrestris or vitamin E along with Cd significantly reversed the Cd induced changes along with significant reduction in Cd load.
take wheat germ oil or any oils that are high in E–alnond–sunflower-olive–and take the tincture or extract and blend together in equal parts for about 5 minutes this will fuse the 2 –and then use 1/2 – 1 tsp increments
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Wild blueberries (bilberries) can help tackle adverse effects of high-fat diet
Date:
December 18, 2014
Source:
University of Eastern Finland
Eating bilberries diminishes the adverse effects of a high-fat diet, according to a recent study at the University of Eastern Finland. For the first time, bilberries were shown to have beneficial effects on both blood pressure and nutrition-derived inflammatory responses.—Low-grade inflammation and elevated blood pressure are often associated with obesity-related diseases. The study focused on the health effects of bilberries on mice that were fed high-fat diet for a period of three months. Some of the mice were fed either 5% or 10% of freeze-dried bilberries in the diet. The researchers assessed the effects of the diets by looking at inflammatory cell and cytokine levels, systolic blood pressure, glucose tolerance, insulin sensitivity and weight gain.–Mice on the high-fat diet experienced significant weight gain and detrimental changes in glucose and lipid metabolism, inflammation factors and blood pressure. Bilberries diminished the pro-inflammatory effects of the high-fat diet, indicated by an altered cytokine profile and a reduced relative prevalence of inflammation supporting T-cells. Bilberries also prevented elevated blood pressure caused by the high-fat diet.—Bilberries constitute an integral part of the Nordic diet and they could be better utilized also elsewhere in the world. Bilberries are associated with several beneficial health effects and their use involves plenty of traditional wisdom. The beneficial health effects of bilberries are thought to be explained by polyphenols, especially anthocyanins, the levels of which are significantly higher in bilberries than in commercially cultivated blueberries.–Story Source-The above story is based on materials provided by University of Eastern Finland. Note: Materials may be edited for content and length.–
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Creation of ‘rocker’ protein opens way for new smart molecules in medicine, other fields
Date:
December 18, 2014
Source:
Dartmouth College
Gevorg Grigoryan, an assistant professor of computer science at Dartmouth College, and researchers from other institutions have built the first artificial transporter protein that carries individual atoms across membranes, opening the possibility of engineering a new class of smart molecules with applications in fields as wide ranging as nanotechnology and medicine[F1].—Human cells are protected by a largely impenetrable molecular membrane, but researchers have built the first artificial transporter protein that carries individual atoms across membranes, opening the possibility of engineering a new class of smart molecules with applications in fields as wide ranging as nanotechnology and medicine[F2].–The study, which appears Dec. 19, in the journal Science, is a milestone in designing and understanding membrane proteins. The study was conducted by researchers from Dartmouth College, the University of California-San Francisco, Massachusetts Institute of Technology and National Institute of Science Educational and Research in India.–Each human cell is surrounded by a lipid membrane, a molecular barrier that serves to contain the cellular machinery and protect it from the surrounding elements. This cellular “skin” is impenetrable to most biological molecules but also presents a conundrum: if chemicals can’t get in or out, how is a cell to receive nutrients (food) and remove unwanted products of metabolism (trash)[F3]? Nature has come up with an elegant solution to this logistical problem — transporter proteins (or transporters). These molecular machines are embedded in the cellular membrane and serve as gatekeepers, allowing specific chemicals to shuttle in and out when needed. Though biologists have known about transporters for many decades, their precise mechanism of action has been elusive.–The researchers set out to “build” an artificial transporter protein from scratch, to learn how transporters work, and to open the possibility of engineering a new class of smart molecules. They developed new computational techniques to model the necessary molecular physics, enabling them to design a transporter protein through computer simulation. Specifically, computer simulations suggested which amino-acid building blocks should comprise the future transporter, so that it would carry ionic atoms of metal zinc in one direction across membranes, while pumping protons in the other. Using this computational blueprint, they created the molecule in the lab, referring to it as “Rocker” due to its predicted molecular dynamic properties: the protein was expected to “rock” between two alternating states, allowing it to drive atoms through.