COPPER AND ZINC SALICYLATES—-Two Excellent Inflammation Fighters
By Walter Last
Copper is an essential trace mineral. All tissues of the body need it for normal metabolic functions. Sometimes there is too much of the inorganic form in drinking water (acid water flowing through copper pipes). It can then gradually accumulate in the body and lead to toxicity symptoms with signs of zinc deficiency, over-stimulation, psychosis and liver damage.However, in organic form as chelates or copper complexes it is excellent for reducing inflammations, strengthening connective tissue, restoring hair colour and the oxidative energy metabolism as well as fighting parasites and cancer and may sometimes improve brain and liver functions.—If you give animals a choice between drinking normal water and water in which a copper pipe has been immersed, they will reportedly prefer the high copper water. This helps to keep them free of parasites. Copper armbands are well known to reduce arthritis. Copper serum levels are elevated up to threefold above normal with inflammations and with many chronic and infectious diseases, apparently because the body mobilises all tissue stores of copper to fight the condition. During remissions the copper levels return back to normal.—The most effective anti-inflammatory agents are copper complexes. Commonly these are related to salicylic acid. In addition, copper ascorbate has strong anti-viral properties. Copper salicylate has a better anti-inflammatory effect than cortisone but without the side effects. In addition it has also good anti-cancer, anti-tremor and anti-convulsive properties, suitable for treatment of epilepsy and possibly Parkinson’s disease. Children with severe copper deficiency constantly have convulsive seizures. Another feature of severe copper deficiency is degeneration of the central nervous system. There are at least 6 important copper-dependent enzymes in the brain. One of these is required for the conversion of tyrosine into dopamine which is lacking in Parkinson’s disease. A copper enzyme is also needed for the synthesis of adrenalin (epinephrine).–In experiments copper salicylate prevented chemically induced skin cancers. Furthermore, a single application resulted in a 55% reduction in experimental animal tumours in 20 weeks. The main metabolic defect of cancer cells, according to Dr Johanna Budwig and other researchers, is a deficiency of the enzyme cytochrome oxidase. This causes a blockage in the cellular respiration or oxidative energy production of the affected cells. Budwig claims that plenty of linseed oil and sulphur amino acids (L-cysteine and especially L-methionine) help to correct this situation.—Cytochrome oxidase is a copper dependent enzyme and additional copper might be of further benefit. In the final stages of this oxidative energy production electrons are transferred to copper (II) and iron (III) in the cytochrome oxidase to form copper (I) and iron (II). In the last step these electrons are then transferred to oxygen, which now can attract hydrogen ions to form water. In cancer cells this transfer of electrons to oxygen is blocked and energy is being produced very inefficiently by converting glucose into lactic acid.–However, practical experience has shown that copper is more important to prevent cancer or a regrowth of tumours and possibly with dormant tumours. If growing tumours are present, then copper is needed to form new blood vessels. Taking high amounts of zinc creates a relative copper deficiency and helps to prevent the formation of new blood vessels.—Copper salicylates have a similar action as superoxide dismutase (SOD) to protect cells from free radicals. Dr John R.J. Sorenson at the University of Arkansas has done most of the research work on copper complexes. In one of his publications he states that with the exception of Wilson’s disease, there are no chronic degenerative diseases in man known to result from non-industrial exposure to copper.–Dr Werner Hangerter, head of medicine at the University of Kiel, successfully used copper salicylates for over 20 years with more than 1100 patients with rheumatoid arthritis and other inflammatory conditions. Of 620 patients with rheumatoid arthritis 65% became symptom free and another 23% improved significantly, only 12% remained unchanged. With acute rheumatic fever 100% became symptom free. Also neuromuscular problems such as sciatica, neuralgia and cervical spine-shoulder problems responded very well. Even short-term treatment of rheumatoid arthritis resulted in long-term remissions or improvements.—The therapeutic potency and safety of the copper complexes of aspirin (acetyl-salicylic acid) and salicylic acid is much better than for aspirin itself or for inorganic copper. These complexes are 5 to 8 times more effective than aspirin but less toxic. The therapeutic index (the margin between effectiveness and toxic effects) has been stated as being significantly greater than for other anti-inflammatory drugs. While aspirin causes or aggravates peptic ulcers, the copper complexes have a better ulcer-healing effect than commonly used anti-inflammatory ulcer drugs. Harmful effects of aspirin, salicylic acid and similar drugs apparently arise because they bind copper in the body and cause a localised copper deficiency in the tissues.—Unfortunately, copper salicylate or other effective copper complexes are not normally available or only in very low doses, presumably because they cannot be patented. However, they are relatively easy to make for someone who wants to experiment. Order salicylic acid through a cooperating pharmacist and dissolve 2 g or about half a teaspoonful in half a litre of hot water.–Use covered glassware and distilled or de-ionised water and several pieces of copper with a large surface area immersed in it. Keep it warm, between 60º and 90ºC or just below boiling. Add more water as required and adjust the final volume to 500 ml. At first a light yellow-greenish colour develops, but at one point the colour considerably deepens. This may happen after 15 to 20 hours of heating and you may now let it cool and fill into a glass bottle.—Near the end of the heating process and during storage black copper oxide starts forming and slowly accumulates at the bottom. This is due to copper being converted from the original one-valent copper (I) salicylate to two-valent copper (II) salicylate. With this, the salicylic acid binds only half of the dissolved copper and the rest becomes copper oxide. The effectiveness of the solution does not seem to be affected by this and the amount of copper in the complex is not related to its potency. From time to time you may decant the solution from any settled copper oxide and crystals or filter it through tissue paper.—Copper (I) salicylate is a strong antioxidant and also appears to have good anti-inflammatory qualities, but all the published papers are on copper (II) salicylate. However the only data for a Cu (I) complex that I could find (penicillamine) showed it to have even stronger anti-inflammatory activity than the corresponding Cu (II) complex. Initially copper (I) will dominate in the self-prepared copper salicylate but the more copper oxide precipitates the more will copper (II) gain the upper hand. While salicylic acid only dissolves in hot water, copper (II) salicylate is easily soluble in cold water and is very stable and generally well tolerated when taken orally.Copper salicylate is also excellent for external use as packs or rubs on sites of tumours and inflammation, also rubbing it on skin prone to skin cancer. To improve its skin absorption you may mix it with some aloe vera gel or follow the copper salicylate rub with some aloe vera.—For internal use with generalised inflammations or other indications 60 mg of copper salicylate have been used in clinical trials once or twice and up to four times daily. Try a teaspoonful (approximately 25 mg of copper salicylate) three times daily in liquids with meals, preferably under professional supervision. For short-term use you may also double this amount. When it produces the desired effect, cut back to a maintenance dose of 1 teaspoonful a
