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Healthy living linked to higher brain function, delay of dementia   
Date:
November 27, 2016 12:59 PM
According to a recent study by York University, fruits, vegetables, and regular exercise have more to do with our well-being than we think. Researchers discovered that people who were normal weight or overweight, but not obese, and ate healthy had much higher cognitive function. The diet high in essential minerals and nutrients helped maintain and increase cognitive function in adults. Key Takeaways:
"It’s tempting to dip into the leftover Halloween treats, but new research has found that eating plenty of fruits and vegetables, combined with regular exercise, leads to better cognitive functioning for younger and older adults, and may delay the onset of dementia." Reference: https://www.sciencedaily.com/releases/2016/11/161101100909.htm
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=3519) Prevent Disease With Discount Vitamins 
Date:
October 24, 2007 09:33 AM
You can prevent disease with discount vitamin just as easy as with those you pay top dollar for on the High Street. Vitamins are vitamins, and they do not lose quality for price as long as you know what to look for and stick with name brands. They are the most purchased supplement in the western world, and there are ways of getting them for less than the normal price. First, though, a definition of what a vitamin is since an astounding number of people have no idea of what actually constitutes a vitamin even though they can recite all the letters. In fact, a vitamin is a molecule, obtained from an organic animal or vegetable source that is essential for life. Without it there can be no animal life and vitamins generally catalyze or act as coenzymes in the biochemistry that makes up all of the chemical reactions of the body. A catalyst allows a reaction to occur without changing itself, and a coenzyme allows enzymes to do their jobs. Let’s have a look at one or two vitamins to provide examples of these statements. In bygone days when sailors used sail to cross the oceans in open boats powered only by sail and oar, a trip that takes us a week in a cruise liner these days could take sailors several months. It was not only the fact that they relied on favorable winds, but also that they did not always know where they were going, and were frequently unable to store up for a whole voyage. They depended on landing at islands on the way to replenish supplies. Disease due to lack of nutrition was common and one of these was scurvy. This condition is not strictly a disease and is due to a lack of vitamin C, or ascorbic acid. In fact the name ‘ascorbic’ comes from the Latin for ‘without scurvy’. The symptoms are liverish spots over the body, spongy gums that cause the teeth to fall out and bleeding from the mucus membranes. Healed scars will open up, and cured and knitted bone fractures will separate. Ultimately it causes death. The first person is used since scurvy still exists. It is due to a breakdown in the synthesis of collagen which heals scars, keeps joints held together, and forms the outside part of cells, and also some inner cell structures. Collagen synthesis is dependent on the amino acids proline and lysine that are hydroxylated by the enzymes lysyl and prolyl hydroxylase. The problem is that these enzymes need ascorbic acid (vitamin C) to do their work. Without it, collagen cannot be made. Although the chemistry was unknown, early sailors soon found that citrus fruits such as lemons and limes prevented this horrible condition. The English used to stock up their ships with fresh limes at any port of call that had them, and this is why the English are frequently referred to a ‘Limeys’. It got them a nickname, but it saved their lives. Scurvy is now rare, but it is not a disease as such that can be eradicated. It occurs now and again in teenagers with poor diets that do not include fresh fruit and vegetables. Vitamin C supplements are now available, and it is one of the most common of the discount vitamins on the market. The same is true of vitamin A that is essential for good eyesight. It has many other uses, as has vitamin C, but without it we could not survive. Without it we will eventually become blind, although the first symptom is night blindness. However, an excess can lead to hypovitaminosis A, a condition common in the developed world. Its absence can kill us, and vitamin A deficiency is one of the more common conditions of the developing world. Vitamins are contrary creatures, and can do us harm as well as good. How about vitamin D, the sunlight vitamin? We don’t think of it, yet it is responsible for the strength of your skeleton and the regulation of calcium and phosphorus levels in the blood. Without it our bones become soft, our children get rickets and we eventually die – frequently through cancer. 1,25-dihydroxycholecalciferol is the chemical name for calcitriol, which is the form of vitamin D found in the body, known as vitamin D3. This has been found to kill some cancer cells in the laboratory, and it is thought that supplements of vitamin D might help to prevent some types of cancer. The reults of a four year cancer study were released in June, 2007, that showed a reduction of 60% in cancers where patients were given a aupplement of 1100 inernational units daily. This rose to 77% where the cancers had been diagnosed in their first year. The effect of vitamin D was emphasized by the reults of a study of more than 4 million cancer patients that showed a marked difference in the risk of cancer according to whether they lived in sunny or less sunny climates. So these are the benefits of some discount vitamin supplements. How, then, do you find vitamins at discount prices? The easiest way is to purchase in bulk. There are those that form online clubs for vitamins and pay a weekly or monthly fee to join. When offers come online for specific supplements at low prices, they are purchased by the groups and distributed. You could do the same yourself with some friends, since it is generally cheaper to purchase 5 Kg of a vitamin that 500g. Your local health food store could also help you out since they are likely to be able to procure discount bulk prices from their supplier. Another way is to wait until your local store makes special offers, or seek offers in the press. These can often be found, but if you are concerned mainly with the common vitamins A, B complex, C, D and E then a large proportion of the population are interested in these and you should not find it difficult to sell several kilos of these. You will not only get yours free, but will a sizeable profit into the bargain. Anything between that and the normal price is an advantage for chemicals that are essential for life. One thing to always remember, buy reputable name brand vitamins because if the vitamins seem to cheap than you’re probably right. Name brand vitamins have quality and can be purchased at discount prices if you look long enough.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=1604) Breast Cancer and Natural Supplements
Date:
May 11, 2007 10:47 AM
Breast Cancer and Nutritional Supplements
There is probably nothing more frightening for a woman than the discovery of a lump in her breast. Cancer and all its consequences quickly come to mind. This quick association may materialize, in part, because no woman is immune. Most have a friend, a sister, a mother, or a coworker who has been diagnosed with the disease. And they know how difficult dealing with this disease can be. Fortunately, 80% of all breast lumps are not cancerous. Most are cysts or a benign clump of tissue.
Over her lifetime, a woman’s breasts undergo many, many changes. From before puberty and on, breast tissue is continually evolving. Breasts often feel different before menstrual cycle, returning to normal a few days after. Pregnancy certainly causes changes in a woman’s breasts, as does breastfeeding. And as women age, breast tissue becomes less dense.
Because of these continual changes, breast tissue especially requires adequate nutrition. While everyone benefits from a healthy diet, there are additional nutrients from which women can specifically benefit.
In this issue of Ask the Doctor, we will discuss breast cancer and the vast amount of research that has explored the role nutrition plays in this serious and still deadly disease. Specifically, we will discuss how two B vitamins, calcium D-glucarate, broccoli extract, green tea, maitake mushrooms, and iodine can all help prevent breast cancer.
