Dairy Diet Myth
You’ve probably seen the ads in magazines or on TV. “Milk, cheese-
yogurt. Burn more fat, lose weight.” Drink 24 ounces
of milk every 24 hours and that skinny hourglass figure will be
yours. Eat three servings of yogurt every day and squeeze into
that itsy-bitsy bikini...
Beginning October 2003 "Drink Milk... Lose Weight" ads ran in over 30 newspapers and magazines when the dairy industry launched an entire "Healthy Weight with Milk" campaign to boost sales. Curiously, that also happened to be the same year a review of that exact subject was published in the Journal of Nutrition. The review found nine randomized controlled studies in the medical literature on body weight and dairy. Seven of the nine studies found no significant change in body weight compared to controls and the last two found that those who increased their dairy consumption gained significantly more weight than the nondairy control groups.[1] Subsequent and even larger studies published in 2004[2] and 2005[3] showed the exact same thing.
So, wait a second. How can the dairy industry's ads claim that "a clinical study shows it helps you burn more fat and lose more weight than just cutting calories alone?" Well, because there are actually three small published studies that found greater weight loss in people who were told to cut calories and eat dairy foods and all were done by one researcher with a patent on the claim. Michael Zemel of the University of Tennessee, found that study participants instructed to eat more dairy did seem to lose more weight. Yes, of course the studies were bought and paid for by the dairy industry, but it goes further than that. This guy Zemel owns a patent on the claim that dairy foods aid weight loss, which is licensed to dairy food manufacturers. As the Center for Science in the Public Interest noted, "In the world of patents and PR, a little science can go a long way."[4] For an in depth analysis of Zemels work and how it is assisting the Dairy Industry check out the Nutrition Action Health Letter Spetember 2005 available online at cspinet.org
Similar maneuverings were involved in the increased dairy recommendation in the new USDA Dietary Guidelines, even though a recent World Health Organization review found no significant relationship at all between low dairy consumption and osteoporotic fracture risk.[5] Assigned to write the dairy guideline was Connie Weaver, head of nutrition at Purdue University and a funding favorite of the National Dairy Council. Walter Willet, head of nutrition at Harvard, calls the guideline committee's report "egregious," accusing them of ignoring the evidence linking dairy to cancer. "There is no nutritional requirement for dairy," Dr. Willet told the Wall Street Journal, "at all."[6]
To hopefully clear up the dairy/weight question once and for all, on June 6, 2005, Harvard researchers published what may be considered the definitive study on the subject in the Archives of Pediatrics and Adolescent Medicine. A study which followed the milk-drinking habits of not 11 kids, or even 12 kids, but over 12,000 kids! After following these 9- though 14-year-olds for years, they found that "children who reported higher total milk intake experienced larger weight gains." The more milk they drank, the heavier they became. Boys who drank the "recommended" three servings of milk a day were 35% more likely to become overweight and girls who drank three servings were 36% more likely to become overweight over time.[7]
"Given the high prevalence of lactose intolerance, the energy content and saturated fat in milk, and evidence that dairy products may promote both male (prostate) and female (ovarian) cancers, we should not assume that high intakes [of dairy] are beneficial," the researchers told reporters. "Furthermore, these cancers may be linked to consumption during adolescence."[8]
What most surprised the researchers was that those who drank low-fat milk (skim and 1%) gained the most weight of all! The weight gain seemed tied more to the dairy protein intake than the dairy fat intake (extra whey protein is often added to low-fat milk during processing). Although there are at least four human studies that show that the dairy protein whey itself may promote weight gain, the researchers guessed that the blame lay in the growth hormones in milk, like the sex steroid estrone found in whey. After all, milk is designed by mother nature to start an 80-pound calf on her way to 1,400 pounds by her second birthday.
This new study has serious implications for our childhood obesity epidemic, which not only has devastating health consequences but social consequences as well. A study released the same week by researchers at the Centers for Disease Control found that teens who perceived themselves as overweight were more than twice as likely to attempt suicide.[9]
[1] Barr SI. "Increased Dairy Product or Calcium Intake: Is Body Weight or Composition Affected in Humans?" Journal of Nutrition 133(2003):245-8S.