day or interrupt the intake after 2 weeks to see what happens.—Copper (I) salicylate is a strong antioxidant and may interfere with oxygen therapy. Therefore, it is advisable to alternate periods of taking high doses of copper salicylate with periods of intensive oxygen therapy. However, external application of copper salicylate should still be fine during oxygen therapy.—Another possibility of making copper salicylate yourself is by ingesting sodium salicylate and a copper chelate together. Copper salicylate then appears to form in the stomach. In some countries sodium salicylate is available as tablets, in others it may be obtained from a friendly chemist/pharmacist as a crystallised powder. Copper chelate, commonly as amino acid chelate or gluconate, may be available from a health food shop or over the Internet. Taking a 650 mg tablet of sodium salicylate together with 5 mg of copper in chelated form has reportedly eliminated severe arthritic pain. As maintenance dose a 350 mg tablet of sodium salicylate together with 2.5 mg of copper have been taken up to three times a day. If the sodium salicylate is available as powder, you may assume that a level teaspoonful is about 4 g. By dividing this into 6 equal portions you will have about 650 mg per portion.—You also find a source of copper salicylate tablets on the Internet or you may be able to obtain copper (II) salicylate crystals from a supplier of laboratory or fine chemicals. In this case you could divide a rounded teaspoonful into 100 equal parts, each part would then be approximately 50 mg.——–For a potent anti-viral remedy you may produce copper ascorbate. This is not difficult either. The only problem is that ascorbic acid easily becomes oxidised in contact with metal. Therefore, it is best to exclude all air. Bring some distilled or de-ionised water to boiling and, as hot as possible, fill a 500 ml glass or hard plastic container nearly to the top. Immerse a piece of copper and add 4 to 5 g or about one teaspoon of ascorbic acid powder. Keep refrigerated and remove the copper after a few days. After part of it has been used minimise the air space by filling it into a smaller bottle or jar. As an infection fighter try a teaspoonful several times a day for up to 2 weeks.—Copper salicylate is a very stable complex and most of it appears to be excreted unchanged. Therefore, it may be regarded more as a remedy rather than a food supplement. Nevertheless, when taking this or other copper complexes, colloids or chelates over a longer period it is advisable to take additional zinc, about 30 mg a day, in order to avoid a zinc deficiency from developing.—Finally I want to stress that the use of copper salicylate and ascorbate, especially when you make these yourself, is strictly experimental and no one can take any responsibility for what you are doing. If in doubt, then use it only externally. Individuals who are sensitive to salicylates need to be extra careful but I believe that even then it will generally be well tolerated. Handle copper salicylate with care, it stains garments.–I believe that colloidal copper has similar beneficial properties as copper salicylate and you might alternate using both with some longer breaks in-between. You can make colloidal copper in the same way as colloidal silver, just use two strips of copper instead of silver electrodes. However, the use of colloidal copper is experimental as well and you have to find out by yourself how much to take and how beneficial it is for you.—The Schweitzer Formula—Zinc has strong anti-inflammatory and antibiotic properties as well but can become deficient with a high copper intake. Therefore, it is usually best to increase the intake of both minerals together. With a high copper intake, also a high zinc supplementation should be used. This may be best in the form of Schweitzer Formula, a complex formed by zinc (oxide or carbonate), boron (boric acid) and salicylic acid. This is an excellent antibiotic, disinfectant, fungicide, anti-inflammatory and healing remedy.—-The Schweitzer Formula was developed 1915 in Germany and sold worldwide since 1920. In addition to any kind of infection or inflammation, it has been used in cancer treatment, to improve the immune response and blood oxygenation. Applied externally it helps to heal injuries and skin diseases, including acne, scarring varicose veins and varicose ulcers.—You can easily make the Schweitzer Formula yourself. Dissolve 9.2 g of salicylic acid, 2.1 g of boric acid and 2.7 g of zinc oxide or 4 g of zinc carbonate in 2 litres of hot water. You may get these ingredients from a pharmacist or supplier of fine chemicals and have exact quantities weight out. However, it is sufficient to use approximate amounts. You may use 2 level teaspoons of salicylic acid and half a teaspoon each of boric acid and zinc oxide or one level teaspoon of zinc carbonate.—-However, in Australia boric acid has now been scheduled as a prescription poison. Apparently eating large amounts of boric acid mixed with castor sugar that the parents had used to eliminate ants poisoned some infants. If you cannot obtain boric acid from a friendly chemist, you may use borax instead. This introduces some additional sodium ions. While this is not desirable, I do not expect this to significantly reduce the healing qualities of the Schweitzer Formula. To get the same amount of boron you may use about 30% more borax than boric acid.—-Use distilled or de-ionised water and a non-metal container. Heat for about an hour and stir occasionally with a non-metal spoon until no more of the zinc oxide or zinc carbonate at the bottom of the container seems to dissolve. Then decant or filter into a glass container and store in a dark and cool place. Any surplus of zinc oxide or carbonate that remains undissolved shows that all the boric acid and salicylic acid have been used up. However, any surplus of boric acid would be beneficial and just supply additional boron.–As a biochemist I do not see a difference between using this solution directly and letting it crystallise and then dissolving the crystals. However, I have not been able to verify this in a clinical trial. If you do want to crystallise the complex, then let the water evaporate very slowly in a flat non-metal tray covered with fine gauze. As a general rule, the slower the crystallisation, the bigger the crystals. Therefore, keep the tray undisturbed in a cool place. For quick crystallisation and smaller crystals you may expose the tray to direct sunlight. For use you may then dissolve the crystals again in 2 litres of hot water.—–As with copper salicylate, there are no exact guidelines on how much to take. A tablespoonful has been taken 3 times daily with liquid or meals for extended periods. For shorter periods this dose has been doubled. It is also good to rub onto the skin, especially where there are any problems.—You may take this at the ratio of one tablespoon of Schweitzer Formula to one teaspoon of copper salicylate. For long-term use I would take one spoonful of each daily. I believe that long-term use of copper or zinc should be balanced by taking the other mineral as well, be it as salicylate complex, colloid or conventional remedy. I also believe that copper and zinc as complexes or colloids are safer and more effective than the long-term use of aspirin or other anti-inflammatory drugs.—-One tablespoonful of Schweitzer contains about 15 mg of zinc, 15 mg of boric acid or 2.5 mg of boron and 70 mg of salicylic acid. As with copper salicylate, most of these can be expected to be eliminated from the body as a complex. Therefore, Schweitzer Formula cannot be regarded as a zinc or boron supplement and these may need to be additionally supplemented in a different form. However, to assess any potential toxicity, we may assume that the complex completely disintegrates in the body. This would then supply only relatively low levels of the individual ingredients. Twice these amounts of zinc and boron are recommended as being beneficial and much higher amounts have been used in nutritional t
herapy. Therefore, I cannot see any possible toxicity at least up to 3 tablespoons daily.—Also many commonly used foods are quite high in salicylates. Some individuals, especially hyperactive children are sensitive to salicylates and get a reaction from it. However, I believe that this is due to the chelating effect of salicylic acid, which may cause zinc and copper deficiency in the body. Therefore, in the form of zinc and copper complexes, salicylates may not normally cause a reaction in susceptible individuals.–After a period of use, it is advisable to interrupt using these remedies for a while and observe any effects., I want to stress again, that the use of these remedies over long periods or in high doses is experimental and you must be prepared to take responsibility for any side effects yourself.