Q. How can these nutrients prevent breast cancer?
A. Scientists learn a lot about disease from simply observing what is happening around them. One observation that has been recognized for many years is that certain cultures have very low incidence of breast cancer. Women n
Moms (and dads) have also learned a lot about diseases simply by observing what is happening in their families. They have notices that certain vegetables play a large role in the prevention of all types of diseases, including cancer. And, accordingly, they have been urging their offspring to eat their vegetables for several generations.
Building on these observations, scientists have designed and carried out many studies to determine what it is about these nutrients that can prevent breast cancer. What they have discovered, so far, follows. Let’s start with the B vitamins.
Vitamin B12
Deficiencies of this vitamin can result in a serious type of anemia. Nerve damage can also occur if B12 levels are too low. Researchers are now investigating whether breast cancer may, in part, be caused by a B12 deficiency as well.
At
Another study, this one taking place in a laboratory setting, discovered that vitamin B12, applied directly against experimental breast cancer cells, actually stopped the cancer cells from growing. The researchers conducting the experiment believe that giving vitamin B12 to women with breast cancer as part of a chemotherapy regime, might help keep the cancer in check.
Folic Acid
Low folic acid intake is linked to the development of all cancers. This is because folic acid is crucial to the making and continual repair of DNA, the molecule that carries our genetic code. A recent study discovered that high intakes of folic acid might actually reduce the risk of breast cancer. The researchers looked at the diets of over 2600 women. During interviews with the researchers, the women reported what they usually ate. Once the data was collected, the results showed that women, who ate lots of foods that contained folic acid, had much lower rates of breast cancer.
There is no clear-cut, single cause of breast cancer. Many factors are required for the disease to appear. One such factor is estrogen. A recent study showed that women who developed breast cancer tended to have higher levels of estrogen circulating in their bodies than women without breast cancer. This means that women who got their periods before age eleven or entered menopause after age fifty-five have a higher risk of breast cancer. This also supports the theory that the number of menstrual cycles a woman has affects her risk for breast cancer.
Another factor is drinking alcohol. Because alcohol raises estrogen levels, if a woman consumes even moderate amounts of alcohol her risk of breast cancer also is increased. The link between alcohol and breast cancer may even be stronger than other dietary links. However, an important study has discovered that folic acid may uncouple this link.
A very large study of over 34,000 women recently studied the effect of folic acid on the risk of breast cancer. This project was part of the Nurses’ Health Study, an ongoing, long-term study that looks at nutrition’s role in the development of disease. The women in the folic acid and breast cancer study were followed for 12 years. The participants completed detailed food questionnaires that provided the researchers with important data.
The women were divided into four groups:
1. Women with low folic acid levels and drink alcohol
2. Women with high folic acid levels and rink alcohol
3. Women with low folic acid levels and don’t drink alcohol
4. Women with high folic acid levels and don’t drink alcohol
Within these four groups the women were further divided into subgroups according to the amount of alcohol they consumed each day and their specific folic acid intake.
The researchers found that women who consumed the lowest amounts of folic acid and drank at least one alcoholic beverage a day had the highest rate of breast cancer. In contrast, women who had high intakes of folic acid and also drank at least one alcoholic beverage a day, had the same rate of breast cancer as the women with high folic acid intakes who did not drink. In other words, women who had high levels of folic acid in their diet erased their alcohol-related increase in breast cancer risk.
Calcium D-Glucarate
It seems estrogen can be both friend and foe. While women need the hormone to soften skin, thicken hair, and fill out hips and breasts, estrogen can also nourish breast tumors, helping them grow bigger, stronger, and more deadly. Thanks, in part, to good nutrition, American women get their periods early and go through menopause alter in life. Women today also have fewer pregnancies; families with one or two children are quite common.
All of these factors increase the time women’s bodies are exposed to estrogen. As we discussed before, longer exposure means increased opportunities for estrogen to cause trouble. It is also a troubling fact of modern life that we are continuously exposed to cancer-causing chemicals and toxins. These toxins come in part from contaminants in the food we eat and pollutants in the air we breathe.
The body does have a system that eliminates some of the excess estrogen and toxic chemicals before they can cause harm. In the liver, they are bound or attached to a chemical called glucuronic acid. The bound toxin or estrogen is then excreted in bile and eventually eliminated as a waste product in the stool.
However, an enzyme called beta-glucuronidase can break this bond between estrogen and glucuronic acid. When this happens, the hormone or toxin is released from its bone, capable of causing harm once more. Increased beta-glucuronidase activity is associated with an increased risk for various cancers, particularly hormone-dependant cancers like breast cancer.
Fortunately, scientists have discovered that a natural substance found in foods calcium D-glucarate (CDG) can stop the activity of beta-glucuonidase. CDG keeps the harmful estrogen bound to glucuronidase. While CDG is found in fruits and vegetables, the amounts may not be sufficient to maintain effective levels to stop beta-glucuronidase.
CDG has been shown in experimental studies to significantly stop beast cancer growth. And several human trials are currently underway with CDG to determine its capability to decrease the breast cancer risk in women at high risk for the disease.
Iodine
There are some very interesting connections between breast tissue and thyroid tissue. Iodine is an essential trace element present in a hormone of the thyroid gland and is involved in several metabolic functions. One iodine function is the protection of breast tissue from cancerous cells.
In a laboratory study, researchers exposed breast cancer cells and breast tissue without any cancer to a type of seaweed that contains high levels of iodine. The seaweed killed all of the cancerous cells, yet did not harm the normal breast cells. Japanese women frequently eat this type of seaweed and have very low rates of breast cancer. The study’s researchers believe one reason for this low incidence of breast cancer may be the iodine in the seaweed.
And, for some as yet unknown reasons, women who have thyroid cancer are at higher risk of developing breast cancer. While they are unsure why this happens, researchers are continuing to study this link, and support of healthy thyroid function remains an important consideration.
Broccoli
For quite some time, scientists have observed that cruciferous vegetables, such as broccoli, cabbage, and cauliflower, significantly reduce the risk of disease, including cancer. It seems a phytochemical in broccoli sulforaphane, is one of the chemicals responsible for this beneficial activity. Sulforaphane increases certain enzymes in the body called phase 2 enzymes that deactivate cancer-causing chemicals.
Breast cancer cells exposed to sulforaphane in several lab experiments showed that the compound inhibited the growth of the cancer cells up to 80 percent. Researchers are in the process of setting up clinical trials to study sulforaphane’s effect in women who have breast cancer.
Green Tea
There is a tall amount of research, including finding from the Nurses’ Health Study, that suggest green tea beverage consumption is associated with a lower incidence of breast cancer. In fact, researchers have long noted the low rates of breast cancer in
The active compound in green tea responsible for breast cancer inhibition is epigallocatechin-3 gallate or EGCG. When breast cancer cells are exposed to EGCG in lab experiments, the cells stop growing, lose their ability to replicate, and die.
In a recent study, researchers discovered that drinking green tea prevented the recurrence of breast cancer in women who have previously been diagnosed and treated for the disease. This study involved over 1100 Japanese women. The women who drank green tea every day had very low rates of their breast cancer returning.
