EK
Age Not Factor in Immunity to Viruses, Researchers Find
Dec. 13, 2012 — Our immune system does not shut down with age, says a new study led by McMaster University researchers.—A study published in PLOS Pathogens today shows a specialized class of immune cells, known as T cells, can respond to virus infections in an older person with the same vigour as T cells from a young person.—“For a long time, it was thought the elderly were at a higher risk of infections because they lacked these immune cells, but that simply isn’t the case,” said Jonathan Bramson, the study’s principal investigator. “The elderly are certainly capable of developing immunity to viruses.”–Researchers at McMaster, University of Toronto and the University of Pennsylvania examined individuals, younger than 40, between 41 to 59 years of age and older than 60, infected with three different viruses, including West Nile, and found the older group demonstrated perfectly normal immune responses.—Both the number of virus-fighting T cells and the functionality of the T cells were equivalent in all three groups.—“So as we age, our bodies are still able to respond to new viruses, while keeping us immune to viruses we’ve been exposed to in the past,” Bramson said.—He added that these results have important implications for vaccination of elderly individuals.—Currently, vaccines for the elderly aren’t designed to elicit responses from these immune cells, and this might explain the lack of effective protection from the flu vaccine, he said.—Vaccines specifically designed to generate T-cell immunity may be more effective at protecting older adults, Bramson said.–The research was funded by the Canadian Institutes for Health Research and the U.S. National Institutes of Health. PLOS Pathogens is an open-access, peer-reviewed journal of the Public Library of Science.—Story Source-The above story is reprinted from materials provided by McMaster University, via Newswise. Journal Reference–Alina Lelic, Chris P. Verschoor, Mario Ventresca, Robin Parsons, Carole Evelegh, Dawn Bowdish, Michael R. Betts, Mark B. Loeb, Jonathan L. Bramson. The Polyfunctionality of Human Memory CD8+ T Cells Elicited by Acute and Chronic Virus Infections Is Not Influenced by Age. PLoS Pathogens, 2012; 8 (12): e1003076 DOI: 10.1371/journal.ppat.1003076
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Cancer– Exercise Reduces Tiredness
Nov. 13, 2012 — Aerobic exercise can help relieve the fatigue often associated with cancer and cancer treatment, according to Cochrane researchers. Their updated systematic review strengthens findings from an earlier version on cancer-related fatigue published in The Cochrane Library.–Fatigue is a common and potentially long-lasting side-effect of cancer and cancer treatment. It may last for months or years. Dealing with cancer-related fatigue is crucial because those who suffer its effects may be less inclined to continue with treatment. Although in the past, people with cancer-related fatigue have been advised to rest, long periods of inactivity may lead to muscle wasting and increased tiredness, whereas balancing rest with physical activity may help to reduce fatigue. A 2008 Cochrane systematic review on the benefits of exercise found some benefits of physical activity for fatigue in cancer based on limited studies.—The new review adds a further 28 studies to those included in the 2008 review. Altogether, 56 studies involving a total of 4,068 people with cancer were included. Half of the studies were carried out in people with breast cancer. Those with solid tumours benefited from aerobic exercise, such as walking or cycling, both during and after cancer treatment. Other forms of exercise, including resistance training, did not significantly reduce fatigue.—“The evidence suggests that exercise may help reduce cancer-related fatigue and should therefore be considered as one component of a strategy for managing fatigue that may include a range of other interventions and education,” said lead researcher Fiona Cramp of the Faculty of Health & Life Sciences at the University of the West of England in Bristol, UK. “This updated review provides a more precise conclusion, showing specifically that aerobic exercise, both during and after cancer treatment, can be beneficial.”—It remains to be seen how cancer treatment alters the beneficial effects of exercise on cancer-related fatigue. Further research is also needed to understand how the frequency and duration of exercise, and type of cancer, affect the results. “Twenty eight of the studies we included were carried out in breast cancer patients, so we need to know more about how exercise can help people with a broad range of diagnoses, including patients with advanced disease,” said Cramp.–The research was funded by the UK’s National Institute for Health Research (NIHR) –Story Source–The above story is reprinted from materials provided by Wiley. —Journal Reference–Fiona Cramp, James Byron-Daniel. Exercise for the management of cancer-related fatigue in adults. The Cochrane Library, 2012; DOI: 10.1002/14651858.CD006145.pub3
********************************************************************************
Easy, At-Home Exercise Program Can Help Cancer Patients
Dec. 13, 2012 — It has been known for some time that exercise is important for cancer patients, but few studies have looked at the practicality of exercise programs and whether even a minimal workout can help. Exercise can reduce cancer-related fatigue, improve sleep, boost a sense of wellness, and reduce the recurrence of certain types of tumors. A Mayo Clinic study published in the Journal of Pain and Symptom Management found that a brief, at-home exercise program — dubbed the Rapid, Easy, Strength Training program, or REST, — was sufficient to increase cancer patients’ mobility and reduce fatigue.—“We talk a lot about how important it is for cancer patients to exercise, but until now, nobody has questioned whether less may be more for patients negotiating the demands of cancer treatment,” says lead author Andrea Cheville, M.D., of the Mayo Clinic Department of Physical Medicine and Rehabilitation. “This was the first trial to investigate what’s feasible and helpful for patients with limited time and energy.”–An interdisciplinary team of Mayo Clinic researchers developed an at-home exercise regimen, involving a pedometer-based walking program and a series of gentle resistance movements — lifts and curls using a resistance band — that can be done standing or seated. The workout takes only a few minutes a day, with minimal cost to patients.—In a randomized, controlled study of 66 adults with stage IV lung or colorectal cancer, researchers found that patients who exercised at least four times a week for two months showed improved mobility, had less fatigue and slept better when compared with those who didn’t exercise. Though other measures such as pain were unaffected, the study suggests that the exercises can address several important disabling effects of disease and that even patients with late-stage cancer are able to perform the brief regimens.—The exercise program and study have significant implications for cancer care, Dr. Cheville says. Other studies have suggested that cancer-related exercise programs may impose financial burdens; patients can learn the REST regimen in a single physical therapy session. A muscle-building exercise regimen may help patients at all stages of cancer treatment.–“Muscles may atrophy during cancer care,” Dr. Cheville adds. “Our regimen preserves muscle mass so that if patients develop complications from cancer or treatment, or require hospitalization, they have the reserves necessary to ensure that their bodies heal.”–The study was funded by the National Institutes of Health; grant number KL2 RR024151-01. Other authors include Jenny Kollasch, Justin Vandenberg, Tiffany Shen, Axel Grothey, M.D., and Jeffrey Basford, M.D., Ph.D., all of Mayo Clinic, and Gail Gamble, M.D., of the Rehabilitation Institute of Chicago.–Story Source–The above story is reprinted from materials provided by Mayo Clinic.
TOP C
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
TOP D
HOME
Show of the Month December 17 2012
Antioxidant and antiproliferative activity of Laurus nobilis
Sesquiterpenes from the leaves of Laurus nobilis L
Aluminum phosphide-induced genetic and oxidative damages in rats: attenuation by Laurus nobilis leaf extract.
The antitumoral effect of the American mistletoe Phoradendron serotinum
Michael Schmidt-Court Case
********************************************************************************
Antioxidant and antiproliferative activity of Laurus nobilis L. (Lauraceae) leaves and seeds essential oils against K562 human chronic myelogenous leukaemia cells.