[2] Obesity Research 12(2004):A23.
[3] Gunther CW, Legowski PA, Lyle RM, et al. "Dairy Products Do Not Lead to Alterations in Body Weight or Fat Mass in Young Women In A 1-Y Intervention." Am J Clin Nutr 2005;81:751-6.
[4] "Dairy Does Diets." Nutrition Action Healthletter September 2004:8.
[5] Kanis JA, et al."A Meta-Analysis of Milk Intake and Fracture Risk: Low Utility For Case Finding." Osteoporisis International 21 October 2004.
[6] Zamiska N. "How Milk Got a Major Boost By Food Panel." Wall Street Journal 30 August 2004:B1.
[7] Berkey CS, et al. "Milk, Dairy Fat, Dietary Calcium, and Weight Gain ." Archives of Pediatrics and Adolescent Medicine 1599(2005):543-50.
[8] Fox M. "Milk may make for heavier kids, study finds." Reuters 6 June 2005.
[9] Eaton DK, et al. "Associations of Body Mass Index and Perceived Weight With Suicide Ideation and Suicide Attempts Among US High School Students." Archives of Pediatrics and Adolescent Medicine 1599(2005):513-9.
Showing posts with label Cancer Promoting Foods. Show all posts
Showing posts with label Cancer Promoting Foods. Show all posts
Thursday, March 22, 2007
Thursday, March 8, 2007
California Dairy Giant Rejects Hormone Treated Milk
Consumer groups and public health organizations give cheers to California’s dairy industry after the Associated Press, along with other news agencies, reported yesterday that members of the largest dairy cooperative in California will be required to supply milk that is free of the hormone RBST. California Dairies Company's 650 members produce approximately 40% of California's milk and 10% of the nation's. By August First, they'll have to stop injecting their herds with the genetically engineered hormone or pay a premium for the co-op to truck their milk to other markets.
The industry wide shockwaves expected will assist in bringing US production regulations closer to that of our trading partners. In Europe and Canada US dairy exports recently have faced increasing resistance because of the refusal by American producers to discontinue using the hormone. European and Canadian authorities banned the hormone, recognize RBST as a threat to human health and have linked it to cancer. Several years ago documents came to public attention that showed Monsanto lied about their studies in order to gain approval from the FDA. The evidence on this is stunning and I have included an exhaustive list of references and hope that everyone gives them at least a quick glance.[1-58]
The good news for the consumers and the cows is not in any case good news for Monsanto, they are going to lose billions of dollars. Monsanto is the only supplier of the hormone, sold under the name Posilac, and sales have been estimated at close to $300 million annually, although Monsanto refuses disclosure of actual figures. Monsanto Corporation, in case anyone has forgotten, is that esteemed member of the American corporate community that has brought us such wonders as Agent Orange, Roundup and is the world's leader in GMO's (genetically modified organism).
RBST or Posilac is also an excellent example of corporate welfare. Posilac causes cows to produce more milk. So... what is wrong with that you ask? American taxpayers pay farmers not to produce milk and have been doing so for years. [59] There is an excess of dairy products in this country and our government buys it using our money. They buy it to keep the prices stable. If the supply exceeds demand, the price of dairy drops. The government steps in and keeps product from reaching the market. It ends up in government warehouses where much of it is simply thrown away. This is where “government cheese” came from. What is not eaten by our poor, elderly, and native populations ends up in the trash. Do you think that Monsanto cares about the fact that their product is contributing to this? I think Monsanto sees the bottom line.
The trouble with this continues because not only has Posilac been recognized as a human health threat, but so is the milk it helps produce more of! Dairy proteins and fats have been linked to heart disease, stroke [60,6], cancer [62-66], diabetes (types 1&2) [67,68], multiple sclerosis, arthritis, Crohn’s disease, irritable bowl syndrome, fibromyalgia, osteoporosis [69-78], and more. So where did Monsanto get the bright idea for such a great product? Since great minds think alike, maybe it was a friend of one of Monsanto’s other top executives; Donald Rumsfeld was a CEO for Monsanto. Hmmmm.