Maitake Mushrooms
For thousands of years, maitake mushrooms have been linked to good health in those who eat them. Called “dancing mushrooms” (possibly due to their wavy, rippling appearance or possibly due to the little dance of joy mushroom hunters perform when they find them in the woods), maitakes contain an important compound called D-fraction.
Not only does the D-fraction in maitake mushrooms stop the growth of cancerous tumors, it also alerts and stimulates immune cells (including macrophages and natural killer cells) to fight the disease. Maitake also inhibits some of the mechanism that promotes metastasis, or spread, of cancer cells in the lymph and bloodstream.
Because of this success, maitake is now being used in clinical trials of women with breast cancer. One study reported significant improvement of symptoms, including reduction of the tumor. The maitake was given to breast cancer patients in addition to standard chemotherapy.
Q. Should these nutrients be used in place of traditional treatment for breast cancer?
A. Absolutely not. None of these nutrients can cure breast cancer. However, they can be a part of a validated plan of treatment. If you have breast cancer, talk to your health care practitioner about these nutrients. Remember, nutritional supplements are just that: supplements to food, medication, and treatment. They are intended to enhance and prevent, not replace.
Conclusion
Despite apprehension in performing self-breast exams, women are very proactive in their health. Yearly mammograms and pap tests have been an important part of their lives for many years, and newer and more accurate diagnoses are emerging. The prevention of health problems in themselves and their families has always been a high priority for women. And for women, nutrition has played an important part of health problem prevention.
Nutritionally speaking, what benefits your breasts benefit your whole body. However, as we have learned, there are specific links between nutrition and developing breast cancer that seem to be fairly strong.
Making a few changes may reduce the risk of developing the disease. The nutrients listed here, vitamin B12, folic acid, calcium d-glucarate, iodine, broccoli, green tea, and maitake mushrooms can be an important part of a woman’s preventative health regimen.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=1537) TMG Fact Sheet
Date:
December 07, 2005 02:13 PM
TMG Fact SheetNeil E. Levin, CCN, DANLA 03/07/05LIKELY USERS: People with high homocysteine levels; People with risks of developing Alzheimer’s Disease; People needing greater metabolism of fats; People with liver detoxification challenges; People consuming alcohol KEY INGREDIENTS: TMG is composed of three methyl groups attached to a glycine atom. It can “donate” methyl groups. MAIN PRODUCT FEATURES: TMG is a metabolite of the B vitamin family product called Choline. Choline has 4 methyl groups, TMG has 3 and DMG has 2. These substances plus Folic acid, Vitamin B-12 and SAM-e are all methyl donors. Methyl donors can contribute methyl groups to biological processes such as liver function, detoxification and cellular replication (production of new cells). Methylation protects the kidneys and stimulates production of the fat-transporting molecule l-carnitine. TMG helps the liver metabolize fats, preventing the accumulation of fats in the liver. It also helps to detoxify chemicals in the liver, while protecting the liver from being damaged by those chemicals. Methylation with TMG helps to convert the dangerous, inflammatory chemical homocysteine into the amino acid methionine. TMG may lower homocysteine when B-6, B-12 and folic acid cannot. ADDITIONAL PRODUCT INFORMATION: TMG is also known as Betaine and is a component of Betaine hydrochloride (Betaine HCl), a stomach acid supplement that is very acidic. But Betaine HCl is not used in the same way as TMG. TMG is not highly acidic and will not supplement low stomach acid. TMG may be useful for autistic children, along with B-6 and magnesium. It may also be useful in strengthening the body’s immune response against pathogenic bacteria. There is very preliminary evidence that TMG and methyl donors may help against some forms of seizures. DMG has been used as a sports supplement. TMG is 50% more effective than DMG in any application where the methyl groups are useful. Otherwise, they can used interchangeably. SERVING SIZE & HOW TO TAKE IT: One serving per day, or up to 6,000 mg., as needed. COMPLEMENTARY PRODUCTS: SAM-e, Milk Thistle (Silymarin), Dr. Verghese’s Liver Detoxifier & Regenerator, Antioxidants, NAC, Homocysteine Regulators, D-Flame, Detox Support CAUTIONS: Pregnant and lactating women and people using prescription drugs should consult their physician before taking any dietary supplement. People with Parkinson’s or taking L-dopa should not use methyl donors like TMG without a physician’s specific approval and supervision. There are no other known drug interactions with TMG. This information is based on my own knowledge and references, and should not be used as diagnosis, prescription or as a specific product claim. This is not an official publication by any company, nor has this information been screened or approved by the FDA or any private company. Disclaimer: These statements have not been evaluated by the FDA. This product is not intended to diagnose, treat, cure or prevent any disease. REFERENCES: General: Craig SA. Betaine in human nutrition. Am J Clin Nutr. 2004 Sep;80(3):539-49. Review. PMID: 15321791 Methylation: Barak AJ, Tuma DJ. Betaine, metabolic by-product or vital methylating agent? Life Sci 1983;32:771-4 [review]. Benson R, Crowell B, Hill B, et al. The effects of L-dopa on the activity of methionine adenosyltransferase: relevance to L-dopa therapy and tolerance. Neurochem Res 1993;18:325–30. Chambers ST. Betaines: their significance for bacteria and the renal tract. Clin Sci 1995;88:25-7 [review]. Charlton CG, Crowell B Jr. Parkinson’s disease-like effects of S-adenosyl-L-methionine: effects of L-dopa. Pharmacol Biochem Behav 1992;43:423–31. Charlton CG, Mack J. Substantia nigra degeneration and tyrosine hydroxylase depletion caused by excess S-adenosylmethionine in the rat brain. Support for an excess methylation hypothesis for parkinsonism. Mol Neurobiol 1994;9:149–61. Cheng H, Gomes-Trolin C, Aquilonius SM, et al. Levels of L-methionine S-adenosyltransferase activity in