Nat Prod Res. 2012;26(18):1741-5
Authors: Saab AM, Tundis R, Loizzo MR, Lampronti I, Borgatti M, Gambari R, Menichini F, Esseily F, Menichini F
Abstract–The antioxidant and antiproliferative activities of the essential oils from Laurus nobilis leaves and seeds in relation to their composition were analysed. The most abundant components of the leaf essential oil were 1,8-cineole, 1-p-menthen-8-ethyl acetate, linalool and sabinene, while the seed oil was characterised by β-ocimene, 1,8-cineole, α-pinene and β-pinene as main constituents. Both seed and leaf essential oils exhibited a scavenging effect on the DPPH radical, with IC₅₀ values of 66.1 and 53.5 µg mL⁻¹, respectively. The leaf essential oil- showed the strongest antioxidant activity in the β-carotene/linoleic acid system, with an IC₅₀ value of 35.6 µg mL⁻¹ after 30 min of incubation. Both leaf and seed oils inhibited proliferation of the K562 tumour cell line with IC₅₀ values of 95 and 75 µg mL⁻¹, respectively. The L. nobilis leaf oil showed a percentage of erythroide differentiation of 15% at a concentration of 10 µg mL⁻¹. A value of 12% was found for the seed essential oil at a concentration of 50 µg mL⁻¹. When the oils were added to a suboptimal concentration of the commercial drug, cytosine arabinoside, a clear synergic effect was observed.–PMID: 22017546 [PubMed – indexed for MEDLINE]
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Sesquiterpenes from the leaves of Laurus nobilis L.
Julianti E, Jang KH, Lee S, Lee D, Mar W, Oh KB, Shin J.
Source
Natural Products Research Institute, College of Pharmacy, Seoul National University, San 56-1, Sillim, Gwanak, Seoul 151-742, Republic of Korea.
Abstract–Ten sesquiterpenes, together with 12 known compounds were isolated from leaves of Laurus nobilis L. Based on spectroscopic analyses, the 10 compounds were determined to be eudesmane lactones and their corresponding methyl esters. Most of these compounds exhibited moderate-to-significant cytotoxicity towards K562 leukemia cells. One compound had a higher cytotoxicity than doxorubicin, while other compounds had moderate to no activity.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Aluminum phosphide-induced genetic and oxidative damages in rats: attenuation by Laurus nobilis leaf extract.
Turkez H, Togar B.–Source
Department of Molecular Biology and Genetics, Faculty of Sciences, Erzurum Technical University, Turkey.
Abstract–Aluminum phosphide (AlP) is a colorless, flammable, liquefied pesticide that is commonly used to control insects, nematodes, weeds, and pathogens in crops, forests, ornamental nurseries, and wood products. Early investigations of AlP-poisoned mammalian cells led to the proposed involvement of oxidative damage in its toxicity mechanism. Therefore, this study was aimed to evaluate the effect of Laurus nobilis (L) leaf extract (LNE) against AlP-induced genetic and oxidative damages in rats. Selected animals were assigned to four groups (n = 6), namely, group A: control (only distilled water is injected); group B: AlP (4 mg kg(-1) injected intraperitoneally (i.p.)); group C: LNE (200 mg kg(-1) injected i.p.), and group D: AlP plus LNE, respectively. The experimental period lasted for 14 successive days. Chromosomal aberrations (CAs) and micronucleus (MN) assay were used for monitoring genotoxic damage. In addition, biochemical parameters such as total antioxidant capacity (TAC) and total oxidative status (TOS) were examined in serum samples to determine oxidative damage. Our results indicated that AlP caused increase in CA and MN assay rates and alterations in TAC and TOS levels when compared with control group. On the contrary, LNE did not change the rates of both the analyzed cytogenetic end points and led to increase in TAC level. Moreover, we observed that LNE suppressed the genetic damage by AlP to bone marrow cells in vivo. Interestingly AlP-induced oxidative stress was also strongly reduced by LNE. The results of the present study indicated that the protective effect of LNE might be ascribable to its antioxidant and free radical scavenging properties
In vivo (Latin for “within the living”)
TAC—Total Antioxidant Capacity
Here is another means to protect against chemtrail fallout of aluminum –by either making teas with this –adding to broths—or extracting with water-alcohol or vinegar
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
The antitumoral effect of the American mistletoe Phoradendron serotinum (Raf.) M.C. Johnst. (Viscaceae) is associated with the release of immunity-related cytokines.
J Ethnopharmacol. 2012 Aug 1;142(3):857-64—Authors: Alonso-Castro AJ, Juárez-Vázquez Mdel C, Domínguez F, González-Sánchez I, Estrada-Castillón E, López-Toledo G, Chávez M, Cerbón MA, García-Carranca A
Abstract
ETHNOPHARMACOLOGICAL RELEVANCE: Phoradendron serotinum is commonly used in Mexican traditional medicine for the empirical treatment of cancer. However, there are no studies regarding the antitumoral or immunomodulatory activities of Phoradendron serotinum.
MATERIALS AND METHODS: The in vivo toxicity of ethanolic extracts of Phoradendron serotinum (PSE) was evaluated in mice according to the Lorke procedure. The in vitro immunomodulatory effects of PSE were evaluated estimating the effects of PSE on the pinocytosis, NO production and lysosomal enzyme activity in murine macrophages RAW 264.7. The effects of PSE on the proliferation of murine splenocytes and NK cell activity were also assayed. The cytotoxic effects on TC-1 (lung murine cancer cells) were evaluated using the MTT assay, whereas the apoptotic effect of PSE on TC-1 cells was evaluated using TUNEL assay. Also, different doses of PSE were injected intraperitoneally daily into C57BL/6 mice bearing tumors of TC-1 cells during 25 days. The growth and weight of tumors was measured. In addition, the levels of IL-2, IL-6, IL-12, IL-23 and IFN-γ in murine serum and supernatants of K562 cell-murine splenocyte cocultures were measured.
RESULTS: PSE stimulated the proliferation, pinocytosis and lysosomal enzyme activity in murine macrophages with a similar potency than lypopolisaccharides 1 μg/ml. In addition, PSE stimulated the proliferation of murine splenocytes and induced the NK cell activity. PSE showed cytotoxic (IC(50)=1.9 μg/ml) and apoptotic effects against TC-1 cells. The LD(50) was 125 mg/kg by intraperitoneal route (i.p.) and 375 mg/kg by oral route. PSE administrated at 1, 5 and 10 mg/kg i.p. inhibited the tumor growth by 18%, 40% and 69%, respectively, in mice bearing TC-1 tumor. PSE increased the in vitro and in vivo release of IL-2, IL-6 and IFN-γ but lacked effect on IL-12 and IL-23 release.