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Bacterial Cause Found for Skin Condition Rosacea
ScienceDaily (Aug. 28, 2012) — Scientists are closer to establishing a definitive bacterial cause for the skin condition rosacea. This will allow more targeted, effective treatments to be developed for sufferers, according to a review published in the Journal of Medical Microbiology.—Rosacea is a common dermatological condition that causes reddening and inflammation of the skin mostly around the cheeks, nose and chin. In severe cases skin lesions may form and lead to disfigurement. Rosacea affects around 3% of the population — usually fair-skinned females aged 30-50 and particularly those with weak immune systems. The condition is treated with a variety of antibiotics, even though there has never been a well-established bacterial cause.–A new review carried out by the National University of Ireland concludes that rosacea may be triggered by bacteria that live within tiny mites that reside in the skin.–The mite species Demodex folliculorum is worm-like in shape and usually lives harmlessly inside the pilosebaceous unit which surrounds hair follicles of the face. They are normal inhabitants of the face and increase in number with age and skin damage — for example, following exposure to sunlight. The numbers of Demodex mites living in the skin of rosacea patients is higher than in normal individuals, which has previously suggested a possible role for the mites in initiating the condition.—More recently, the bacterium Bacillus oleronius was isolated from inside a Demodex mite and was found to produce molecules provoking an immune reaction in rosacea patients. Other studies have shown patients with varying types of rosacea react to the molecules produced by this bacterium — exposing it as a likely trigger for the condition. What’s more, this bacterium is sensitive to the antibiotics used to treat rosacea.—Dr Kevin Kavanagh who conducted the review explained, “The bacteria live in the digestive tracts of Demodex mites found on the face, in a mutually beneficial relationship. When the mites die, the bacteria are released and leak into surrounding skin tissues — triggering tissue degradation and inflammation.”—“Once the numbers of mites increase, so does the number of bacteria, making rosacea more likely to occur. Targeting these bacteria may be a useful way of treating and preventing this condition,” said Dr Kavanagh. “Alternatively we could look at controlling the population of Demodex mites in the face.. Some pharmaceutical companies are already developing therapies to do this, which represents a novel way of preventing and reversing rosacea, which can be painful and embarrassing for many people.”—-Story Source-The above story is reprinted from materials provided by Society for General Microbiology, via AlphaGalileo. —Journal Reference-Stanisław Jarmuda, Niamh O’Reilly, Ryszard Żaba, Oliwia Jakubowicz, Andrzej Szkaradkiewicz and Kevin Kavanagh. The potential role of Demodex folliculorum mites and bacteria in the induction of rosacea. Journal of Medical Microbiology, 2012 DOI: 10.1099/jmm.0.048090-0
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Aqueous garlic extract and its phytochemical profile– special reference to antioxidant status.
Int J Food Sci Nutr. 2012 Jun;63(4):431-9—Authors: Rasul Suleria HA, Sadiq Butt M, Muhammad Anjum F, Saeed F, Batool R, Nisar Ahmad A
Abstract—Garlic (Allium sativum L) has distinct nutritional profile with special reference to its bioactive components and is used in different diet-based therapies to cure various lifestyle-related disorders. For this purpose, characterization and extraction of garlic were carried out followed by antioxidant assays. Different solvents (50% aqueous ethanol, 50% aqueous methanol and water) at different time intervals (4, 5 and 6 h) at 60°C were used to optimize aqueous extraction efficiency of garlic. Among the solvents, water extract resulted in better extraction yield (31.85 ± 2.09 g/25 g) at 5 h. The antioxidant potential of all these solvents was estimated through in vitro studies. In this context, it was observed that higher amount of total phenolic contents was present in aqueous methanol 71.87 ± 1.69% at 45 min. Antiradical (1,1-diphenyl-2-picrylhydrazyl assay) and antioxidant activity showed that the maximum value was 73.80 ± 3.69 and 83.83 ± 0.16%, respectively, in methanolic extract at 45 min while glucose diffusion and ferric reducing antioxidant power were 97.00 ± 0.20 and 32.66 ± 0.72% at p < 0.05, respectively. Aqueous garlic extract was selected as the best treatment on the basis of percentage yield and safety modulation in human body absorption. Aqueous garlic extract was subjected to pH, acidity, total soluble solids (TSS) and colour. It was observed that the pH of aqueous garlic extract decreased with the passage of time while acidity increased. It was also concluded that storage affected the value of TSS and colour significantly. L* values for colour on 0 day were 34.18 ± 0.08, whereas those on 28th day were 38.84 ± 0.03. It was predicted that 28 days storage resulted in significant increase in L* value, while a* value decreased from 4.31 ± 0.01 to 0.32 ± 0.01 at the end of storage study.—PMID: 22098476 [PubMed – indexed for MEDLINE]
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Hexavalent chromium and its effect on health- possible protective role of garlic (Allium sativum Linn).
J Basic Clin Physiol Pharmacol. 2011;22(1-2):3-10—Authors: Das KK, Dhundasi SA, Das SN
Abstract—Hexavalent chromium or chromium (VI) is a powerful epithelial irritant and a confirmed human carcinogen. This heavy metal is toxic to many plants, aquatic animals, and bacteria. Chromium (VI) which consists of 10%-15% total chromium usage, is principally used for metal plating (H2Cr2O7), as dyes, paint pigments, and leather tanning, etc. Industrial production of chromium (II) and (III) compounds are also available but in small amounts as compared to chromium (VI). Chromium (VI) can act as an oxidant directly on the skin surface or it can be absorbed through the skin, especially if the skin surface is damaged. The prooxidative effects of chromium (VI) inhibit antioxidant enzymes and deplete intracellular glutathione in living systems and act as hematotoxic, immunotoxic, hepatotoxic, pulmonary toxic, and nephrotoxic agents. In this review, we particularly address the hexavalent chromium-induced generation of reactive oxygen species and increased lipid peroxidation in humans and animals, and the possible role of garlic (Allium sativum Linn) as a protective antioxidant.–PMID: 22865357 [PubMed – indexed for MEDLINE]
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http://www.thecehf.org/morgellons-disease-research-update-august-2012.html
Morgellons Disease Research Update August 2012
Research Update …
Scientists Pursue Connection between Infectious Disease Afflicting Cattle and Morgellons Disease Affecting Humans
Progress moves forward as more research shows Morgellons disease has a physiologic (physical not mental) basis. ——-
The Morgellons break through started with the research publication, Filament Formation Associated with Spirochetal Infection: a comparative approach to Morgellons Disease by Marianne Middelveen, a Canadian veterinary microbiologist and Raphael Stricker, MD. The CEHF first announced this news last fall when this peer reviewed publication appeared in the November, 2011 issue of Clinical, Cosmetic and Investigational Dermatology.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3257881
Why is this important? —-In November, 2011, Middelveen and Stricker reported to have found evidence of a veterinary analog to Morgellons (MD). BDD, an infectious disease which has plagued cattle for decades, has fibers/filaments within their tissue and lesions that were recognized as a match to those found in the controversial disease known as Morgellons (MD) in humans. Studies on fibers/filaments from cattle with the bovine hoof disease and those found in MD suffers provided startling evidence challenging the dermatologists’ unfounded assumption that MD is a psychiatric disorder called “Delusions of Parasitosis”. Anyone who suffers from Morgellons knows how real these symptoms are and how disheartening it is to be told it is all in your head. Although the publication stated that the etiology (cause) of MD was not yet known, the findings by Middelveen and Stricker provided corroborative evidence to support a physiological and, perhaps, infectious etiology, lending a new direction for further research.