erythrocytes and concentrations of S-adenosylmethionine and S-adenosylhomocysteine in whole blood of patients with Parkinson’s disease. Exp Neurol 1997;145:580–5. Crowell BG Jr, Benson R, Shockley D, Charlton CG. S-adenosyl-L-methionine decreases motor activity in the rat: similarity to Parkinson’s disease-like symptoms. Behav Neural Biol 1993;59:186–93. Selhub J. Homocysteine metabolism. Annu Rev Nutr 1999;19:217-46 [review]. Homocysteine: Brosnan JT, Jacobs RL, Stead LM, Brosnan ME. Methylation demand: a key determinant of homocysteine metabolism. Acta Biochim Pol. 2004;51(2):405-13. Review. PMID: 15218538 Gahl WA, Bernardini I, Chen S, et al. The effect of oral betaine on vertebral body bone density in pyridoxine-non-responsive homocystinuria. J Inherit Metab Dis 1988;11:291-8. Olthof MR, van Vliet T, Boelsma E, Verhoef P. Low dose betaine supplementation leads to immediate and long term lowering of plasma homocysteine in healthy men and women. J Nutr. 2003 Dec;133(12):4135-8. PMID: 14652361 Olthof MR, Verhoef P. Effects of betaine intake on plasma homocysteine concentrations and consequences for health. Curr Drug Metab. 2005 Feb;6(1):15-22. PMID: 15720203 Schwab U, Torronen A, Toppinen L, Alfthan G, Saarinen M, Aro A, Uusitupa M. Betaine supplementation decreases plasma homocysteine concentrations but does not affect body weight, body composition, or resting energy expenditure in human subjects. Am J Clin Nutr. 2002 Nov;76(5):961-7. PMID: 12399266 Selhub J. Homocysteine metabolism. Annu Rev Nutr 1999;19:217-46 [review]. van Guldener C, Janssen MJ, de Meer K, et al. Effect of folic acid and betaine on fasting and postmethionine-loading plasma homocysteine and methionine levels in chronic haemodialysis patients. J Intern Med 1999;245:175-83. Wendel U, Bremer HJ. Betaine in the treatment of homocystinuria due to 5,10-methylenetetrahydrofolate reductase deficiency. Eur J Pediatr 1984;142:147-50. Wilcken DE, Wilcken B, Dudman NP, Tyrrell PA. Homocystinuria—the effects of betaine in the treatment of patients not responsive to pyridoxine. N Engl J Med 1983;309:448-53. Wilcken DE, Dudman NP, Tyrrell PA. Homocystinuria due to cystathionine beta-synthase deficiency--the effects of betaine treatment in pyridoxine-responsive patients. Metabolism. 1985 Dec;34(12):1115-21. PMID: 3934499 Liver function: Babucke G, Sarre B. Clinical experience with betain citrate. Med Klin 1973;68:1109-13 [in German]. Barak AJ, Beckenhauer HC, Badakhsh S, Tuma DJ. The effect of betaine in reversing alcoholic steatosis. Alcohol Clin Exp Res 1997;21:1100-2. Barak AJ, Beckenhauer HC, Matti J, Tuma DJ. Dietary betaine promotes generation of hepatic S-adenosylmethioine and protects the liver from ethanol-induced fatty infiltration. Alcohol Clin Exp Res 1993;17:552-5. Barak AJ, Beckenhauer HC, Tuma DJ. Betaine, ethanol, and the liver: a review. Alcohol 1996;13:395-8 [review]. PMID: 8836329 Freed WJ. Prevention of strychnine-induced seizures and death by the N-methylated glycine derivatives betaine, dimethylglycine and sarcosine. Pharmacol Biochem Behav. 1985 Apr;22(4):641-3. PMID: 2581277 Junnila M, Barak AJ, Beckenhauer HC, Rahko T. Betaine reduces hepatic lipidosis induced by carbon tetrachloride in Sprague-Dawley rats. Vet Hum Toxicol 1998;40:263-6. Ji C, Kaplowitz N. Betaine decreases hyperhomocysteinemia, endoplasmic reticulum stress, and liver injury in alcohol-fed mice. Gastroenterology. 2003 May;124(5):1488-99. PMID: 12730887 Kettunen H, Tiihonen K, Peuranen S, Saarinen MT, Remus JC. Dietary betaine accumulates in the liver and intestinal tissue and stabilizes the intestinal epithelial structure in healthy and coccidia-infected broiler chicks. Comp Biochem Physiol A Mol Integr Physiol. 2001 Nov;130(4):759-69. PMID: 11691612 Kim SK, Kim YC, Kim YC. Effects of singly administered betaine on hepatotoxicity of chloroform in mice. Food Chem Toxicol 1998;36:655-61. McCarty MF. Co-administration of equimolar doses of betaine may alleviate the hepatotoxic risk associated with niacin therapy. Med Hypotheses. 2000 Sep;55(3):189-94. PMID: 10985907 Murakami T, Nagamura Y, Hirano K. The recovering effect of betaine on carbon tetrachloride-induced liver injury. J Nutr Sci Vitaminol 1998;44:249-55. Poschl G, Stickel F, Wang XD, Seitz HK. Alcohol and cancer: genetic and nutritional aspects. Proc Nutr Soc. 2004 Feb;63(1):65-71. Review. PMID: 15070439 Semmler F. Treatment of liver diseases, especially of fatty liver with betaine citrate. Ther Ggw 1977;116:2113-24 [in German]. Zapadniuk VI, Panteleimonova TN. [Cholagogic effect of trimethylglycine in normal animals of different ages and in experimental atherosclerosis] Biull Eksp Biol Med. 1987 Jul;104(7):30-2. Russian. PMID: 3620644 Autism & Seizures: Rimland B. Seizures, Vitamin B6, DMG, and Sudden Speech. Autism Research Review International. 1996;10(2):1. Roach ES, Carlin L. N,N-dimethylglycine for epilepsy. N Engl J Med. 1982;307:1081-82. Vitamin B6/DMG. Letters to the Editor, Autism Research Interview International. 1994;8(2):6. Immunity: Reap EA, Lawson JW. Stimulation of the immune response by dimethylglycine, a nontoxic metabolite. J Lab Clin Med. Apr1990;115(4):481-6. Safety: Hoorn AJ. Dimethylglycine and chemically related amines tested for mutagenicity under potential nitrosation conditions. Mutat Res. 1989 Apr;222(4):343-50. PMID: 2468082
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=988) REFERENCES
Date:
June 25, 2005 08:13 PM
REFERENCES 1 a. The Surgeon General’s “Nutrition and Health Report.” b. The Centers for Disease Control and Prevention’s “National Health and Examination Survey (NHANES III)” c. The National Academy of Science’s. Diet and Health Report: Health Promotion and Disease Objectives (DHHS Publication No. (PHS) 91-50213, Washington, DC: US Government Printing Office, 1990). e. Dietary Guidelines for Americans. 2 Rolls BJ. Carbohydrates, fats, and satiety. Am J Clin Nutr 1995; 61(4 Suppl):960S-967S. 3 McDowell MA, Briefel RR, Alaimo K, et al. Energy and macronutrient intakes of persons ages 2 months and over in the United States: Third National Health and Nutrition Examination Survey, Phase 1:1988-91. Advance data from vital and health statistics of the Centers for Disease Control and Prevention; No. 255. Hyattsville, Maryland: National Center for Health Statistics; 1994. 4 Center for Science in the Public Interest and McDonald’s Nutrition and You—A guide to Healthy Eating at McDonald’s: McDonald’s Corp,1991. 