CONCLUSIONS: Phoradendron serotinum shows moderate toxic effects in vivo, exerts cytotoxic and apoptotic effects on TC-1 cells. Phoradendron serotinum also has antitumor effects in mice bearing TC-1 tumor and induces immunomodulatory activities in vivo. The results suggest that antitumoral effects of PSE are related with the production of immunity-related cytokines.—-PMID: 22732726 [PubMed – indexed for MEDLINE]
☞Making mistletoe tea can assist in the reduction of tumours and have an anti cancer effect— in any usage in dealing with tumours the use of high profile enzymes or highly equipped foods that are high in enzymes will also assist in removing what is broken down and the renewing of the blood with tonics and foods as well☜
*********************************************************************************
Michael Schmidt-Court Case
Michael Schmidt Takes Solace from Resistance of Another German, Sees His Own Case “Going in the Right Direction”; New U.S. Intrusion Mechanism
The legal situation confronting Michael Schmidt could hardly look more ominous.—-He faces four counts of conspiracy, in connection with the disappearance last April of 31 rare Shropshire sheep suspected by Canadian health authorities of harboring scrapies disease. Conviction could mean a lengthy jail term of up to 14 years, he has been told. Three other farmers charged in the alleged plot to move the sheep and save them from mandated slaughter by the Canadian Food Information Agency (CFIA) are Montana Jones, Suzanne Atkinson, and Robert Pinnell.—Schmidt has been forced to surrender his passport in connection with the charges–a not insignificant penalty for a man who has over the last few years become the spiritual leader of North America’s budding food rights movement, and been in ever-greater demand as a speaker around the U.S. and Canada.—He was arraigned last week, to have mug shots taken and be fingerprinted, and it’s unclear when his trial will be held.—
While Schmidt has faced much legal travail since his Glencolton Farm in Ontario was first raided in 1993 for selling raw milk–his conviction in 2011 of violating provincial dairy laws has been accepted for appeal by Ontario’s highest court–this current legal challenge is potentially the most serious the native of Germany has encountered.—
Yet in the face of it all, he is not only at peace, but optimistic about the outcome. “It’s going in the right direction,” he told me earlier this week.—He has excellent legal representation, he feels. And when the case goes to trial, he is convinced, “it will open people’s eyes” to the real issues at stake–the state’s determination to control his nation’s food supply and, in the process, destroy crop and animal diversity and the small farms committed to providing good food. Last April, after the sheep disappeared from Montana Jones’ Ontario farm in advance of their intended slaughter under CFIA orders, Schmidt stated last spring, “The actions of the CFIA remind me of the history of my native Germany, where genetic cleansing became a tragic and horrible national policy.”—-The connections to Germany’s history continue to reverberate for Schmidt in the Canadian government’s new legal offensive against him and the other farmers. He says he has taken much solace from a documentary film, “The Top Secret Trial of the Third Reich”, which contains film of the 1944 trial of German officers who failed in a planned assassination attempt of Adolph Hitler. —One of the defendants in that case was Adam von Trott, who was a close friend of the Schmidt family in Germany during World War II. “I knew of him from my grandmother,” says Schmidt. The outcome of the case against von Trott was pre-ordained, and together with other conspirators, he was hanged in August 1944.—
The Nazis circulated film of the trial, intending to scare the populace and stimulate loyalty to Hitler, but when the Nazis learned it instead encouraged sympathy for the would-be assassins, the government ordered all copies destroyed. One copy survived, though, and it became the basis of the documentary Schmidt has been studying.—He finds it ironic that both the plotters against Hitler and the farmers in the Canadian sheep case were charged with conspiracy. In his case, he takes heart from conspiracy charges. “When they cannot convict you of anything, they throw up conspiracy charges.” He says that in his case, the authorities won’t find a conspiracy, “because there wasn’t any.”—Schmidt identifies with von Trott, who was “a humble man” willing to die to rid the world of Hitler and his “genetic cleansing” madness.–To some, it may seem a wild leap to compare the Nazis’ genocide with what is happening in Canada and the U.S. But to Schmidt, the similarities are uncanny. Today’s rulers in Canada and the U.S. seek the same kind of control via intimidation as the Nazis, to satisfy corporate benefactors. Because mass murder can’t be tolerated today, our rulers must be more sophisticated, more gradual, in their consolidation of control. As it moves along its inevitable path, he predicts, the consolidation will become ever more ruthless, and the political targets, like Schmidt, more numerous. —Schmidt also sees the case against him over the sheep as a statement by his government that dialog about such matters as control of the food supply is out. “Why is there no dialog? Why do you have to have blood on your hands before you meet?” The ultimate irony, he says, is that “those who order the killings go after the people who try to prevent the killings” of the sheep.—Schmidt expects to mount a serious defense, and also expects to be raising funds to pay for his legal defense. More to come on that matter. —The latest legal offensive against Michael Schmidt must be seen in a larger context of expanding government control intrusion into our lives, with the goal of rooting out those considered to be politically dangerous. (The U.S. and Canada, in this context, are one and the same.) The latest salvo is detailed on the front page of today’s Wall Street Journal. The Obama administration, reports the WSJ via government documents it obtained, has just implemented rules that “now allow the little-known National Counterterrorism Center to examine the government files of U.S. citizens for possible criminal behavior, even if there is no reason to suspect them. That is a departure from past practice, which barred the agency from storing information about ordinary Americans unless a person was a terror suspect or related to an investigation.—“Now, NCTC can copy entire government databases—flight records, casino-employee lists, the names of Americans hosting foreign-exchange students and many others. The agency has new authority to keep data about innocent U.S. citizens for up to five years, and to analyze it for suspicious patterns of behavior. Previously, both were prohibited.”
TOP D
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
TOP E
HOME
Show of the Month December 21 2012
Flavonoid intake and bone health.
Human & Synthetic Hormones Now Contaminate Fresh Produce
Postmenopausal bleeding and dietary supplements- a possible causal relationship with hop- and soy-containing preparations
Countering Brain Chemical Could Prevent Suicides, Research Suggests
Age-Associated Changes In Oxidative Stress and NAD(+) Metabolism In Human Tissue.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Flavonoid intake and bone health.
J Nutr Gerontol Geriatr. 2012;31(3):239-53-Authors: Weaver CM, Alekel DL, Ward WE, Ronis MJ
Abstract
Flavonoids, found in a wide diversity of plant foods from fruits and vegetables, herbs and spices, essential oils, and beverages, have the most potential of dietary components for promotion of bone health beyond calcium and vitamin D. Recent epidemiological studies show flavonoid consumption to have a stronger association with bone than general fruit and vegetable consumption. Bioactive flavonoids are being assessed for properties beyond their chemical antioxidant capacity, including anti-inflammatory actions. Some have been reported to enhance bone formation and to inhibit bone resorption through their action on cell signaling pathways that influence osteoblast and osteoclast differentiation. Future research is needed to determine which of the flavonoids and their metabolites are most effective and at what dose, as well as the mechanism of modulating cellular events, in order to set priorities for clinical trials.–PMID: 22888840 [PubMed – indexed for MEDLINE]
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Human and Synthetic Hormones Now Contaminate Fresh Produce
Hormones and/or hormone-mimicking chemicals are omnipresent environmental contaminants. Already found in places as varied as our teeth (dental sealant) to our paper products (receipts, money), our meat to our canned foods, new research now indicates that even fresh, whole vegetables and fruits are no longer immune to this growing biological and chemical threat.—A newly released study has found that a variety of substances with hormone-disrupting properties now widely contaminate commercially available fresh vegetables and fruits, in some cases at concentrations exceeding the recommended acceptable daily intake (ADI) for children as recommended by the Joint FAO/WHO Expert Committee on Food Additives (JECFA).—Published this month in the Journal of Agricultural and Food Chemistry, researchers at the Indian River Research and Education Center, University of Florida/IFAS, found the synthetic endocrine-disrupting chemicals bisphenol A (BPA), nonylphenol (NP), and the natural steroidal estrogen 17-β-estradiol, in vegetables and fruits randomly sampled from local markets, using gas chromotagraphy with tandem mass spectrometry.—
According to the researchers, the “BPA was detected in all vegetable and fruit samples, ranging from 0.2±0.1 to 9.0±4.9 µg kg-1, indicating significant exposure potential for humans.” Nonylphenol (NP), a chemical in the alkylphenol class mainly used to manufacturer detergents, was detected in pumpkin, sweet potato, citrus, and apple samples. Concentrations of 17-β-estradiol in vegetables and fruits ranged from 1.3±0.4 to 2.2±1.0 µg kg-1 except those in tomato and strawberry.—Notably, the highest concentrations of BPA were found in potatoes, lettuce contained the highest concentration of natural estrogens, and pumpkin the highest concentration of alkylphenols (APs).