Second Study Announced by the CEHF on May 16, 2012 –Morgellon Fibres
http://www.omicsonline.org/2155-9554/2155-9554-3-140.pdf
Indeed, their second study, Morgellons Disease: A Chemical and Light Microscopic Study, published May, 2012 in the peer reviewed publication, Journal of Clinical & Experimental Dermatology Research, continued this BDD and MD comparison in greater detail. Researchers were able to conduct a more in-depth analysis of dermatological specimens from three Morgellons patients and biopsies from cattle with proliferative late stage BDD. Examinations were conducted by light microscopy, by chemical experiments and by immunohistological testing.
Results of the Study … These findings confirmed that filaments/fibers from both bovine and human samples were similar in formation at the cellular level and had the chemical and physical properties of keratin. The composition of MD filaments from humans was confirmed to be keratin by immunohistological staining with antibodies specific for human keratins. Fibers from three human patients were found to be biological in origin and are produced by keratinocytes in epithelial and follicular tissues. —An interesting side note is that researchers Middelveen and Stricker found filaments/fibers associated with MD beneath unbroken skin as well as in lesions, thus, demonstrating they are not self-implanted. This confirms previous research from Dr. Randy Wymore at the OSU-Center for the Investigation of Morgellons Disease.
Why is this important? —-The original premise–that MD is physiological is holding up to the test of scientific scrutiny.
Morgellons Study Cited by Faculty of 1000
http://www.thecehf.org/morgellons-study-cited-by-faculty-of-1000.html
The quality and importance of this research is highlighted in Faculty of 1000 Award.
Faculty of 1000 (F1000) is a global community of over 10,000 experts who select, rate and evaluate the very best articles in biology and medicine. The core mission of the F1000 is to identify and evaluate the most important articles in biology and medical research publications. The organization highlights and brings awareness to significant new research. The selection of Morgellons Disease: A Chemical and Light Microscopic Study places the work in this work in the top 2% of published articles in these fields. It classifies the study as “must read” and is certainly an honor for the entire research team. More information can be accessed at the F1000 website (http://f1000.com/716597867).
Thank You and Congratulations to Our Researchers!! —-No one can apply to be considered for this. This research was chosen and recognized on its merits and for the importance it holds worldwide. Everyone at The Charles E. Holman Foundation and from the Morgellons community wish to express our congratulations to Marianne Middelveen, Elizabeth Rasmussen, Douglas Kahn, and Raphael Stricker for this recognition. The award was indeed serendipity. We now have documented, peer reviewed evidence published, corroborating MD is not Delusions of Parasitosis.
MD, like BBD, has a true physical cause. “ … Because BDD is a disease in which spirochetes have been identified as primary etiologic agents, and spirochetal sero-reactivity has been associated with MD, it is reasonable to assume that spirochetal infection plays an important role in MD… Further immunohistological and electron microscopy studies are needed to solve the mystery of Morgellons …” (Middelveen and Stricker). This points the way to the next step in our research. To paraphrase Paul Harvey, stay tuned in and signed up for the next edition of Keeping You in the Loop …for the “rest of the story.”
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Show of the Month Sepetember 17- 2012
Brain-Eating Amoeba-From Tap Water
Coconut Oil Could Combat Tooth Decay
High Doses of Vitamin D Help Tuberculosis Patients Recover More Quickly
DETAILED DESCRIPTION OF SOME SPECIFIC EMBODIMENTS
Cannabidiol blocks glutamate
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Brain-Eating Amoeba-From Tap Water
Now even TAP WATER isn’t safe! Brain-eating amoeba fatal in 99% of cases ‘could come from your own faucet’
In 2011, two people in Louisiana died after using tap water for nasal irrigation
Amoeba known as Naegleria fowleri can infect brain and enters through nasal passage
Once infected, organism is 99% fatal
By Beth Stebner
PUBLISHED: 12:37 GMT, 24 August 2012 | UPDATED: 12:37 GMT, 24 August 2012 –There could be a deadly killer in your home – the kitchen tap.Last year in Louisiana, two people died from a single-celled organism that thrives in warm, freshwater after using tap water for flushing their sinuses.The amoeba, known as Naegleria fowleri, can cause primary amoebic meningoecephalitis (PAM), which is fatal in 99 per cent of cases.–Deadly infection: The amoeba, known as Naegleria fowleri, can cause primary amoebic meningoecephalitis (PAM), which is fatal in 99 per cent of cases The nose knows: In 2011, two people in Louisiana who used tap water in neti pots to flush out their sinuses caught the deadly infection Both victims, a 51-year-old woman and a 28-year-old man, had used tap water in neti pots to flush out their sinuses and died days later. They lived in separate areas of the state. Neti pots are generally safe for use for clearing out excess mucus in the nasal cavity, but when amoebas are present, the infection has a frighteningly fatal rate. According to the Centers for Disease Control, the amoeba enters the brain through the nasal passage, especially when people go swimming in warm freshwater lakes and ponds. -In a report published by Dr Jonathan Yoder, who works at the National Center for Emerging and Zoonotic Infectious Diseases, a division of the CDC, concluded that in both cases, the victims had only come in contact with the amoeba from tap water.-He and a group of researchers tested the water from both houses. Their results were published in Clinical Infectious Diseases on August 23. Dr Yoder and the other authors found the amoeba in the kitchen spigot, shower, bathtub, and bathroom sink in the woman’s home.