5 Bray GA. Appetite Control in Adults. In: Fernstrom JD, Miller GD eds. Appetite and Body Weight Regulation. Boca Raton: CRC Press, 1994:1-92. 6 Michnovicz JJ. How to Reduce Your Risk of Breast Cancer. New York: Warner Book Inc. 1994:54. 7 Carcinogens and Anticarcinogens in the Human Diet. National Research Council Report, National Academy of Sciences, 15 Feb. 1996. 8 Van Tallie TB. Obesity: adverse effects on health and longevity. Am J Clin Nutr 1979:32: 2723-33. 9 Somer E, M.A. R.D. Nutrition for Women. New York: Henry Hold and Company, 1993:273. 10 Swaneck GE, Fishman J. Covalent binding of the endogenous estrogen 16A-hydroxyestrone to estradiol in human breast concer cells: characterization and intranuclear localization. Proc Natl Acad Sci USA 1988:85;7831-5. 11 Colditz GA. Epidemiology of breast cancer. Findings from the nurses’ health study. Cancer1993;714:1480-9. 12 Hennen WJ. Breast Cancer Risk Reduction. The effects of supplementation with dietary indoles. Unpublished report 1992. 13 Deslypere BJ. Obesity and cancer. Metabolism 1995;44(93):24-7. 14 Somer E, M.A. R.D. Nutrition for Women. New York: Henry Hold and Company, 1993:281. 15 Whittemore AS, Kolonel LN, John M. Prostate cancer in relation to diet, physical activity, and body size in blacks, whites, and Asians in the United States and Canada. J Natl Cancer Inst 1995;87(9):629-31. 16 Key T. Risk factors for prostate cancer. Cancer Survivor 1995;23:63- 77. 17 Kondo Y, Homma Y, Aso Y, Kakizoe T. Promotional effects of twogeneration exposure to a high-fat diet on prostate carcinogenisis in ACI/Seg mice. Cancer Res 1994;54(23):6129-32. 18 Wang Y, Corr JG, Taler HT, Tao Y, Fair WR, Heston WD. Decreased growth of established human prostate LNCaP tumors in nude mice fed a low-fat diet. J Natl Cancer Inst. 1995;87(19):1456-62. 19 Nixon DW. Cancer prevention clinical trials. In-Vivo 1994;8(5):713-6. 20 Key T. Micronutrients and cancer aetiology: the epidmiological evidence. Proceed Nutr Soc 1994;53(3):605-14. 21 Gorbach SL, Goldin BR. The intestinal microflora and the colon cancer connection. Reviews of Infectious Diseases 1990;12(Suppl 2):S252-61. 22 Shrapnel WS, Calvert GD, Nestel PJ, Truswell AS. Diet and coronary heart disease. The National Heart Foundation of Australia. Med J Australia. 1995;156(Suppl):S9-S16. 23 Ellis JL, Campos-Outcalt D. Cardiovascular disease risk factors in native Americans: a literature review. Am. J. Preventive Med 1994;10(5):295-307. 24 DiBianco R. The changing syndrome of heart failure: an annotated review as we approach the 21st century. J. Hypertension 1994; 12(4 Suppl):S73- S87. 25 Van Itallie TB. Obesity: adverse effects on health and longevity. Am J Clin Nutr 1979;32(suppl):2723-33. 26 Kestin M, Moss R, Clifton PM, Nestel PJ. Comparative effects of three cereal brans on plasma lipids, blood pressure and glucose metabolism in mildly hyper-cholesterolemic men. Am J Clin Nutr 1990;52(4):661-6. 27 Story JA. Dietary fiber and lipid metabolism. In: Spiller GA, Kay RM. eds. Medical Aspects of Dietary Fiber. Penun Medical; New York, 1980, p.138. 28 Stein PP, Black HR. The role of diet in the genesis and treatment of hypertension. Med. Clin. North America. 1993;77(4):831-47. 29 Olin JW. Antihypertensive treatment in patients with peripheral vascular disease. Cleve. Clin. J. Medicine. 1994;61(5):337-44. 30 Tinker LF. Diabetes Mellitus—a priority health care issue for women. J. Am. Dietetic Association. 1994;94(9):976-85. 31 Gaspard UJ, Gottal JM, van den Brule FA. Postmenopausal changes of lipid and glucose metabolism: a review of their main aspects. Maturitas. 1995;21(3):71-8. 32 Coordt MC, Ruhe RC, McDonald RB. Aging and insulin secretion. Proc. Soc. Exp. Biology and Medicine. 1995;209(3):213-22. 33 Felber JP. From Obesity to Diabetes. Pathophysiological Considerations. Int. Journal of Obesity 1992;16:937-952. 34 Gillum RF. The association of body fat distribution with hypertension, hypertensive heart disease, coronary heart disease, diabetes, and cardiovascular risk factors in men and women age 18-79. J Chronic Diseases 1987;40:421-8. 35 Haffner SM, Stern MP, Hazuda HP, et al. Role of obesity and fat distribution in non-insulin-dependent diabetes mellits in Mexican Americans and non- Hispanic whites. Diabetes Care 1986;9:153-61. 36 Bonadonna RC, deFronzo RA. Glucose metabolism in obesity and type 2 diabetes. Diabetes and Metabolism. 1991;17(1 Pt. 2):12-35. 37 Shoemaker JK, Bonen A. Vascular actions of insulin in health and disease. Canadian J. of Applied Physiology. 1995;20(2):127-54. 38 Resnick LM. Ionic Basis of Hypertension, Insulin Resistaince, Vascular Disease, and Related Disorders. The Mechanism of ‘Syndrome X’. Am. J. Hypertension. 1993;6(suppl):123S-134S. 39 Trautwein EA. Dietetic influences on the formation and prevention of cholesterol gallstones. Z. Ernahrugswiss. 1994;33(1):2-15. 40 Cicuttini FM, Spector TD. Osteoarthritis in the aged. Epidemiological issues and optimal management. Drugs and Aging. 1995;6(5):409-20. 41 Melnyk MG, Wienstein E. Preventing obesity in black women by targeting adolescents: a literature review. J Am. Diet. Association. 1994;94(4):536-40. 42 Robinson BE, Gjerdingen Dk, Houge DR. Obesity: a move from traditional to more patient-oriented management. J. Am. Board of Family Practice. 1995;8(2):99-108. 43 Dulloo AG, Miller DS. Reversal of Obesity in the Genetically Obese fa/fa Zucker Rat with an Ehpedrine/Methylxanthines Thermogenic Mixture. J. Nutrition. 1987;117:383-9. 44 Dulloo AG, Miller DS. The thermogenic properties of ephedrin/methylxanthine mixtures: animal studies. Am J Clinical Nutr. 1986;43:388-394. 45 Richelsen B. Health risks of obesity. Significance of the regional distri-bution of adipose tissue. Ugeskr. Laeger. 1991;153(13):908-13. 46 Lissner L, Heitmann BL. Dietary fat and obesity: Evidence from epidemiology. European J. Clinical Nutrition. 1995;49(2):79-90. 47 Lissner L, Heitmann BL. The dietary fat: Carbohydrate ratio in relation to body weight, Current Opinion in Lipidology. 1995;6(1):8-13. 48 Ravussin E. Energy metabolism in obesity. Studies in the Pima Indians. Diabetes Care. 1993;16(1):232-8. 49 O’Dea K. Westernisation, insulin resistance and diabetes in Australian aborigines. Med J. Australia. 1991;155(4):258-64. 50 Bailey C. Fit or Fat . Houghton Mifflen, Boston, 1991. 51 McCarty MF. Optimizing Exercise for Fat Loss. Unpublished report. 