How Did These Chemicals End Up In Our Food?—-The answer is wastewater and sewage sludge — two things that, as many would be surprised to find, are commonly used to grow our food. While wastewater may contain as much as 95% water, the other 5% remaining is a biological and chemical atrocity. Even the sewage used in this degenerate, albeit highly productive (though unsustainable), form of farming has been renamed and transformed euphemistically into “biosolids,” to make it somehow sound more palatable.-The reuse of wastewater for irrigation of agricultural land is a well established practice that introduces many contaminants into our environment and crops including pharmaceuticals, hormones and personal care products.—-Wastewater may contain human sewage, industrial site drainage, toxic waste (e.g. pesticide manufacturing), petroleum waste products or byproducts, for instance.
Other wastewater constituents include:
Pathogens such as bacteria, viruses, parasites
Soluble organic materials such as urea, drugs, pharmaceuticals
Macro-solids such as condoms, needles, diapers, sanitary napkins
Emulsions such as paint, adhesives, hair colorants
Gases such as hydrogen sulfide, methane, carbon dioxide
Animals such as insects, protozoa, small fish
It is estimated that 90% of the global wastewater being used in agriculture today is untreated, meaning that it contains hundreds, if not thousands of potential biological and chemical toxicants that may ultimately end up in your food and body.—With the increasing use of raw or processed sewage to grow conventional food, it has become prone to overgrowth with pathogenic (even deadly) bacteria, which is why the USDA promotes food irradiation to nuke (“cold pasteurize”) the intrinsically unsanitary food into the kind of sterility that also entails the destruction of its nutrition value.—Even when sewage is pretreated in order to remove chemicals, foreign materials, and microorganisms, up to 93% of highly concentrated active drug compounds still remain, including hormones and hormone metabolites that remain biologically active.[ii]—With the latest research now indicating that our modern, industrialized agricultural system is creating a toxic nightmare within our food, it is time for us to face the gravity of the situation, and make some real changes. All the more reason to support AQUAPONICALLY OR HYDROPONICALLY OR HOME OR CHEMICAL FREE –HORMONAL FREE –SOY FREE AND CANOLA FREE-GMO-GE FREE, and preferably locally, produced food by voting with our fork, as it does not utilize these intrinsically toxic farming practices.
Resources
Jian Lu, Jun Wu, Peter J Stoffella, Patrick Wilson. Analysis of Bisphenol A, Nonylphenol and Natural Estrogens in Vegetables and Fruits Using Gas Chromatography-Tandem Mass Spectrometry. J Agric Food Chem. 2012 Dec 6. Epub 2012 Dec 6. PMID: 23215552
[ii] Watershedcouncil.org, Medicines in Our Waterways
**********************************************************************************
Postmenopausal bleeding and dietary supplements- a possible causal relationship with hop- and soy-containing preparations.
[Article in Dutch]
van Hunsel FP, Kampschöer P.
Source–Nederlands Bijwerkingen Centrum Lareb, ‘s-Hertogenbosch, the Netherlands. [email protected]
BACKGROUND–Many women suffering from menopausal symptoms choose to use dietary supplements made from plants for the relief of their symptoms. These herbal preparations can have phyto-oestrogenic properties. Although probably regarded as ‘safe’, such preparations can cause adverse drug reactions.
CASE DESCRIPTION:
We describe four patient reports to the Netherlands Pharmacovigilance Centre Lareb. All of these patients suffered from postmenopausal bleeding and used hop- and soy-containing dietary supplements. The reports were all from the same gynaecologist.
CONCLUSION:
Postmenopausal bleeding has many possible causes. The use of dietary supplements containing ingredients with phyto-oestrogenic properties, such as hop and soy, may give rise to proliferation of the endometrium[U1] . The four reports to Lareb illustrate the association between the use of these supplements and postmenopausal bleeding. Such products are available as over-the-counter preparations and consumers often mistakenly believe that they do not cause adverse drug reactions. During the diagnostic phase, it is important to be aware that the use of a dietary supplement or an herbal drug having phyto-oestrogenic properties may be a possible cause of postmenopausal bleeding.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Countering Brain Chemical Could Prevent Suicides, Research Suggests
MSU experimental psychiatry professor Lena Brundin studies biological causes of suicidal behavior in order to find new ways to save lives—Dec. 13, 2012 — Researchers have found the first proof that a chemical in the brain called glutamate is linked to suicidal behavior, offering new hope for efforts to prevent people from taking their own lives.—Writing in the journal Neuropsychopharmacology, Michigan State University’s Lena Brundin and an international team of co-investigators present the first evidence that glutamate is more active in the brains of people who attempt suicide. Glutamate is an amino acid that sends signals between nerve cells and has long been a suspect in the search for chemical causes of depression[U2] .—“The findings are important because they show a mechanism of disease in patients,” said Brundin, an associate professor of experimental psychiatry in MSU’s College of Human Medicine. “There’s been a lot of focus on another neurotransmitter called serotonin for about 40 years now. The conclusion from our paper is that we need to turn some of that focus to glutamate.”–Brundin and colleagues examined glutamate activity by measuring quinolinic acid — which flips a chemical switch that makes glutamate send more signals to nearby cells — in the spinal fluid of 100 patients in Sweden. About two-thirds of the participants were admitted to a hospital after attempting suicide and the rest were healthy.–They found that suicide attempters had more than twice as much quinolinic acid in their spinal fluid as the healthy people, which indicated increased glutamate signaling between nerve cells. Those who reported the strongest desire to kill themselves also had the highest levels of the acid.—The results also showed decreased quinolinic acid levels among a subset of patients who came back six months later, when their suicidal behavior had ended.—The findings explain why earlier research has pointed to inflammation in the brain as a risk factor for suicide. The body produces quinolinic acid as part of the immune response that creates inflammation.–Brundin said anti-glutamate drugs are still in development, but could soon offer a promising tool for preventing suicide. In fact, recent clinical studies have shown the anesthetic ketamine — which inhibits glutamate signaling — to be extremely effective in fighting depression, though its side effects prevent it from being used widely today.–In the meantime, Brundin said physicians should be aware of inflammation as a likely trigger for suicidal behavior. She is partnering with doctors in Grand Rapids, Mich., to design clinical trials using anti-inflammatory drugs.–“In the future, it’s likely that blood samples from suicidal and depressive patients will be screened for inflammation,” Brundin said. “It is important that primary health care physicians and psychiatrists work closely together on this.”—Story Source–The above story is reprinted from materials provided by Michigan State University. –Journal Reference–Sophie Erhardt, Chai K Lim, Klas R Linderholm, Shorena Janelidze, Daniel Lindqvist, Martin Samuelsson, Kristina Lundberg, Teodor T Postolache, Lil Träskman-Bendz, Gilles J Guillemin, and Lena Brundin. Connecting Inflammation with Glutamate Agonism in Suicidality. Neuropsychopharmacology, 2012; DOI: 10.1038/npp.2012.248
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Age-Associated Changes In Oxidative Stress and NAD(+) Metabolism In Human Tissue.
Hassina Massudi, Ross Grant, Nady Braidy, Jade Guest, Bruce Farnsworth, Gilles J Guillemin
Department of Pharmacology, School of Medical Sciences, Faculty of Medicine, University of New South Wales, Sydney, New South Wales, Australia.