Path of infection: N. fowleri can only enter the body through the nasal passage or broken skin, not through drinking water Growth process: The single-celled amoeba is also called a brain-eating amoeba; later symptoms can include hallucinations and seizures—They found Naegleria fowleri in a tankless water heater in the home of the 28-year-old man. The authors noted that the municipal water sources were not contaminated in either case. The residents lived in different parts of the state. The CDC says that one cannot contract the organism simply through drinking water, and urges those using nasal irrigation systems to either use distilled or bottled water, or boil their tap water for at least a minute to ensure the Naegleria fowleri amoeba is killed. The centre also notes that there have been few infections in the U.S. throughout the past decades. Preventative measures: The CDC recommends that those near warm, fresh water avoid swimming in it, or holding your nose when going underwater–From 2002 to 2011, there were 32 infections reported. Included in those statistics are the two people from Louisiana who used neti pots to flush out their noses.—Initial symptoms begin five days after infection, but could take as long as seven, and include headache, fever, nausea, and even vomiting.—In the later phases when the amoeba reaches the brain tissue, those suffering from the infection may lose balance, hallucinate, and experience seizures, and in 99 per cent of cases, die. The CDC notes that only one person out of 123 infected has survived. It reminds those who will be swimming in warm, fresh water to use nasal plugs, hold one’s nose shut, or avoid going under water altogether, though infection from N. fowleri is extremely rare
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Coconut Oil Could Combat Tooth Decay
ScienceDaily (Aug. 30, 2012) — Digested coconut oil is able to attack the bacteria that cause tooth decay. It is a natural antibiotic that could be incorporated into commercial dental care products, say scientists presenting their work at the Society for General Microbiology’s Autumn Conference at the University of Warwick. The team from the Athlone Institute of Technology in Ireland tested the antibacterial action of coconut oil in its natural state and coconut oil that had been treated with enzymes, in a process similar to digestion. The oils were tested against strains of Streptococcus bacteria which are common inhabitants of the mouth. They found that enzyme-modified coconut oil strongly inhibited the growth of most strains of Streptococcus bacteria including Streptococcus mutans — an acid-producing bacterium that is a major cause of tooth decay.—Many previous studies have shown that partially digested foodstuffs are active against micro-organisms. Earlier work on enzyme-modified milk showed that it was able to reduce the binding of S. mutans to tooth enamel, which prompted the group to investigate the effect of other enzyme-modified foods on bacteria.—Further work will examine how coconut oil interacts with Streptococcus bacteria at the molecular level and which other strains of harmful bacteria and yeasts it is active against. Additional testing by the group at the Athlone Institute of Technology found that enzyme-modified coconut oil was also harmful to the yeast Candida albicans that can cause thrush. The researchers suggest that enzyme-modified coconut oil has potential as a marketable antimicrobial which could be of particular interest to the oral healthcare industry. Dr Damien Brady who is leading the research said, “Dental caries is a commonly overlooked health problem affecting 60-90% of children and the majority of adults in industrialized countries. Incorporating enzyme-modified coconut oil into dental hygiene products would be an attractive alternative to chemical additives, particularly as it works at relatively low concentrations. Also, with increasing antibiotic resistance, it is important that we turn our attention to new ways to combat microbial infection.”-The work also contributes to our understanding of antibacterial activity in the human gut. “Our data suggests that products of human digestion show antimicrobial activity. This could have implications for how bacteria colonize the cells lining the digestive tract and for overall gut health,” explained Dr Brady. “Our research has shown that digested milk protein not only reduced the adherence of harmful bacteria to human intestinal cells but also prevented some of them from gaining entrance into the cell. We are currently researching coconut oil and other enzyme-modified foodstuffs to identify how they interfere with the way bacteria cause illness and disease,” he said.—Story Source-The above story is reprinted from materials provided by Society for General Microbiology, via AlphaGalileo.
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High Doses of Vitamin D Help Tuberculosis Patients Recover More Quickly
ScienceDaily (Sep. 3, 2012) — For decades before antibiotics became generally available, sunshine was used to treat tuberculosis, with patients often being sent to Swiss clinics to soak up the sun’s healing rays. Now, for the first time scientists have shown how and why heliotherapy might, indeed, have made a difference.–A study led by researchers at Queen Mary, University of London, conducted in collaboration with the Medical Research Council’s National Institute for Medical Research, has shown that high doses of vitamin D, given in addition to antibiotic treatment, appear to help patients with tuberculosis (TB) recover more quickly.—The research, which will be published online this week in the Proceedings of the National Academy of Sciences of the USA (PNAS), is the first to investigate the effect of vitamin D on the immune responses of patients receiving treatment for an infectious disease. The findings indicate that high doses of the vitamin can dampen down the body’s inflammatory response to infection, enabling patients to recover faster, with less damage to their lungs.– In addition to stimulating recovery in TB patients, the authors say their results suggest that vitamin D supplementation might help patients recover better from other diseases such as pneumonia.–Dr Adrian Martineau, senior lecturer in respiratory infection and immunity at the Blizard Institute, part of Queen Mary, University of London, who led the research, said: “These findings are very significant. They indicate that vitamin D may have a role in accelerating resolution of inflammatory responses in tuberculosis patients. This is important, because sometimes these inflammatory responses can cause tissue damage leading to the development of cavities in the lung. If we can help these cavities to heal more quickly, then patients should be infectious for a shorter period of time, and they may also suffer less lung damage.”More broadly, the ability of vitamin D to dampen down inflammatory responses without compromising the actions of antibiotics raises the possibility that supplementation might also have benefits in patients receiving antimicrobial therapy for pneumonia, sepsis and other lung infections.”–Dr Martineau and his colleagues from a number of London hospitals and institutions randomised 95 TB patients receiving standard antibiotic treatment into two groups: for the first eight weeks of their treatment, 44 received additional high dose vitamin D, while 51 received a placebo. Dr Anna Coussens at the MRC’s National Institute for Medical Research measured levels of inflammatory markers in blood samples taken from these patients, and conducted statistical analyses to determine the effects that vitamin D had on the immune response.—“We found that a large number of these inflammatory markers fell further and faster in patients receiving vitamin D,” said Dr Coussens. -The researchers also found that Mycobacterium tuberculosis, the bacterium that causes TB, was cleared from the patients’ sputum (the phlegm coughed up from deep in the lungs) faster in those who were taking vitamin D, taking an average of 23 days to become undetectable under the microscope compared to 36 days in the patients who were taking the placebo. Dr Martineau said it was probably too early to be recommending that all TB patients should take high-dose vitamin D in addition to the standard antibiotic treatment for the disease; more research with more patients was needed before clinical recommendations could be made. “We are hoping to do more work to evaluate the effects of higher doses and different forms of vitamin D to see if they have a more dramatic effect,” he said. The study was funded by the UK’s Medical Research Council and the British Lung Foundation. In addition to Barts and the London School of Medicine and Dentistry, part of Queen Mary, University of London, the other institutions involved in the research were the MRC’s National Institute of Medical Research, Imperial College London, Homerton University NHS Foundation Trust, Newham Chest Clinic, Whipps Cross University Hospital, Northwick Park Hospital, Guy’s and St Thomas’ NHS Foundation Trust, Lewisham Hospital, and King’s College Hospital. Story Source—The above story is reprinted from materials provided by Queen Mary, University of London, via EurekAlert!, a service of AAAS.