52 Weinsier RL, Schutz Y, Bracco D. Reexamination of the relationship of resting metabolic rate and fat-free mass and the the metabolically active components of fat-free mass in humans. Am. J. Clinical Nutrition. 1992;55(4):790-4. 53 Evans WJ. Exercise, nutrition and aging. J. Nutrition. 1992;122(3 suppl):796-801. 54 Schlicker SA, Borra ST, Regan C. The weight and fitness status of United States children. Nutrition Reviews. 1994;52(1):11-7. 55 Raben A, Jensen ND, Marckmann P, Sandstrom B and Astrup A. Spontaeous weight loss during 11 weeks’ ad libitum intake of a low fat/high fiber diet in young, normal weight subjects. Stockholm Press. 1995;916-23. 56 Blundell JE, Cotton JR, Delargy H, Green S, Greenough A, King NA, Lawton, CL. The fat paradox: fat-induced satiety signals versus high fat overconsumption. Short Communication 1995:832-835. 57 Reinhold RB. Late results of gastric bypass surgery for morbid obesity. J Am Coll Nutr 1994;13(4):307-8. 58 McCredie M, Coates M Grulich A. Cancer incidence in migrants to New South Wales (Australia) from the Middle East, 1972-1991. Cancer Causes Control 1994:5(5):414-21. 59 Schiff ER, Dietschy JM. Steatorrhea Associated with Disordered Bile Acid Metabolism. Am. J. Digestive Diseases. 1969;14(6) 60 Nauss JL , Thompson JL and Nagyvary J. The binding of micellar lipids to Chitosan. Lipids. 1983;18(10):714-19. 61 Braconnot H, Sue la natrue ces champignons. Ann Chim Phys 1811;79:265. 62 Odier A. Memoire sur la composition chemique des parties cornees des insectes. Mem Soc Hist Nat Paris 1823;1:29. 63 Johnson EL, Peniston QP. Utilization of shellfish waste for chitin and Chitosan production. Chp 19 In: Chemistry and Biochemistry of Marine Food Products. Martin RE, Flick GJ, Hebard CE and Ward DR (eds.) 1982. p.415-. AVI Publishing Co., Westport, CT. 64 Shahram H. Seafood waste: the potential for industrial use. Kem Kemi 1992;19(3),256-8. 65 Rouget C. Des substances amylacees dans le tissue des animux, specialement les Articules (Chitine). Compt Rend 1859;48:792. Commission on Natural Health Products. 1995 67 Peniston QP and Johnson EL. Method for Treating an Aqueous Medium with Chitosan and Derivatives of Chitin to Remove an Impurity. US Patent 3,533,940. Oct. 30:1970. 68 Poly-D-Glucosamine (Chitosan); Exemption from the Requirement of a Tolerance. Federal Register. 1995;60(75):19523-4. Rules and Regulations. Environmental Protection Agency 40 CFR Part 180. April, 19, 1995. 69 Arul J. “Use of Chitosan films to retard post-harvest spoilage of fruits and vegetables,” Chitin Workshop. ICNHP, North Carolina State University, Raleigh, NC. 70 Karlsen J, Skaugrud O. “Excipient properties of Chitosan,” Manufacturing Chemist. 1991;62:18-9. 71 Winterowd JG, Sandford PA. Chitin and Chitosan. In: Food Polysaccharides and their Applications. Ed: Stephen AM. Marcel Dekker 1995. 72 Chitin Workshop. ICNHP, North Carolina State University, Raleigh, NC. 73 Advances in Chitin and Chitosan. Eds: CJ Brine, PA Sandford, JP Zikakis. Elsevier Applied Science. London. 1992. 74 Chitin in Nature and Technology. Eds: R Muzzarelli, C Jeuniaux, GW Gooday. Plenum Press, New York. 1986. 75 Zikakis, JP. Chitin, Chitosan and Related Enzymes. Academic Press, Inc. 1984. 76 Abelin J and Lassus A. Fat binder as a weight reducer in patients with moderate obesity. ARS Medicina, Helsinki, Aug- October, 1994. 77 Kanauchi O, Deuchi K, Imasato Y, Shizukuishi M, Kobayashi E. Increasing effect of a Chitosan and ascorbic acid mixture on fecal dietary fat excretion. Biosci Biotech Biochem 1994;58(9):1617-20. 78 Maezaki Y, Tsuji K, Nakagawa Y, et al. Hypocholesterolemic effect of Chitosan in adult males. Biosci Biotchnol Biochem1993;57(9):1439-44. 79 Kobayashi T, Otsuka S, Yugari Y. Effect of Chitosan on serum and liver cholesterol levels in cholesterol-fed rats. Nutritional Rep. Int., 1979;19(3):327-34. 80 Sugano M, Fujikawa T, Hiratsuji Y, Hasegawa Y. Hypocholesterolemic effects of Chitosan in cholesterol-fed rats. Nutr Rep. Int. 1978;18(5):531-7. 81 Vahouny G, Satchanandam S, Cassidy M, Lightfoot F, Furda I. Comparative effects of Chitosan and cholestryramine on lymphatic absorption of lipids in the rat. Am J Clin Nutr, 1983;38(2):278-84 82 Suzuki S, Suzuki M, Katayama H. Chitin and Chitosan oligomers as hypolipemics and formulations containing them. Jpn. Kokai Tokkyo Koho JP 63 41,422 [88,422] 22 Feb1988. 83 Ikeda I, Tomari Y, Sugano M. Interrelated effects of dietary fiber on lymphatic cholesterol and triglyceride absorption in rats. J Nutr 1989;119(10):1383- 7. 84 LeHoux JG and Grondin F. Some effects of Chitosan on liver function in the rat. Endocrinology. 1993;132(3):1078-84. 85 Fradet G, Brister S, Mulder D, Lough J, Averbach BL. “Evaluation of Chitosan as a New Hemostatic Agent: In Vitro and In Vivo Experiments In Chitin in Nature and Technology. Eds: R Muzzarelli, C Jeuniaux, GW Gooday. Plenum Press, New York. 1986. 86 Malette W, Quigley H, Gaines R, Johnson N, Rainer WG. Chitosan A New Hemostatic. Annals of Thorasic Surgery. 1983;36:55. 87 Malette W, Quigley H, Adickes ED. Chitosan effect in Vascular Surgery, Tissue Culture and Tissue Regeneration. In R Muzzarelli, C Jeuniaux, GW Gooday, Eds: Chitin in Nature and Technology. Plenum Press, New York. 1986. 88 Okamoto Y, Tomita T, Minami S, et al. Effects of Chitosan on experimental abscess with Staphylococcus aureus in dogs. J. Vet. Med., 1995;57(4):765-7. 89 Klokkevold PR, Lew DS, Ellis DG, Bertolami CN. Effect of Chitosan on lingual hemostasis in rabbits. Journal of Oral-Maxillofac-Surg, 1991;Aug. 49(8):858-63. 89 Surgery, Tissue Culture and Tissue Regeneration. In Chitin in Nature and Technology. Eds: R Muzzarelli, C Jeuniaux, GW Gooday. Plenum Press, New York. 1986. 90 Hiroshi S, Makoto K, Shoji A, Yoshikazu S. Antibacterial fiber blended with Chitosan. Sixth International Conference on Chitin and Chitosan. Sea Fisheries Institute, Gdynia, Poland. August 1994;16-19. 91 Shimai Y, Tsukuda K, Seino H. Antiacne preparations containing chitin, Chitosan or their partial degradation products. Jpn. Kikai Tokkyo Koho JP 04,288,017 [92,288,017] 13 Oct 1992. 92 Suzuki K, Okawa Y, Suzuki S, Suzuki M. Candidacidal effect of peritoneal exudate cells in mice administered with chitin or Chitosan: the role of serine protease in the mechanism of oxygen-independent candidacidal effect. Microbiol Immunol. 1987;31(4):375-9. 93 Sawada G, Akaha Y, Naito H, Fujita M. Synergistic food preservatives containing organic acids, Chitosan and citrus seed extracts. Jpn, Kokai Kokkyo Koho JP 04 27,373 [92 27,373] 30 Jan 1992. 