My hat is off to the California dairy producers for standing up to Monsanto and their money grubbing schemes regardless of the reason. It is a rare day when I have anything positive to say about the dairy industry, today just happens to be one of them.
References
1. Conyers, John. Letter to Richard R. Kusserow, Inspector General, Department of
Health and Human Services. May 9, 1990.
2. Kennelly J & DeBoer G. Bovine somatotropin. In Proceedings of the Alberta Dairy Seminar. Banff, Alberta, March 9-11, 1998.
3. Baer RJ, et al. Composition and flavor of milk produced by cows injected with recombinant bovine somatotropin. Journal of Dairy Science 72:1424-1434, 1989.
4. Capuco, AV et al. Somatotropin increases thyroxine-5’-monodeiodinase activity in lactating mammary tissue of the cow. Journal of Endocrinology 121(2):205-211, 1989.
5. Epstein, SS. Potential public health hazards of biosynthetic milk hormones.
International Journal of Health Services 20:73-84, 1990.
6. Kronfeld, DS. Safety of bovine growth hormone. Science 251:256-257, 1991.
7. U.S. General Accounting Office. rBGH. FDA Approval Should Be Withheld Until the Mastitis Issues is Resolved. 1992.
8. Mepham TB. Public health implications of bovine somatotropin use in dairying: discussion paper. Journal of the Royal Society of Medicine 85:736-739, 1992.
9. Millstone E, et al. Plagiarism or protecting public health? Nature 371:647-648, 1994.
10. U.S. General Accounting Office. Recombinant bovine growth hormone. FDA approval should be withheld until the mastitis issue is resolved. 1992.
11. Davis SR, et al. Effects of injecting growth hormone of thyroxine on milk production and blood plasma concentrations of insulin-like growth factors I and II in dairy cows.
Journal of Endocrinology 114:17-24, 1987.
12. Prosser CG, et al. Changes in concentrations of IGF-1 in milk during BGH treatment in the goat. Journal of Endocrinology 112 (March Supplement): Abstract 65, 1987.
13. McBride BW, et al. The influence of bovine growth hormone (somatotropin) on animals and their products. Research and Development in Agriculture 5:1-21, 1988. page 5
14. Francis GL, et al. Insulin-like growth factors 1 and 2 in bovine colostrum. Sequences and biological activities compared with those of a potent truncated form. Biochem J. 251:95-103, 1988.
15. Prosser CG, et al. Increased secretion of insulin-like growth factor-1 into Milk of cows treated with recombinantly derived bovine growth hormones. Journal of Dairy Research 56:17-26, 1989.
16. Juskevich JC & Guyer CG. Bovine growth hormone food safety evaluation.
Science 249:875-884, 1990.
17. National Institutes of Health. Technology Assessment Conference Statement on
Bovine Somatotropin. Journal of the American Medical Association 265:1423-1425, 1991.
18. Joint FAO/WHO Expert Committee on Food Additives (JECFA). Fortieth Report,
Geneva. June 9-18, 1992. Cited six unpublished industry studies confirming increased IGF-1 levels in rBGH milk. These included one by Monsanto (Schams et al, 1988) reporting a four-fold increase, and another (Miller et al, 1989) reporting a further 50% increase following pasteurization.
19. Epstein SS. BST and cancer. New Scientist U.K., October 29, 1994.
20. Mepham TB, et al. Safety of milk from cows treated with bovine somatotropin.
The Lancet 2:197, 1994
21. Mepham TB & Schofield PN. International Dairy Federation Nutrition Week, Paris, June 1995.
22. Epstein SS. Unlabeled milk from cows treated with biosynthetic growth hormones:
a case of regulatory abdication. International Journal of Health Services 261:173-185, 1996.
23. Furlanetto RW & DiCarlo JN. Somatotropin-C receptors and growth effects in human breast cells maintained in long-term tissue culture. Cancer Research 44:2122-2128, 1984.
24. Glimm DR, et al. Effect of bovine somatotropin in the distribution of immunoreactive insulin-like growth factor-1 in lactating bovine mammary tissue.