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Detailed Descripition of Some Specific Embodiments
This invention provides antioxidant compounds and compositions, such as pharmaceutical compositions, that include cannabinoids that act as free radical scavengers for use in prophylaxis and treatment of disease. The invention also includes methods for using the antioxidants in prevention and treatment of pathological conditions such as ischemia (tissue hypoxia), and in subjects who have been exposed to oxidant inducing agents such as cancer chemotherapy, toxins, radiation, or other sources of oxidative stress. The compositions and methods described herein are also used for preventing oxidative damage in transplanted organs, for inhibiting reoxygenation injury following reperfusion of ischemic tissues (for example in heart disease), and for any other condition that is mediated by oxidative or free radical mechanisms of injury. In particular embodiments of the invention, the compounds and compositions are used in the treatment of ischemic cardiovascular and neurovascular conditions, and neurodegenerative diseases. However the present invention can also be used as an antioxidant treatment in non-neurological diseases.—Molecular oxygen is essential for aerobic organisms, where it participates in many biochemical reactions, including its role as the terminal electron acceptor in oxidative phosphorylation. However excessive concentrations of various forms of reactive oxygen species and other free radicals can have serious adverse biological consequences, including the peroxidation of membrane lipids, hydroxylation of nucleic acid bases, and the oxidation of sulfhydryl groups and other protein moieties. Biological antioxidants include tocopherols and tocotrieneols, carotenoids, quinones, bilirubin, ascorbic acid, uric acid, and metal binding proteins.————–
However these endogenous antioxidant systems are often overwhelmed by pathological processes that allow permanent oxidative damage to occur to tissue.—-Free radicals are atoms, ions or molecules that contain an unpaired electron, are usually unstable, and exhibit short half-lives. Reactive oxygen species (ROS) is a collective term, designating the oxygen radicals (e.g. .O2- superoxide radical), which by sequential univalent reduction produces hydrogen peroxide (H2 O2) and hydroxyl radical (.OH). The hydroxyl radical sets off chain reactions and can interact with nucleic acids. Other ROS include nitric oxide (NO.) and peroxy nitrite (NOO.), and other peroxyl (RO2.) and alkoxyl (RO.) radicals
DEFINITIONS
“Oxidative associated diseases” refers to pathological conditions that result at least in part from the production of or exposure to free radicals, particularly oxyradicals, or reactive oxygen species. It is evident to those of skill in the art that most pathological conditions are multifactorial, and that assigning or identifying the predominant causal factors for any particular condition is frequently difficult. For these reasons, the term “free radical associated disease” encompasses pathological states that are recognized as conditions in which free radicals or ROS contribute to the pathology of the disease, or wherein administration of a free radical inhibitor (e.g. desferroxamine), scavenger (e.g. tocopherol, glutathione) or catalyst (e.g. superoxide dismutase, catalase) is shown to produce detectable benefit by decreasing symptoms, increasing survival, or providing other detectable clinical benefits in treating or preventing the pathological state.–Oxidative associated diseases include, without limitation, free radical associated diseases, such as ischemia, ischemic reperfusion injury, inflammatory diseases, systemic lupus erythematosis, myocardial ischemia or infarction, cerebrovascular accidents (such as a thromboembolic or hemorrhagic stroke) that can lead to ischemia or an infarct in the brain, operative ischemia, traumatic hemorrhage (for example a hypovolemic stroke that can lead to CNS hypoxia or anoxia), spinal cord trauma, Down’s syndrome, Crohn’s disease, autoimmune diseases (e.g. rheumatoid arthritis or diabetes), cataract formation, uveitis, emphysema, gastric ulcers, oxygen toxicity, neoplasia, undesired cellular apoptosis, radiation sickness, and others. The present invention is believed to be particularly beneficial in the treatment of oxidative associated diseases of the CNS, because of the ability of the cannabinoids to cross the blood brain barrier and exert their antioxidant effects in the brain. In particular embodiments, the pharmaceutical composition of the present invention is used for preventing, arresting, or treating neurological damage in Parkinson’s disease, Alzheimer’s disease and HIV dementia; autoimmune neurodegeneration of the type that can occur in encephalitis, and hypoxic or anoxic neuronal damage that can result from apnea, respiratory arrest or cardiac arrest, and anoxia caused by drowning, brain surgery or trauma (such as concussion or spinal cord shock).—As used herein, an “antioxidant” is a substance that, when present in a mixture containing an oxidizable substrate biological molecule, significantly delays or prevents oxidation of the substrate biological molecule. Antioxidants can act by scavenging biologically important reactive free radicals or other reactive oxygen species (.O2-, H2 O2, .OH, HOCl, ferryl, peroxyl, peroxynitrite, and alkoxyl), or by preventing their formation, or by catalytically converting the free radical or other reactive oxygen species to a less reactive species. Relative antioxidant activity can be measured by cyclic voltametry studies of the type disclosed in Example 5 (and FIG. 3), where the voltage (x-axis) is an index of relative antioxidant activity. The voltage at which the first peak occurs is an indication of the voltage at which an electron is donated, which in turn is an index of antioxidant activity.
“Therapeutically effective antioxidant doses” can be determined by various methods, including generating an empirical dose-response curve, predicting potency and efficacy of a congener by using quantitative structure activity relationships (QSAR) methods or molecular modeling, and other methods used in the pharmaceutical sciences. Since oxidative damage is generally cumulative, there is no minimum threshold level (or dose) with respect to efficacy. However, minimum doses for producing a detectable therapeutic or prophylactic effect for particular disease states can be established.
As used herein, a “cannabinoid” is a chemical compound (such as cannabinol, THC or cannabidiol) that is found in the plant species Cannabis saliva (marijuana), and metabolites and synthetic analogues thereof that may or may not have psychoactive properties. Cannabinoids therefore include (without limitation) compounds (such as THC) that have high affinity for the cannabinoid receptor (for example Ki <250 nM), and compounds that do not have significant affinity for the cannabinoid receptor (such as cannabidiol, CBD). Cannabinoids also include compounds that have a characteristic dibenzopyran ring structure (of the type seen in THC) and cannabinoids which do not possess a pyran ring (such as cannabidiol). Hence a partial list of cannabinoids includes THC, CBD, dimethyl heptylpentyl cannabidiol (DMHP-CBD), 6,12-dihydro-6-hydroxy-cannabidiol (described in U.S. Pat. No. 5,227,537, incorporated by reference); (3S,4R)-7-hydroxy-Δ6 – tetrahydrocannabinol homologs and derivatives described in U.S. Pat. No. 4,876,276, incorporated by reference; ( )-4-[4-DMH-2,6-diacetoxy-phenyl]-2-carboxy-6,6-dimethylbicyclo[3.1. 1]hept-2-en, and other 4-phenylpinene derivatives disclosed in U.S. Pat. No. 5,434,295, which is incorporated by reference; and cannabidiol (-)(CBD) analogs such as (-)CBD-monomethylether, (-)CBD dimethyl ether; (-)CBD diacetate; (-)3′-acetyl-CBD monoacetate; and . -.AF11, all of which are disclosed in Consroe et al., J. Clin. Phannacol. 21:428S-436S, 1981, which is also incorporated by reference. Many other cannabinoids are similarly disclosed in Agurell et al., Pharmacol. Rev. 38:31-43, 1986, which is also incorporated by reference.