94 Min H-K, Hatai K, Bai S. Some inhibitory effects of Chitosan on fishpathogenic oomycete, Saprolegnia parasitic. Gyobyo Kenkyu, 1994;29(2):73-4. 95 Nelson JL, Alexander JW, Gianotti L, Chalk CL, Pyles T. The influence of dietary fiber on microbial growth in vitro and bacterial translocation after burn injury in mice. Nutr 1994;10(1):32-6. 96 Ochiai Y, Kanazawa Y. Chitosan as virucide. Jpn Kokai Tokkyo Koho 79 41,326. 97 Hillyard IW, Doczi J, Kiernan. Antacid and antiulcer properties of the polysaccharide Chitosan in the rat. Proc Soc Expl Biol Med 1964; 115:1108-1112. 98 Shibasaki K, Sano H, MatsukuboT, Takaesu Y. pH response of human dental plaque to chewing gum supplemented with low molecular Chitosan. Bull- Tokyo-Dent-Coll, 1994:35(2): 61-6. 99 Kato H, Okuda H. Chitosan as antihypertensive. Jpn. Kikoi Tokyo Koho JP 06 56,674 [94 56,674] 100 Kato H, Taguchi T. Mechanism of the rise in blood pressure by sodium chloride and decrease effect of Chitosan on blood pressure. Baiosaiensu to Indasutori 1993;51(12):987-8. 101 Muzzarelli R, Biagini G, Pugnaoni A, Filippini O, Baldassarre V, Castaldini C, and Rizzoli C. Reconstruction of Periodontal Tissue with Chitosan. Biomaterials. 1989;10:598-603. 102 Sapelli P, Baldassarre V, Muzzarelli R, Emanuelli M. Chitosan in Dentistry. In Chitin in Nature and Technology. Eds: R Muzzarelli, C Jeuniaux, GW Gooday. Plenum Press, New York. 1986. 103 Borah G, Scott G, Wortham K. Bone induction by Chitosan in endochrondral bones of the extremities. In Advances in Chitin and Chitosan. Eds: CJ Brine, PA Sandford, JP Zikakis. Elsevier Applied Science. London. 1992. 104 Ito F. Role of Chitosan as a supplementary food for osteoporosis. Gekkan Fudo Kemikaru, 1995;11(2):39-44. 105 Nakamura S, Yoshioka T, hamada S, Kimura I. Chitosan for enhancement of bioavailability of calcium. Jpn. Kokai Tokkyo Koho JP 07 194,316 [95 194,316] 01 Aug 1995. 106 Maekawa A, Wada M. Food Containing chitin or its derivatives for reduction of blood and urine uric acid. Jpn. Kokai Tokkyo Koho JP 03 280,852 [91 280,852], 11 Dec 1991. 107 Weisberg M, Gubner R. Compositions for oral administration comprising Chitosan and a pharmaceutically acceptable carrier. Antacid preparations for alleviating gastric hyperacidity. U.S. patent 3257275 108 Kanauchi O, Deuchi K, Imasato Y, Shizukuishi M, Kobayashi E. Mechanism for the inhibition of fat digestion by Chitosan and for the synergistic effect of ascorbate. Biosci Biotech Biochem1995;59(5):786-90. 109 McCausland CW. Fat Binding Properties of Chitosan as Compared to Other Dietary Fibers. Private communication. 24 Jan1995. 110 Deuchi K, Kanauchi O, Imasato Y, Kobayashi E. Biosci Biotech Biochem. 1994:58,1613-6. 111 Ebihara K, Schneeman BO. Interaction of bile acids, phospholipids, cholesterol and triglyceride with dietary fibers in the small intestine of rats. J Nutr 1989;119(8):1100-6. 112 Weil A, M.D. Natural Health Natural Medicine: Boston: Houghton Mifflin, 1990:182. 113 Chen Y-H, Riby Y, Srivastava P, Bartholomew J, Denison M, Bjeldanes L. Regualtion of CYP1A1 by indolo[3,2-b]carbazole in murine hepatoma cells. J Biol Chem 1995;270(38):22548-55. 114 Intestinal Absorption of metal ions and chelates. Ashmead HD, Graff DJ, Ashmead HH. Charles C Thomas, Springfield, IL 1985. 115 Nutrient Interactions. Bodwell CE, Erdman JW Jr. Marcel Dekker New York 1988. 116 Heleniak EP, Aston B. Prostaglandins, Brown Fat and Weight Loss. Medical Hypotheses 1989;28:13-33. 117 Connor WE, DeFrancesco CA, Connor SL. N-3 fatty acids from fish oil. Effects on plasma lipoproteins and hypertriglyceridemic patients. Ann NY Acad Sci 1993;683:16-34. 118 Conte AA. A non-prescription alternative in weight reduction therapy. The Bariatrician Summer 1993:17-19. 119 McCarty MF. Inhibition of citrate lyase may aid aerobic endurance. Unpublished manuscript. 120 Bray GA. Weight homeostasis. Annual Rev Med 1991;42:205-216. 121 Dulloo AG, Miller DS. The thermogenic properties of Ephedrin/Methylxanthine mixtures: Human studies. Intl J Obesity 986;10:467-481. 122 Arai K, Kinumaki T, Fujita, T. Bulletin Tokai Regional Fisheries Res Lab. 1968;No. 56. 123 Bough WA. Private communication. 124 Freidrich EJ, Gehan, EA, Rall DP, Schmidt LH, Skipper HE. Cancer Chemotherapy Reports 1966;50(4):219-244. 125 A Drovanti, AA Bignamini, AL Rovati. Therapeutic activity of oral glucosamine sulfate in osteoarthritis: A placebo-controlled double-blind investigation. Clinical Therapeutics 1980;3(4):260-272. 126 K Deuchi, O Kanauchi, M Shizukuishi, E Kobayashi. Continuous and massive intake of Chitosan affects mineral and fat-soluble vitamin status in rats fed on a high-fat diet. Biosci. Biotech. Biochemistry. 1995;59(7):1211-6. 127 . BesChitin W in Chitin Wound Healing (video), Unitika Corporation, April 1992.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=507) Home on the Range 
Date:
June 13, 2005 03:52 PM
Home on the Range by Janis Jibrin, RD Energy Times, September 5, 1999 Got chicken? Americans can't seem to get enough of this bird. Last year each of us ate, on average, just about 80 pounds of chicken, a whopping increase over the 49 pounds we each devoured in 1980 and an eight-pound increase from 1995. Part of this food's popularity comes from its lean image as a healthier, less fatty alternative to red meat (don't forget to take the fatty skin off). Chicken's also a cheap protein source: At many popular supermarkets you'll find weekly specials at about a dollar a pound. But at health food markets, chicken can cost upwards of $1.69 a pound. These birds may be touted as raised in an organic, stress-free environment and on a vegetarian diet, free of antibiotics. For many people, this poultry is a better buy. The Alternative Chicken Most of the supermarket chicken you pick up in grocery refrigerated cases are broilers, birds bred to mature in about eight weeks. In comparison, in the '60s, chickens needed 14 weeks to become adult poultry. Conventionally-raised broilers eat grain mixed with whatever's cheapest on the market, such as recycled cooking oil that's been used to fry fast foods and animal parts. These birds reside in chicken coops the size of football fields and don't see the light of day until transported to the slaughterhouse. On the other roost, alternatively raised chickens are brought up in a variety of ways (see box), but usually