Journal of Dairy Science 71:2923-2935, 1988.
25. Reynolds RK, et al. Regulation of epidermal growth factor and insulin-like growth factors I receptors by estradiol and progesterone in normal and neoplastic endometrial cells cultures. Gynecology Oncology 38:396-406, 1990. page 6
26. Lippman A. Growth factors, receptors and breast cancer. National Institutes of Health Research 3:59-62, 1991.
27. Rosen N, et al. Insulin-like growth factors in human breast cancer. Breast Cancer Research Treatment 18 (Suppl):555-562, 1991.
28. Harris JR, et al. Breast Cancer. New England Journal of Medicine 7:473-480, 1992.
29. Pollak MN, et al. Tamoxifen reduced insulin-like growth factor-1 (IGF-1). Breast Cancer Research Treatment 22:91-100, 1992.
30. Lippman ME. The development of biological therapies for breast cancer. Science 259:631-632, 1993.
31. Pappa V, et al. Insulin-like growth facotr-1 receptors are over expressed and predict a low risk in human breast cancer. Cancer Research 53:3736-3740, 1993.
32. Bruning PF, et al. Insulin-like growth factor-binding protein 3 is decreased in early-stage operable pre-menopausal breast cancer. International Journal of Cancer 62(3):266-270, July 1995.
33. Epstein SS. Unlabeled milk from cows treated with biosynthetic growth hormones: a case of regulatory abdication. International Journal of Health Services 261:173-185, 1996.
34. LeRoith D. Insulin-like growth factors and cancer. Annals of Internal Medicine 122(1):54-59, January, 1995.
35. Bohlke K, et al. Insulin-like growth factor-1 in relation to premenopausal ductal carcinoma in situ of the breast. Epidemiology 9(5):570-573, 1998.
36. Del Giudice ME, et al. Insulin and related factors in premenopausal breast cancer risk. Breast Cancer Research and Treatment 47 (2):111-120, 1998.
37. Hankinson SE, et al. Circulating concentrations of insulin-like growth factor-1 and risk of breast cancer. The Lancet 351:1393-1396, 1998.
38. Agurs-Collins T, et al. Insulin-like growth factor-1 and breast cancer risk in post-menopausal American women. Proceedings of the American Association of Cancer Research 40:152, 1999.
39. Toniolo P, et al. Serum insulin-like growth factor-1 and breast cancer.
International Journal of Cancer 88(5):828-832, 2000.
40. Yu H & Rohan T. Role of the insulin-like growth factor family in cancer development and progression. Journal of the National Cancer Institute 92:1472-1484, 2000. page 7
41. Epstein SS. Re Role of the insulin-like growth factors in cancer development and progression. Journal of the National Cancer Institute 93(3):238, 2001.
42. Pines A, et al. Gastrointestinal tumors in acromegalic patients. Am J Gastroenterology 80:266-269, 1985.
43. Orme SM, et al. Cancer incidence and mortality in acromegaly: a retrospective cohort study. Journal of Endocrinology Supplement Number OC22, June 1996.
44. Epstein SS. Unlabeled milk from cows treated with biosynthetic growth hormones: a case of regulatory abdication. International Journal of Health Services 261:173-185, 1996.
45. Manousos O, et al. IGF-I and IGF-II in relation to colorectal cancer. International Journal of Cancer 83:15-17, 1999.
46. Ma J, et al. Prospective study of colorectal cancer risk in men and plasma levels of insulin-like growth factor-1 and IGF-1 binding protein-3. Journal of the National Cancer Institute 91:620-625, 1999.
47. Giovannucci E, et al. Plasma insulin-like growth factor-I and binding protein-3 and risk of colorectal cancer and adenoma in women. Proceedings of the American Association of Cancer Research 40:211, 1999.
48. Renehan AG, et al. Circulating insulin-like growth factor II and colorectal adenomas. Journal of Clinical Endocrinology & Metabolism 85(9):3402-3408, 2000.