As referred to herein, the term “psychoactivity” means “cannabinoid receptor mediated psychoactivity.” Such effects include, euphoria, lightheadedness, reduced motor coordination, and memory impairment. Psychoactivity is not meant to include non-cannabinoid receptor mediated effects such as the anxiolytic effect of CBD.
The “lipoxygenase enzyme activity” refers to the relative level of lipoxygenase enzyme activity for a particular lipoxgenase, such as 5-, 15- or 12-lipoxygenase, as measured in Example 8. A compound would be said to “selectively inhibit a lipoxgenase enzyme” if the concentration of inhibitor required to reduce enzyme activity by 50% was at least about 5 times less than the amount required to reduce activity of a second lipoxgenase enzyme by the same degree (under the same conditions, i.e. temperature, substrate concentration, etc.)
The term “lower alkyl” refers to a cyclic, branched or straight chain monovalent alkyl radical of one to seven carbon atoms. This term is further exemplified by such radicals as methyl, ethyl, n-propyl, i-propyl, n-butyl, t-butyl, i-butyl (or 2-methylpropyl), cyclopropylmethyl, i-amyl, n-amyl, hexyl and heptyl. Lower alkyl groups can also be unsubstituted or substituted, where a specific example of a substituted alkyl is 1,1-dimethyl heptyl.
“Hydroxyl” refers to –OH.
“Alcohol” refers to R–OH, wherein R is alkyl, especially lower alkyl (for example in methyl, ethyl or propyl alcohol). An alcohol may be either linear or branched, such as isopropyl alcohol.
“Carboxyl” refers to the radical –COOH, and substituted carboxyl refers to –COR where R is alkyl, lower alkyl or a carboxylic acid or ester.
The term “aryl” or “Ar” refers to a monovalent unsaturated aromatic carbocyclic group having a single ring (e.g. phenyl) or multiple condensed rings (e.g. naphthyl or anthryl), which can optionally be unsubstituted or substituted with, e.g., halogen, alkyl, alkoxy, alkylthio, trifluoromethyl, acyloxy, hydroxy, mercapto, carboxy, aryloxy, aryl, arylalkyl, heteroaryl, amino, alkylamino, dialkylamino, morpholino, piperidino, pyrrolidin-1-yl, piperazin-1-yl, or other functionality.
The term “alkoxy” refers to a substituted or unsubstituted alkoxy, where an alkoxy has the structure –O–R, where R is substituted or unsubstituted alkyl. In an unsubstituted alkoxy, the R is an unsubstituted alkyl. The term “substituted alkoxy” refers to a group having the structure –O–R, where R is alkyl which is substituted with a non-interfering substituent. The term “arylalkoxy” refers to a group having the structure –O–R–Ar, where R is alkyl and Ar is an aromatic substituent. Arylalkoxys are a subset of substituted alkoxys. Examples of useful substituted alkoxy groups are: benzyloxy, naphthyloxy, and chlorobenzyloxy.
The term “aryloxy” refers to a group having the structure –O–Ar, where Ar is an aromatic group. A particular aryloxy group is phenoxy.
The term “heterocycle” refers to a monovalent saturated, unsaturated, or aromatic carbocyclic group having a single ring (e.g. morpholino, pyridyl or faryl) or multiple condensed rings (e.g. indolizinyl or benzothienyl) and having at least one heteroatom, defined as N, O, P, or S, within the ring, which can optionally be unsubstituted or substituted with, e.g. halogen, alkyl, alkoxy, alkylthio, trifluoromethyl, acyloxy, hydroxy, mercapto, carboxy, aryloxy, aryl, arylakyl, heteroaryl, amino, alkylamino, dialkylamino, morpholino, piperidino, pyrrolidin-1-yl, piperazin-1-yl, or other functionality.
“Arylalkyl” refers to the groups –R–Ar and –R–HetAr, where Ar is an aryl group. HetAr is a heteroaryl group, and R is a straight-chain or branched chain aliphatic group. Example of arylaklyl groups include benzyl and furfuryl. Arylalkyl groups can optionally be unsubstituted or substituted with, e.g., halogen, alkyl, alkoxy, alkylthio, trifluoromethyl, acyloxy, hydroxy, mercapto, carboxy, aryloxy, aryl, arylalkyl, heteroaryl, amino, alkylamino, dialkylamino, morpholino, peperidino, pyrrolidin-1-yl, piperazin-1-yl, or other functionality.
The term “halo” or “halide” refers to fluoro, bromo, chloro and iodo substituents.
The term “amino” refers to a chemical functionality –NR’R” where R’ and R” are independently hydrogen, alkyl, or aryl. The term “quaternary amine” refers to the positively charged group –N.sup. R’R”, where R’R” and R” are independently selected and are alkyl or aryl. A particular amino group is –NH2.
Cannabidiol blocks glutamate toxicity
Cannabidiol blocks glutamate toxicity with equal potency regardless of whether the insult is mediated by NMDA, AMPA or kainate receptors. Cannabidiol and THC have been shown to be comparable to the antioxidant BHT, both in their ability to prevent dihydrorhodamine oxidation and in their cyclic voltametric profiles. Several synthetic cannabinoids also exhibited profiles similar to the BHT, although anandamide, which is not structurally related to cannabinoids, did not. These findings indicate that cannabinoids act as antioxidants in a non-biological situation, which was confirmed in living cells by showing that cannabidiol attenuates hydroperoxide induced neurotoxicity. The potency of cannabidiol as an antioxidant was examined by comparing it on an equimolar basis with three other commonly used compounds.
In the AMPA/kainate receptor dependent neurotoxicity model, cannabidiol neuroprotection was comparable to the potent antioxidant, BHT, but significantly greater than that observed with either α-tocopherol or ascorbate. This unexpected superior antioxidant activity (in the absence of BHT tumor promoting activity) shows for the first time that cannabidiol, and other cannabinoids, can be used as antioxidant drugs in the treatment (including prophylaxis) of oxidation associated diseases, and is particularly useful as a neuroprotectant. The therapeutic potential of nonpsychoactive cannabinoids is particularly promising, because of the absence of psychotoxicity, and the ability to administer higher doses than with psychotropic cannabinoids, such as THC. Previous studies have also indicated that cannabidiol is not toxic, even when chronically administered to humans or given in large acute doses (700 mg/day).