Nicotinamide adenine dinucleotide (NAD(+)) is an essential electron transporter in mitochondrial respiration and oxidative phosphorylation. In genomic DNA, NAD(+) also represents the sole substrate for the nuclear repair enzyme, poly(ADP-ribose) polymerase (PARP) and the sirtuin family of NAD-dependent histone deacetylases. Age associated increases in oxidative nuclear damage have been associated with PARP-mediated NAD(+) depletion and loss of SIRT1 activity in rodents. In this study, we further investigated whether these same associations were present in aging human tissue. Human pelvic skin samples were obtained from consenting patients aged between 15-77 and newborn babies (0-1 year old)(n = 49) previously scheduled for an unrelated surgical procedure. DNA damage correlated strongly with age in both males (p = 0.029; r = 0.490) and females (p = 0.003; r = 0.600) whereas lipid oxidation (MDA) levels increased with age in males (p = 0.004; r = 0.623) but not females (p = 0.3734; r = 0.200). PARP activity significantly increased with age in males (p<0.0001; r = 0.768) and inversely correlated with tissue NAD(+) levels (p = 0.0003; r = -0.639). These associations were less evident in females. A strong negative correlation was observed between NAD(+) levels and age in both males (p = 0.001; r = -0.706) and females (p = 0.01; r = -0.537). SIRT1 activity also negatively correlated with age in males (p = 0.007; r = -0.612) but not in females. Strong positive correlations were also observed between lipid peroxidation and DNA damage (p<0.0001; r = 0.4962), and PARP activity and-NAD(+) levels (p = 0.0213; r = 0.5241) in post pubescent males. This study provides quantitative evidence in support of the hypothesis that hyperactivation of PARP due to an accumulation of oxidative damage to DNA during aging may be responsible for increased NAD(+) catabolism in human tissue. The resulting NAD(+) depletion may play a major role in the aging process, by limiting energy production, DNA repair and genomic signalling.
TOP E
[U1]THIS IS WHY THERE IS A ENDOMETRIS ISSUE OVERLOADING THE UTERUS AND NOT ENOUGH IODINE TO ASSIST INBALANCING THE HORMONES
[U2]Soy and Soy based products are loaded with this and It Is added in every food we consume—so if a childs blood brain barrier is not developed then what will occur will be permanent damage to the person in adult stages of life—could even explain why some people are more prone to drug addiction then others
*********************************************************************************
TOP F
HOME
Show Of the Month December 24-2012
Stress and the α7 nicotinic acetylcholine receptor.
Nicotine as a potential neuroprotective agent for Parkinson’s disease.
Cotinine Reduces Amyloid-β Aggregation and Improves Memory in Alzheimer’s Disease Mice.
Caffeine induces beneficial changes in PKA signaling and JNK and ERK activities in the striatum and cortex of Alzheimer’s transgenic mice.
Cotinine- A Potential New Therapeutic Agent against Alzheimer’s disease
Effects of cholinesterase inhibiting sage (Salvia officinalis) on mood, anxiety and performance on a psychological stressor battery.
**************************************************************************************
Stress and the α7 nicotinic acetylcholine receptor.
Richard G Hunter
Laboratory of Neuroendocrinology, 1230 York Ave., Rockefeller University, New York, NY 10065, USA. [email protected]
Nicotine is well known for its deleterious effects on human health, and it has long been known that nicotine interacts with the stress axis in both man and in laboratory animals. Nicotine also has beneficial effects upon cognition, and an emerging literature has demonstrated that it may play a protective or palliative role in diseases such as Alzheimer’s disease and schizophrenia. Recent advances have permitted scientists to identify the specific subtypes of nicotinic receptors responsible for the drugs varied physiological effects. The α7 subunit of the nicotinic acetylcholine receptor (NAchRα7), has been identified as a significant mediator of nicotine’s interactions with the stress axis and human disease. The NAchRα7 has also been shown to have neuroprotective effects via multiple pathways, making it a logical target for the treatment of a number of brain disorders.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Nicotine as a potential neuroprotective agent for Parkinson’s disease.
Maryka Quik, Xiomara A Perez, Tanuja Bordia
Center for Health Sciences, SRI International, Menlo Park, California, USA. [email protected]
Converging research efforts suggest that nicotine and other drugs that act at nicotinic acetylcholine receptors (nAChRs) may be beneficial in the management of Parkinson’s disease. This idea initially stemmed from the results of epidemiological studies that demonstrated that smoking is associated with a decreased incidence of Parkinson’s disease. The subsequent finding that nicotine administration protected against nigrostriatal damage in parkinsonian animal models led to the idea that nicotine in tobacco products may contribute to this apparent protective action. Nicotine most likely exerts its effects by interacting at nAChRs. Accumulating research indicates that multiple subtypes containing nAChRs, including α4β2, α6β2, and/or α7, may be involved. Stimulation of nAChRs initially activates various intracellular transduction pathways primarily via alterations in calcium signaling. Consequent adaptations in immune responsiveness and trophic factors may ultimately mediate nicotine’s ability to reduce/halt the neuronal damage that arises in Parkinson’s disease. In addition to a potential neuroprotective action, nicotine also has antidepressant properties and improves attention/cognition. Altogether, these findings suggest that nicotine and nAChR drugs represent promising therapeutic agents for the management of Parkinson’s disease. © 2012 Movement Disorder Society.
Neurobiol Aging. 2012 Mar 26;: 22459600
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Cotinine Reduces Amyloid-β Aggregation and Improves Memory in Alzheimer’s Disease Mice.
Valentina Echeverria, Ross Zeitlin, Sarah Burgess, Sagar Patel, Arghya Barman, Garima Thakur, Magorzota Mamcarz, Li Wang, David B Sattelle, Daniel A Kirschner, Takashi Mori, Roger M Leblanc, Rajeev Prabhakar, Gary W Arendash
Bay Pines VA Healthcare System, Bay Pines, FL, USA Department of Molecular Medicine, University of South Florida, Tampa, FL, USA.
Alzheimer’s disease (AD) affects millions of people world-wide and new effective and safe therapies are needed. Cotinine, the main metabolite of nicotine, has a long half-life and does not have cardiovascular or addictive side effects in humans. We studied the effect of cotinine on amyloid-β (Aβ) aggregation as well as addressed its impact on working and reference memories. Cotinine reduced Aβ deposition, improved working and reference memories, and inhibited Aβ oligomerization in the brains of transgenic (Tg) 6799 AD mice. In vitro studies confirmed the inhibitory effect of cotinine on Aβ1-42 aggregation. Cotinine stimulated Akt signaling, including the inhibition of glycogen synthase kinase 3β (GSK3β), which promotes neuronal survival and the synaptic plasticity processes underlying learning and memory in the hippocampus and cortex of wild type and Tg mice. Simulation of the cotinine-Aβ1-42 complex using molecular dynamics showed that cotinine may interact with key histidine residues of Aβ1-42, altering its structure and inhibiting its aggregation. The good safety profile in humans and its beneficial effects suggest that cotinine may be an excellent therapeutic candidate for the treatment of AD.
Neuroscience. 2009 May 14;: 19447162 Cit:5
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Caffeine induces beneficial changes in PKA signaling and JNK and ERK activities in the striatum and cortex of Alzheimer’s transgenic mice.
Ross Zeitlin, Sagar Patel, Sarah Burgess, Gary W Arendash, Valentina Echeverria
Research and Development, Department of Veterans Affairs, Bay Pines VA Healthcare System, Bay Pines, FL 33744, USA.