49. Mantzoros CS, et al. Insulin-like growth factor 1 in relation to prostate cancer and benign prostatic hyperplasia. British Journal of Cancer 76:1115-1118, 1997.
50. Chan JM, et al. Plasma insulin-like growth factor-I and prostate cancer risk: a prospective study. Science 279:563-566, 1998.
51. Wolk A, et al. Insulin-like growth factor 1 and prostate cancer risk: a population-based, case-control study. Journal of the National Cancer Institute 90:911-915, 1998.
52. Signorello LB, et al. Insulin-like growth factor-binding protein-1 and prostate cancer.
Journal of the National Cancer Institute 91:1965-1967, 1999.
53. Stattin P, et al. Plasma insulin-like growth factor-binding proteins, and prostate
cancer risk: a prospective study. Journal of the National Cancer Institute 92:1910-1917, 2000.
54. Harman SM, et al. Serum levels of insulin-like growth factor I (IGF-1), IGF-II, IGF-binding protein-3, and prostate-specific antigen as predictors of clinical prostate cancer.
Journal of Clinical Endocrinology & Metabolism 85(11):4258-4265, 2000. page 8
55. Juul A, et al. The ratio between serum levels of IGF-1 and the IGF binding protein decreases with age in healthy patients and is increased in acromegalic patients. Clinical Endocrinology 41:85-93, 1994.
56. Tremble JM & McGregor AM. In Treating Acromegaly, editor Wass p. 5-12.
Journal of Endocrinology Ltd., Bristol, England, 1994.
57. Resnicoff M, et al. The insulin-like growth factor-I receptor protects tumor cells from apoptosis in vivo. Cancer Research 55(11):2463-2469, June 1,1995.
58. Epstein SS. Re: role of the insulin-like growth factor family in cancer development and progression. Journal of the National Cancer Institute 93(3):238, 2001
59. Milk Pricing in the United States. By Alden C. Manchester and Don P. Blayney.
Market and Trade Economics Division, Economic Research Service, U.S. Department
of Agriculture. Agriculture Information Bulletin No. 761.
60. Pennington JAT. Bowes and Churches Food Values of Portions Commonly Used, 17th ed. New York: Lippincott, 1998.
61. Ornish D, Brown SE, Scherwitz LW, Billings JH, Armstrong WT, Ports TA. Can lifestyle changes reverse coronary heart disease? Lancet 1990;336:129-33.
62. Cramer DW, Harlow BL, Willet WC. Galactose consumption and metabolism in relation to the risk of ovarian cancer. Lancet 1989;2:66-71.
63. Outwater JL, Nicholson A, Barnard N. Dairy products and breast cancer: the IGF-1, estrogen, and bGH hypothesis. Medical Hypothesis 1997;48:453-61.
64. Chan JM, Stampfer MJ, Giovannucci E, et al. Plasma insulin-like growth factor-1 and prostate cancer risk: a prospective study. Science 1998;279:563-5.
65. World Cancer Research Fund. Food, Nutrition, and the Prevention of Cancer: A Global Perspective. American Institute of Cancer Research. Washington, D.C.: 1997.
66. Cadogan J, Eastell R, Jones N, Barker ME. Milk intake and bone mineral acquisition in adolescent girls: randomised, controlled intervention trial. BMJ1997;315:1255-69.
67. Scott FW. Cow milk and insulin-dependent diabetes mellitus: is there a relationship? Am J Clin Nutr 1990;51:489-91.
68. Karjalainen J, Martin JM, Knip M, et al. A bovine albumin peptide as a possible trigger of insulin-dependent diabetes mellitus. N Engl J Med 1992;327:302-7.
69. Feskanich D, Willet WC, Stampfer MJ, Colditz GA. Milk, dietary calcium, and bone fractures in women: a 12-year prospective study. Am J Public Health 1997;87:992-7.
70. Cumming RG, Klineberg RJ. Case-control study of risk factors for hip fractures in the elderly. Am J Epidemiol 1994;139:493-505.
71. Huang Z, Himes JH, McGovern PG. Nutrition and subsequent hip fracture risk among a national cohort of white women. Am J Epidemiol 1996;144:124-34.