These studies with the nonpsychotropic marijuana constituent, cannabidiol, demonstrate that protection can be achieved against both glutamate neurotoxicity and free radical induced cell death. THC, the psychoactive principle of cannabis, also blocked glutamate neurotoxicity with a potency similar to cannabidiol. In both cases, neuroprotection is unaffected by the presence of a cannabinoid receptor antagonist. These results therefore surprisingly demonstrate that cannabinoids can have useful therapeutic effects that are not mediated by cannabinoid receptors, and therefore are not necessarily accompanied by psychoactive side effects. Cannabidiol also acts as an anti-epileptic and anxiolytic, which makes it particularly useful in the treatment of neurological diseases in which neuroanatomic defects can predispose to seizures (e.g. subarachnoid hemorrhage).
A particular advantage of the cannabinoid compounds of the present invention is that they are highly lipophilic, and have good penetration into the central nervous system. The volume of distribution of some of these compounds is at least 100 L in a 70 kg person (1.4 L/kg), more particularly at least 250 L, and most particularly 500 L or even 700 L in a 70 kg person (10 L/kg). The lipophilicity of particular compounds is also about as great as that of THC, cannabidiol or other compounds that have excellent penetration into the brain and other portions of the CNS.
Cannabinoids that lack psychoactivity or psychotoxicity are particularly useful embodiments of the present invention, because the absence of such side effects allows very high doses of the drug to be used without encountering unpleasant side effects (such as dysphoria) or dangerous complications (such as obtundation in a patient who may already have an altered mental status). For example, therapeutic antioxidant blood levels of cannabidiol can be 5-20 mg/kg, without significant toxicity, while blood levels of psychoactive cannabinoids at this level would produce obtundation, headache, conjunctival irritation, and other problems. Particular examples of the compounds of the present invention have low affinity to the cannabinoid receptor, for example a Ki of greater than 250 nM, for example Ki≥500-1000 nM. A compound with a Ki≥1000 nM is particularly useful, which compound has essentially no psychoactivity mediated by the cannabinoid receptor
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Show Of the Month September 21-2012
Precautions for Tick-Borne Disease Extend ‘Beyond Lyme’
Copper Benefits
Copper—and how it Protects
Copper Proves Effective Against New E. Coli Strains in New Study
Dry Copper Kills Bacteria On Contact
Work With Germ-Killing Copper Could Save Thousands of Lives
Copper Recipes
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Precautions for Tick-Borne Disease Extend ‘Beyond Lyme’
ScienceDaily (Sep. 7, 2012) — This year’s mild winter and early spring were a bonanza for tick populations in the eastern United States. Reports of tick-borne disease rose fast.—While Lyme disease is the most common tick-borne disease in the Northeast and Upper Midwest, new research results emphasize that it is not the greatest cause for concern in most Southeastern states.—The findings are published today in a paper in the journal Zoonoses and Public Health.—The majority of human-biting ticks in the North–members of the blacklegged tick species–cause Lyme disease, but these same ticks do not commonly bite humans south of mid-Virginia.–Biologist Graham Hickling of the University of Tennessee, co-author of the paper, says many patients in Southeastern states, who become sick from a tick-bite, assume they have Lyme disease, but the odds of that being the case are low.—“Ticks in the eastern U.S. collectively carry more than a dozen agents that can cause human disease,” says Hickling.—“Here in Tennessee we regularly collect lone star ticks that test positive for Ehrlichia, [a tick-borne bacterial infection]. Lone stars are an aggressive species that account for most of the human bites that we see in this region. So ehrlichiosis has to be a big concern, yet most people have never heard of it.”—In contrast, says Hickling, there have been no confirmed reports to date of the Lyme disease pathogen among the sparse populations of blacklegged ticks found in Tennessee.–“The Southeast is dominated by different tick species than the ones that attack humans in the North,” says Ellen Stromdahl, an entomologist at the U.S. Army Public Health Command and lead author of the paper.—“The lone star tick is by far the most abundant tick in the Southeast, and which species of tick bites you is critical because different ticks carry different diseases. In the Southeast you are unlikely to be bitten by the blacklegged ticks that spread Lyme disease,” Stromdahl says.–Most bites in the Southeast are from the tick species that spread spotted fever rickettsiosis and ehrlichiosis, but not Lyme disease.–A complicating factor for public health officials is that tick species are on the move, as wildlife populations, forest habitats and weather patterns change across the continent. This spring the Tennessee Department of Health, for example, reported a 500 percent increase in tick-borne rickettsiosis.—“Identifying health risks in the face of changing climates will be critical in coming years,” says Sam Scheiner, National Science Foundation program director for the joint NSF-National Institutes of Health Ecology and Evolution of Infectious Diseases (EEID) program, which funds Hickling’s research.–At NSF, the EEID program is co-funded by the Directorates for Biological Sciences and Geosciences.–“This study will inform public health officials about what diseases are found in which areas,” says Scheiner, “so they can minimize human health problems.”–Hickling’s work is also in collaboration with scientist Jean Tsao of Michigan State University and is part of an EEID project to identify the ecological factors leading to distributions of tick species and pathogens–in particular, where the Lyme disease tick and pathogen are found.–Lyme-infected blacklegged ticks are expanding south through Virginia, and lone star ticks are moving north, the scientists have found.–The bite of the lone star tick can create a bulls-eye rash that appears like that of Lyme disease, but the rash isn’t caused by the Lyme bacteria.—The scientists say that this almost certainly leads to misdiagnosis of some patients in mid-Atlantic states, where both tick species are common.—The best way to distinguish Lyme from other tick-borne diseases is to be vigilant for tick bites, and whenever possible save any tick that manages to bite you, the biologists recommend. Store the tick in your freezer or in a vial of alcohol so it can be identified if you become ill.—In the Northeast, Lyme disease awareness campaigns have focused public attention on the nymphal blacklegged tick–which is responsible for most disease transmission and which is tinier than the adult form.–While nymphal blacklegged ticks and nymphal lone star ticks–which also bite humans–can be distinguished, the two are often confused by the public.–In one study, 13 of 20 patients reporting tick bites to physicians were given antibiotics on the assumption that they were at risk for Lyme disease, yet 53 of the 54 ticks removed from those same patients were lone star ticks, which do not spread Lyme disease.—“Where you live determines which tick species is likely to bite you,” says Tsao, “and therefore which diseases you’re most likely to contract.”–The biologists say they are happy that recent treatment recommendations have begun to emphasize the importance of considering the tick species and its infection status as part of the diagnostic process.–Their advice: Stay open-minded about which tick-borne diseases are most common in your area–and save the tick that bites you.–Story Source-The above story is reprinted from materials provided by National Science Foundation. —Journal Reference–E. Y. Stromdahl, G. J. Hickling. Beyond Lyme: Aetiology of Tick-borne Human Diseases with Emphasis on the South-Eastern United States. Zoonoses and Public Health, 2012; 59: 48 DOI: 10.1111/j.1863-2378.2012.01475.x