Caffeine intake has been associated with a lower incidence of Alzheimer’s disease (AD) in humans. In AD mouse models, caffeine significantly decreases senile plaques and amyloid beta (Aβ) levels while also protecting against or reversing cognitive impairment. To understand the mechanism(s) underlying the protective effects of caffeine against AD pathology, we investigated the effects of a two-week treatment with caffeine (3mg/day) in transgenic (APPswe) mice and non-transgenic (NT) mice on signaling factors involved in neuronal plasticity and survival. We evaluated cAMP-dependent protein kinase A (PKA), phospho-cyclic AMP response-element binding protein (phospho-CREB), and the pro-apoptotic protein kinases extracellular signal-regulated kinase 1/2 (phospho-ERK) and phospho-c-Jun N-terminal kinase 1 (phospho-JNK) in the striatum and frontal cortex of caffeine-treated mice. In the striatum, APPswe control mice exhibited a significant decrease in phospho-CREB, as well as significant increases in phospho-JNK and phospho-ERK in comparison to NT mice. Caffeine treatment stimulated PKA activity, increased phospho-CREB levels, and decreased phospho-JNK and phospho-ERK expression in the striatum of APPswe mice, all of which are thought to be beneficial changes for brain function. Even caffeine-treated NT mice exhibited some of these changes in striatum. In the frontal cortex, caffeine did not significantly increase phospho-CREB and PKA activity, but significantly reduced phospho-JNK and phospho-ERK expression in both APPswe and NT mice. These results suggest that caffeine shifts the balance between neurodegeneration and neuronal survival toward the stimulation of pro-survival cascades and inhibition of pro-apoptotic pathways in the striatum and/or cortex, which may contribute to its beneficial effects against AD.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Cotinine enhances the extinction of contextual fear memory and reduces anxiety after fear conditioning.
Ross Zeitlin, Sagar Patel, Rosalynn Solomon, John Tran, Edwin J Weeber, Valentina Echeverria
Bay Pines VA Healthcare System, Bay Pines, FL 33744, USA.
Posttraumatic stress disorder (PTSD) is an anxiety disorder triggered by traumatic events. Symptoms include anxiety, depression and deficits in fear memory extinction (FE). PTSD patients show a higher prevalence of cigarette smoking than the general population. The present study investigated the effects of cotinine, a tobacco-derived compound, over anxiety and contextual fear memory after fear conditioning (FC) in mice, a model for inducing PTSD-like symptoms. Two-month-old C57BL/6J mice were separated into three experimental groups. These groups were used to investigate the effect of pretreatment with cotinine on contextual fear memory and posttreatment on extinction and stability or retrievability of the fear memory. Also, changes induced by cotinine on the expression of extracellular signal-regulated kinase (ERK)1/2 were assessed after extinction in the hippocampus. An increase in anxiety and corticosterone levels were found after fear conditioning. Cotinine did not affect corticosterone levels but enhanced the extinction of contextual fear, decreased anxiety and the stability and/or retrievability of contextual fear memory. Cotinine-treated mice showed higher levels of the active forms of ERK1/2 than vehicle-treated mice after FC. This evidence suggests that cotinine is a potential new pharmacological treatment to reduce symptoms in individuals with PTSD.
Brain Res. 2011 Oct 12;1417 :127-36 21907331
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Cotinine- A Potential New Therapeutic Agent against Alzheimer’s disease.
Valentina Echeverria, Ross Zeitlin
Bay Pines VA Healthcare System, Bay Pines, Tampa, FL, USA Department of Molecular Medicine, University of South Florida, Tampa, FL, USA.
Tobacco smoking has been correlated with a lower incidence of Alzheimer’s disease (AD). This negative correlation has been attributed to nicotine’s properties. However, the undesired side-effects of nicotine and the absence of clear evidence of positive effects of this drug on the cognitive abilities of AD patients have decreased the enthusiasm for its therapeutic use. In this review, we discuss evidence showing that cotinine, the main metabolite of nicotine, has many of the beneficial effects but none of the negative side-effects of its precursor. Cotinine has been shown to be neuroprotective, to improve memory in primates as well as to prevent memory loss, and to lower amyloid-beta (Aβ)) burden in AD mice. In AD, cotinine’s positive effect on memory is associated with the inhibition of Aβ aggregation, the stimulation of pro-survival factors such as Akt, and the inhibition of pro-apoptotic factors such as glycogen synthase kinase 3 beta (GSK3β). Because stimulation of the α7 nicotinic acetylcholine receptors (α7nAChRs) positively modulates these factors and memory, the involvement of these receptors in cotinine’s effects are discussed. Because of its beneficial effects on brain function, good safety profile, and nonaddictive properties, cotinine may represent a new therapeutic agent against AD.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Effects of cholinesterase inhibiting sage (Salvia officinalis) on mood, anxiety and performance on a psychological stressor battery.
Kennedy DO, Pace S, Haskell C, Okello EJ, Milne A, Scholey AB.
Source
Human Cognitive Neuroscience Unit, Division of Psychology, University of Northumbria, Newcastle upon Tyne, UK. [email protected]
Abstract
Salvia officinalis (sage) has previously been shown both to possess in vitro cholinesterase inhibiting properties, and to enhance mnemonic performance and improve mood in healthy young participants. In this double-blind, placebo-controlled, crossover study, 30 healthy participants attended the laboratory on three separate days, 7 days apart, receiving a different treatment in counterbalanced order on each occasion (placebo, 300, 600 mg dried sage leaf). On each day mood was assessed predose and at 1 and 4 h postdose. Each mood assessment comprised completion of Bond-Lader mood scales and the State Trait Anxiety Inventory (STAI) before and after 20 min performance of the Defined Intensity Stress Simulator (DISS) computerized multitasking battery. In a concomitant investigation, an extract of the sage leaf exhibited dose-dependent, in vitro inhibition of acetylcholinesterase and, to a greater extent, butyrylcholinesterase. Both doses of sage led to improved ratings of mood in the absence of the stressor (that is, in pre-DISS mood scores) postdose, with the lower dose reducing anxiety and the higher dose increasing ‘alertness’, ‘calmness’ and ‘contentedness’ on the Bond-Lader mood scales. The reduced anxiety effect following the lower dose was, however, abolished by performing the DISS, with the same dose also being associated with a reduction of alertness during performance. Task performance on the DISS battery was improved for the higher dose at both postdose sessions, but reduced for the lower dose at the later testing session. The results confirm previous observations of the cholinesterase inhibiting properties of S. officinalis, and improved mood and cognitive performance following the administration of single doses to healthy young participants.
TOP F
***************************************************************************************************
TOP G
HOME
Show of the Month December 28 2012
Antioxidants—and the differences and uses
Natural Antioxidants
FLAVONOIDS and effects
α-Tocopherol and δ-tocopherol
Recipe for Whipped oil
*********************************************************************************************************************
Antioxidants—and the differences and uses
Antioxidants are compounds or systems that delay autoxidation by inhibiting formation of free radicals or by interrupting propagation of the free radical by one (or more) of several mechanisms: (1) scavenging species that initiate peroxidation, (2) chelating metal ions such that they are unable to generate reactive species or decompose lipid peroxides, (3) quenching •O2− preventing formation of peroxides, (4) breaking the autoxidative chain reaction, and/or (5) reducing localized O2 concentrations (Nawar 1996). Chain-breaking antioxidants differ in their antioxidative effectiveness depending on their chemical characteristics and physical location within a food (proximity to membrane phospholipids, emulsion interfaces, or in the aqueous phase). The chemical potency of an antioxidant and solubility in oil influence its accessibility to peroxy radicals especially in membrane, micellar and emulsion systems, and the amphiphilic character required for effectiveness in these systems (Wanatabe and others 2010).