—“To our great excitement, experiments showed that Rocker did indeed transport zinc and protons and it did, in fact, rock between two states just as designed,” says co-lead author Gevorg Grigoryan, an assistant professor of computer science at Dartmouth. “Further, Rocker showed great selectivity, not transporting ions of calcium, another design feature.”– Proteins are nature’s workhorse molecules, performing a great variety of tasks in the cell from catalysis and sensing to generation of mechanical work. Learning to design (from first principles) novel protein molecules to perform specific tasks would mean that the immense richness of function that proteins have to offer can be brought to bear in a variety of applications, from better therapeutics to smart materials and clean energy solutions.–“Our findings are an important step forward in this pursuit, demonstrating that through the use of computer simulations to orchestrate precise properties of atomic structure and molecular dynamics, proteins can now be designed to carry out complex functions that rival those of natural molecular machines,” Grigoryan says. “Further, our work represents a milestone in designing and understanding membrane proteins, a particularly challenging class of proteins.”Story Source–The above story is based on materials provided by Dartmouth College. Note: Materials may be edited for content and length.–Journal Reference-N. H. Joh, T. Wang, M. P. Bhate, R. Acharya, Y. Wu, M. Grabe, M. Hong, G. Grigoryan, W. F. DeGrado. De novo design of a transmembrane Zn2 -transporting four-helix bundle. Science, 2014; 346 (6216): 1520 DOI: 10.1126/science.1261172
[F1]This is horrendously dangerous —this will effect environmental settings—these protens will get out into the field just like Genetics and other nano components but with a protein delivery system the natural protection in the field whether environmental—human-aquatic-mammalian or reptilian will all be impacted—with a vaccine the nano delivery method which is already being utilized is showing high levels of affliction—this has become an experiment —using humans as a guinea pig
[F2]Anyone seeing the connection here with smart dust tech and ligand or protein binding agents—and there already effect on the environment
[F3]That is the nature of defence against viral or fungal or bacterial invaders—when the barrier is penetrated with nano then it has no defence and becomes a re written cell and saturated with nano particles
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Bad air means bad news for seniors’ brainpower
Date-November 16, 2012
Source-The Gerontological Society of America
Living in areas of high air pollution can lead to decreased cognitive function in older adults, according to new research presented in San Diego at The Gerontological Society of America’s (GSA) 65th Annual Scientific Meeting.–This finding is based on data from the U.S. Environmental Protection Agency and the Health and Retirement Study. The analysis was conducted by Jennifer Ailshire, PhD, a National Institute on Aging postdoctoral fellow in the Center for Biodemography and Population Health and the Andrus Gerontology Center at the University of Southern California.–“As a result of age-related declines in health and functioning, older adults are particularly vulnerable to the hazards of exposure to unhealthy air,” Ailshire said. “Air pollution has been linked to increased cardiovascular and respiratory problems, and even premature death, in older populations, and there is emerging evidence that exposure to particulate air pollution may have adverse effects on brain health and functioning as well.”–This is the first study to show how exposure to air pollution influences cognitive function in a national sample of older men and women. It suggests that fine air particulate matter — composed of particles that are 2.5 micrometers in diameter and smaller, thought to be sufficiently small that if inhaled they can deposit deep in the lung and possibly the brain — may be an important environmental risk factor for reduced cognitive function.–The study sample included 14,793 white, black, and Hispanic men and women aged 50 and older who participated in the 2004 Health and Retirement Study (a nationally representative survey of older adults). Individual data were linked with data on 2004 annual average levels of fine air particulate matter from the Environmental Protection Agency’s Air Quality System monitors across the country. Cognitive function was measured on a scale of 1 to 35 and consisted of tests assessing word recall, knowledge, language, and orientation.–Ailshire discovered that those living in areas with high levels of fine air particulate matter scored poorer on the cognitive function tests. The association even remained after accounting for several factors, including age, race/ethnicity, education, smoking behavior, and respiratory and cardiovascular conditions.–Fine air particulate matter exposures ranged from 4.1 to 20.7 micrograms per cubic meter, and every ten point increase was associated with a 0.36 point drop in cognitive function score. In comparison, this effect was roughly equal to that of aging three years; among all study subjects, a one-year increase in age was associated with a drop 0.13 in cognitive function score.–Story Source-The above story is based on materials provided by The Gerontological Society of America. Note: Materials may be edited for content and length.
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