enjoy a more relaxed life and diet. Chickens on the farm receive antibiotics for two reasons: To fight off the diseases that can run rampant through a crowded chicken coop and to encourage faster growth. Antibiotics Stimulate Growth Mark Cook, PhD, professor of animal science at the University of Wisconsin at Madison, explains, "Gut bacteria trigger an immune system assault, which makes chickens a little feverish, suppresses appetite and slows growth. Antibiotics stimulate growth indirectly, by keeping bacteria levels down, and preventing the immune reaction." When birds get sick, they often get dosed with even more antibiotics. This widespread antibiotic use has come home to roost and may contribute to the growth of bacteria that, frequently exposed to chemicals, have evolved ways to keep from being killed by pharmaceuticals. This development threatens human health. Bacterial infections that people contract, once easily cured by penicillin or other drugs, are now tougher to eradicate. For instance, campylobactor, a common bacteria found in chicken, and responsible for some food poisonings, now demonstrates signs of resistance to drugs like floroquinolones. A powerful class of antibiotics, floroquinolones used to dependably conquer this infection. "Floroquinolones are an extremely important class of antibiotics, used to treat many types of infections such as urinary tract infection, a wide variety of gastrointestinal illnesses, pneumonia, almost everything," says Kirt Smith, DVM, PhD, epidemiologist, acute disease epidemiology section, Minnesota Department of Health. A study by Dr. Smith, published in the New England Journal of Medicine (340, 1999: 1525-32), showed that the percent of floroquinolone-resistant campylobactor appearing in infected people in his state-Minnesota-climbed from a little over 1% in infected people during 1992 to 10.2% in 1998. He and other scientists strongly suspect that the rise is a direct consequence of the Food and Drug Administration's (FDA) decision to allow floroquinolones in poultry feed beginning in 1995. Although it was nearly impossible for Dr. Smith to trace the precise origin of campylobactor poisoning, he believes chicken was usually the source-and not just U.S. chicken. Many of the infected people had returned from Mexico and other countries. "Sales of floroquinolones for poultry use in Mexico has increased dramatically," notes Dr. Smith. Many alternative chicken producers do not use any antibiotic-laced feed at all. Other farmers adjust the feed to lower gut pH, making it more acidic and lowering chances of bacteria. At the U. of Wisconsin, Dr. Cook is developing antibodies to suppress the immune response to bacteria so chickens won't need antibiotics to spur growth. Buying and dining on chicken raised with little or no antibiotics could beneficially lower your risk of contracting a hardy bacterial infection. Better to catch campylobactor from an antibiotic-free chicken than a conventional chicken, speculates Dr. Cook. "There's less likelihood the bug will be resistant, and a better chance your problem can be cured with antibiotics," he explains. And, looking beyond your own immediate health risk, buying antibiotic-free chicken makes a small contribution to stopping the spread of antibiotic resistant bugs. A Matter of Taste Conventionally raised chickens get little exercise and live only eight weeks, so they're tender but bland. "There's not much taste in a modern chicken. Free range or organically grown, older birds usually have more taste," notes Dr. Cook. The days of barnyard chickens happily clucking and strutting around in picturesque nature have disappeared with the family farm. Today, chickens lead a meager existence. After hatching, baby chicks are tossed into a gigantic hen house that is home to up to 30,000 birds. Their short lives are lived within the United States Department of Agriculture (USDA) mandated 3/4 square foot per chicken. In that squeeze, birds can catch "chicken influenza," especially in winter when it's too cold to let in much fresh air. Laying hens don't experience much more of a peaceful existence. These birds live their years with about five other hens, so crowded they can't flap their wings. Cages, suspended in the air, let eggs roll into a holding area. So they don't peck each other, hens are often debeaked, a painful process that can cause infection. Hens go through natural laying and "dry" cycles. Growers manipulate this cycle by "forced molting," depriving hens of food for four to 14 days to keep them constantly laying. By the end of two years, hens are worn out. Their inactivity weakens their bones enough that electrical stunning, the usual method for knocking chickens out before slaughter, shatters their bones. So some wind up being plucked and boiled alive, according to Mary Finelli, program director for farm animals and public health at the Humane Society of the United States. The meat from these hens, tougher than other birds, was probably in your deli lunch sandwich. It's also used in the school lunch program or may end up in dog food. "Generally, organically-grown broilers and hens have it better because room to move is part of the organic certification process," says Finelli. Finelli suggests visiting chicken suppliers to find out how chickens are treated. Or, she advocates a Humane Society book listing reliable firms. For a local producer call the society: 202-452-1100. According to a Consumer Report report, some growers force chickens out the last week of their lives to brand them "free range." So free range isn't a prime standard for choosing a decently raised chicken. However, turkeys thrive outdoors, so choosing free-range turkey is often a good idea for better tasting poultry. In any case, organic is your best bet for chicken without pesticides. Make it your main choice for your 80 pound yearly consumption! To fight cruel treatment of poultry: • Forced Molting Ban. Forced molting is shocking hens for more eggs. To support petitions banning forced molting write: Docket Manage-ment Branch, FDA, Dept. Health & Human Serv-ices, 12420 Parklawn Drive, Room 1-23, Rock-ville, MD 20857. Include docket # 98P-0203/CP • Downed Animal Protection Bill (House Bill 443, Senate Bill S515) spares some animals from the tortuous journey from chicken house to slaughterhouse. Mandates humane euthanization.
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