Antioxidant effectiveness is related to activation energy, rate constants, oxidation–reduction potential, ease with which the antioxidant is lost or destroyed (volatility and heat susceptibility), and antioxidant solubility (Nawar 1996). In addition, inhibitor and chain propagation reactions are both exothermic. As the A:H and R:H bond dissociation energies increase, the activation increases and the antioxidant efficiency decreases. Conversely, as these bond energies decrease, the antioxidant efficiency increases.
The most effective antioxidants are those that interrupt the free radical chain reaction. Usually containing aromatic or phenolic rings, these antioxidants donate H• to the free radicals formed during oxidation becoming a radical themselves (see step nr 7). These radical intermediates are stabilized by the resonance delocalization of the electron within the aromatic ring and formation of quinone structures (Nawar 1996). In addition, many of the phenolics lack positions suitable for molecular oxygen attack. Both synthetic antioxidants (BHA, BHT, and propyl gallate) and natural botanicals contain phenolics (flavonoids) function in this manner. Botanical extracts with antioxidant activity generally quench free radical oxygen with phenolic compounds as well.—————-Because bivalent transition metal ions, Fe2+ in particular, can catalyze oxidative processes, leading to formation of hydroxyl radicals, and can decompose hydroperoxides via Fenton reactions, chelating these metals can effectively reduce oxidation (Halliwell and others 1987). Food materials containing significant amounts of these transition metals (red meat) can be particularly susceptible to metal-catalyzed reactions.
*****************************************************************************************
Natural Antioxidants
Food tissues, because they are (or were) living, are under constant oxidative stress from free radicals, reactive oxygen species, and prooxidants generated both exogenously (heat and light) and endogenously (H2O2 and transition metals). For this reason, many of these tissues have developed antioxidant systems to control free radicals, lipid oxidation catalysts, oxidation intermediates, and secondary breakdown products (Nakatani 2003; Agati and others 2007; Brown and Kelly 2007; Chen 2008; Iacopini and others 2008). These antioxidant compounds include flavonoids, phenolic acids, carotenoids, and tocopherols that can inhibit Fe3+/AA-induced oxidation, scavenge free radicals, and act as reductants (Khanduja 2003; Ozsoy and others 2009).
Spices and herbs, used in foods for their flavor and in medicinal mixtures for their physiological effects, often contain high concentrations of phenolic compounds that have strong H-donating activity (Lugasi and others 1995; Muchuweti and others 2007). Many also have high ORAC values (Table 2 and 3). Some plant-derived compounds (carnosol, rosmanol, rosmariquinone, and rosmaridiphenol) are better antioxidants than BHA (Richheimer and others 1996; Carvalho and others 2005).
Table 2–. Total ORAC values (μm TE/100 g; Prior and others 2003) of selected herbs and spices, berries, roots, and teas.
Food
Total ORAC
SEM
The oxygen radical absorbance capacity (ORAC) method is based on the inhibition of the peroxyl-radical-induced oxidation initiated by thermal decomposition of azo compounds. Prior and others (2003) used 2,2′-azo bis (2 amidino propane) dihydrochloride (AAPH) as the azo generator, incubated at 37 °C for 30 min with fluorescein (14 μm) as a fluorescent detector.
Source: USDA (2010).
Basil (fresh)
4805
225
Marjoram (fresh)
27297
1306
Oregano (fresh)
13970
545
Sage (fresh)
32004
1548
Savory (fresh)
9465
436
Basil (dried)
61063
2280
Cinnamon (ground)
131420
13867
Clove (ground)
290283
3292
Ginger (ground)
39041
1835
Nutmeg (ground)
69640
6859
Oregano (dried)
175295
7683
Pepper, black
34053
289
Rosemary (dried)
165280
1391
Sage (ground)
119929
20305
Thyme (fresh)
27426
1251
Thyme (dried)
157380
1629
Turmeric (ground)
127068
11181
Grapes (red, raw)
1837
248
Raspberries (raw)
5065
205
Garlic (raw)
5708
475
Ginger root (raw)
14840
530
Onions, red (raw)
1521
69
Tea brewed
1128
–
Tea, green, brewed
1253
Table 3–. Content of redox-active compounds (antioxidants) of selected foods (mmol/100 g).
Food
Redox-active compound content (mmol/100 g)
Sources: McCormick Institute Antioxidant Comparison (2009) and Halvorsen and others (2006).
Cloves, ground
125.5
Oregano leaf, dried
40.3
Ginger, ground
21.6
Cinnamon, ground
17.7
Turmeric powder
15.7
Basil leaf, dried
12.3
Curry powder
10.0
Paprika
8.6
Pepper, black
4.4
Raspberries
2.3
Wine, red
2.1
Cherries, sour
1.8
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
The major antioxidative plant phenolics can be divided into 4 general groups: phenolic acids (gallic, protochatechuic, caffeic, and rosmarinic acids; Figure 1), phenolic diterpenes (carnosol and carnosic acid; Figure 2), flavonoids (quercetin and catechin; Figure 3), and volatile oils (eugenol, carvacrol, thymol, and menthol; Figure 4; Shan and others 2005). Phenolic acids generally act as antioxidants by trapping free radicals; flavonoids can scavenge free radicals and chelate metals as well (Engeseth and Geldof 2001)
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
FLAVONOIDS and effects
Flavonoids with multiple hydroxyl groups are more effective antioxidants than those with only one. The presence of the ortho-3,4-dihydroxy structure increases the antioxidative activity (Geldof and Engeseth 2002). Flavonoids can dampen transition metal enhancement of oxidation by donating a H• to them, rendering them less proxidative. In addition, flavones and some flavanones (naringenin) can preferentially bind metals at the 5-hydroxyl and 4-oxo groups[U1] (Fernandez and others 2002).
Brown and Kelly (2007) evaluated the antioxidative activity of structurally related (poly)phenols, anthocyan(id)ins, and phenolic acids at physiologically relevant concentrations (100 to 1000 nM) using a Cu2+-mediated low-density lipoprotein oxidation model. (Poly)phenols with an ortho-dihydroxy substituted arrangement (cyanidin-3-glucoside, cyanidin, and protocatechuic acid) were the most effective, while trihydroxy-substituted compounds (gallic acid) had only intermediate efficacy. This was explained, in part, by their ability to chelate Cu2+ ions. It seems likely that the steric relationship of these −OH groups and their arrangement on the ring(s) both play a role in the ability of the substance to chelate metal ions. However, differences in lipid/hydrophilic phase partitioning and in H-donating abilities were also hypothesized to have contributed to the structure-activity relationships.
Alamed and others (2009) reported that the order of free radical-scavenging activity of a group of polar compounds was ferulic acid > coumaric acid > propyl gallate > gallic acid > AA; the free radical-scavenging activity of a group of nonpolar compounds was rosmarinic acid > BHT, tert-butylhydroquinone (TBHQ) > α-tocopherol. Only propyl gallate, TBHQ, gallic acid, and rosmarinic acid inhibited lipid oxidation in an oil-in-water emulsion that may reflect the ability of these compounds to orient at the interface of the oil droplet in the emulsion[U2] .
Evaluating the antioxidative activity of hydroxycinnamic acids with similar structures (caffeic, chlorogenic, o-coumaric, and ferulic acids) in a fish muscle system, Medina and others (2007) found that the capacity of these compounds to donate electrons (bond dissociation energies) appeared to play the most significant role in delaying rancidity, while the ability to chelate metals and the distribution between oily and aqueous phases were not correlated with inhibitory activities. The latter finding may reflect the type of matrix, fish muscle, in which the oxidative activity was studied. Caffeic acid was the most effective of this antioxidant group (similar to propyl gallate).
Potapovich and Kostyuk (2003) reported that, of a variety of flavonoids (rutin, dihydroquercetin[U3] , quercetin, epigallocatechin gallate, and epicatechin gallate), the catechins were most effective in inhibiting microsomal lipid peroxidation. All were able to chelate Fe2+, Fe3+, and Cu2+ and were effective •O2− scavengers to varying degrees. Authors speculate that the relative ability to scavenge •O2− may be responsible for the relative antioxidative difference among these compounds.
Many of the antioxidative flavonoid compounds are naturally occurring pigments. It appears that chloroplast-located flavonoids perform a photo-protective role against •O2− in plants (Agati and others 2007). Anthocyanins are the glycosides of polyhydroxy or polymethoxy derivatives of the flavylium cation. Hydrolysis of the sugar moiety yields an aglycone, anthocyanindin (Figure 5). Anthocyanins and anthocyanindins exhibit visual color because of the extreme mobility of the electrons within the molecular structure (double bonds) in response to light in the visible spectrum (approximately 400 to 700 nm). The pigments are quite water-soluble and 4 −OH groups are bound to the aromatic rings. pH has a significant effect on anthocyanin pigments. These −OH groups can give up H+ (in a basic solution) or H• to an oxidizing lipid (ROO•).
Proanthocyanidins also contain multiple −OH groups that can donate hydrogen, quench •O2−, and chelate metals (Shahidi and Wanasundara 1992; Fukumoto and Mazza 2000). Free radical-scavenging ability increases as the number of phenolic −OH groups increases (Kondo and others 2001).
Some phenols can polymerize into polyphenols that can bind minerals. Proanthocyanidins often occur as oligomers or polymers of monomeric flavonoids, polyhydroxy flavan-3-ols such as [+]-catechin and [−]-epicatechin (Dixon and others 2005; Figure 3 and 5). The polymeric procyanidins are better antioxidants than the corresponding monomers, catechin, and epicatechin (Ursini and others 2001). Catechin and epicatechin can combine to form esters, such as catechin/epicatechin gallate, or bond with sugars and proteins to yield glycosides and polyphenolic proteins. Glycosylation of flavonoids at the 3 −OH group usually decreases the antioxidative activity due to the reduction of the number of phenolic groups (quercetin/rutin; Figure 3).
Proanthocyanidins with demonstrated antioxidant activity and potential biologically therapeutic effects occur in fruits (apples and cherries), some berries (rosehips, raspberries, blackberries, and strawberries), as well as in the leaves (tea), seeds (grape, sorghum, and cocoa bean), and bark of many plants (Dixon and others 2005; Buricova and Reblova 2008; Bak and others 2010).
[U1]This is good news to assist in the binding of metals that we come across in the air we breathe as well as in the foods we consume—so having a good dose of flavonoids can be of great benefit
[U2]Fat saving or lipid periodization is regulated better with these compounds
[U3]To quench oxygen free radicals as well as fats is a extreme bonus—both of these components are necessary for the body but oxygen can be a proxidant and fats can get oxidized as well
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
α-Tocopherol and δ-tocopherol
α-Tocopherol (vitamin E) is a fat-soluble carotenoid whose antioxidative capacity has been studied extensively (Figure 6). α-Tocopherol is the major vitamin E compound in plant leaves where it is located in the chloroplast envelope and thylakoid membranes in proximity to phospholipids (Onibi and others 2000). It deactivates photosynthesis-derived reactive oxygen species (especially •O2−) and prevents the propagation of lipid peroxidation by scavenging lipid peroxyl radicals in thylakoid membranes (Munné-Bosch 2005).
Figure 6–. Natural antioxidants (alpha- and gamma-tocopherol, ascorbic acid, ascorbyl palmitate, propyl gallate, and resveratrol).image
Trolox is a water-soluble derivative of vitamin E. Structurally related lipid-soluble antioxidants that differ in the number of methyl groups (δ-tocopherol compared with α-tocopherol)[U1] have different free radical-scavenging activities and different surface activities (Figure 6; Chaiyasit and others 2005). Giuffrida and others (2007) evaluated the ability of α-tocopherol, δ-tocopherol, ascorbyl palmitate, and propyl gallate (300 mg/kg; Figure 6) to prevent oxidation in sunflower oil and high-oleic sunflower oil, both rich in di-unsaturated fatty acids, and in partially hydrogenated palm oil containing monounsaturated fatty acids. δ-Tocopherol was[U2] the most effective antioxidant in sunflower oil, and propyl gallate was the most effective in the more saturated oils. Yeum and others (2009) reported synergistic effects between AA and α-tocopherol in protecting an in vitro biological model system. It may be that AA regenerates α-tocopherol after α-tocopherol donates a H• to an oxidizing lipid.
α-Tocopherol can also inhibit oxidation of protein. Estévez and Heinonen (2010) demonstrated that α-tocopherol reduced formation of α-aminoadipic and γ-glutamic semialdehydes from oxidized myofibrillar proteins[U3] .—In general, vitamin E added to water-based food systems using an oil carrier targets the neutral lipid fraction (triacylglycerols) rather than the polar lipid fraction (phospholipids) and is not an effective antioxidant. However, δ-tocopherol added using a polar carrier can be incorporated into the phospholipid fraction and is an effective antioxidant (Wills and others 2007). In a lard model system, the antioxidative activity of the tocopherols is temperature dependent (Reblova 2006). At 80 °C, the antioxidative activity of δ-tocopherol is about twice that of α-tocopherol; however, it decreases as temperature increases. Antioxidative activity of α-tocopherol decreases above 110 °C, and both lose their activity above 150 °C[U4] .
Dietary supplementation of α-tocopherol increases incorporation of the antioxidant into the phospholipid membrane region where the polyunsaturated fatty acids are located. Including α-tocopherol in livestock diets has been shown to have significant effects on the antioxidative activities of their tissues and the stability of meat derived from them (Formanek and others 2001; Swigert and others 2004; Guo and others 2006; Boler and others 2009; Lahucky and others 2010).
[U1] Alpha Tocopherol
[U2]δ-Tocopherol= Delta Tocopherol—there are 4 tocopherols in vitamin E and 4 toctrienols as well
Alpha-Beta-Delata and Gamma and the tocotrienols as well have 4 alpha, beta, gamma, delta
[U3]It would appear to squelch the free radical effect of glutamic acid which may cause neuron death of the brain
[U4]So if you cook above 110 cel or about 230 fahr the free radical neutralizing effect will lose it’s ability to work
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Recipe for Whipped oil— take rosemary extract that you made and add it to a thick oil like wheat germ oil or rice bran oil or olive oil or avocado–you can add different things like vitamin C or even other essential oils to this recipe or even any fat soluble antioxidant or other herbals or even essential oils add it to the extractor I have shown or in a blender and apply mid range speed and gradually turn it up to full—what you will see is the oil and extract will fuse and form a buttery like consistency—jar it and freeze it asap—if it seperates then reapply the method again and re freeze—it will hold and solidify like butter
the benefits to this will out weigh almost any fat your consuming now—with the rosemary you have several antioxidants in there that will perform a variety of effects from brain support–heart support–liver protection pancreas support—blood flow–hormonal balancing of estrogens-radiation protection–this will assist in the brain fatty cells as well as other lipid supplying and defending cells to reinforce neurol connection and cellular communication and remve metals from the body—anti fungal-anti bacterial-anti viral