72. Cummings SR, Nevitt MC, Browner WS, et al. Risk factors for hip fracture in white women. N Engl J Med 1995;332:767-73.
73. Finn SC. The skeleton crew: is calcium enough? J Women’s Health 1998;7(1):31-6.
74. Nordin CBE. Calcium and osteoporosis. Nutrition 1997;3(7/8):664-86.
75. Reid DM, New SA. Nutritional influences on bone mass. Proceed Nutr Soc 1997;56:977-87.
76. Tucker KL, Hannan MR, Chen H, Cupples LA, Wilson PWF, Kiel DP. Potassium, magnesium, and fruit and vegetable intakes are associated with greater bone mineral density in elderly men and women. Am J Clin Nutr 1999;69:727-36.
77. Prince R, Devine A, Dick I, et al. The effects of calcium supplementation (milk powder or tablets) and exercise on bone mineral density in postmenopausal women. J Bone Miner Res 1995;10:1068-75.
78. The Cornell-China-Oxford Project. The China Study- Dr. T .Colin Campbell 2006
The industry wide shockwaves expected will assist in bringing US production regulations closer to that of our trading partners. In Europe and Canada US dairy exports recently have faced increasing resistance because of the refusal by American producers to discontinue using the hormone. European and Canadian authorities banned the hormone, recognize RBST as a threat to human health and have linked it to cancer. Several years ago documents came to public attention that showed Monsanto lied about their studies in order to gain approval from the FDA. The evidence on this is stunning and I have included an exhaustive list of references and hope that everyone gives them at least a quick glance.[1-58]
The good news for the consumers and the cows is not in any case good news for Monsanto, they are going to lose billions of dollars. Monsanto is the only supplier of the hormone, sold under the name Posilac, and sales have been estimated at close to $300 million annually, although Monsanto refuses disclosure of actual figures. Monsanto Corporation, in case anyone has forgotten, is that esteemed member of the American corporate community that has brought us such wonders as Agent Orange, Roundup and is the world's leader in GMO's (genetically modified organism).
RBST or Posilac is also an excellent example of corporate welfare. Posilac causes cows to produce more milk. So... what is wrong with that you ask? American taxpayers pay farmers not to produce milk and have been doing so for years. [59] There is an excess of dairy products in this country and our government buys it using our money. They buy it to keep the prices stable. If the supply exceeds demand, the price of dairy drops. The government steps in and keeps product from reaching the market. It ends up in government warehouses where much of it is simply thrown away. This is where “government cheese” came from. What is not eaten by our poor, elderly, and native populations ends up in the trash. Do you think that Monsanto cares about the fact that their product is contributing to this? I think Monsanto sees the bottom line.
The trouble with this continues because not only has Posilac been recognized as a human health threat, but so is the milk it helps produce more of! Dairy proteins and fats have been linked to heart disease, stroke [60,6], cancer [62-66], diabetes (types 1&2) [67,68], multiple sclerosis, arthritis, Crohn’s disease, irritable bowl syndrome, fibromyalgia, osteoporosis [69-78], and more. So where did Monsanto get the bright idea for such a great product? Since great minds think alike, maybe it was a friend of one of Monsanto’s other top executives; Donald Rumsfeld was a CEO for Monsanto. Hmmmm.
My hat is off to the California dairy producers for standing up to Monsanto and their money grubbing schemes regardless of the reason. It is a rare day when I have anything positive to say about the dairy industry, today just happens to be one of them.
References
1. Conyers, John. Letter to Richard R. Kusserow, Inspector General, Department of
Health and Human Services. May 9, 1990.
2. Kennelly J & DeBoer G. Bovine somatotropin. In Proceedings of the Alberta Dairy Seminar. Banff, Alberta, March 9-11, 1998.
3. Baer RJ, et al. Composition and flavor of milk produced by cows injected with recombinant bovine somatotropin. Journal of Dairy Science 72:1424-1434, 1989.
4. Capuco, AV et al. Somatotropin increases thyroxine-5’-monodeiodinase activity in lactating mammary tissue of the cow. Journal of Endocrinology 121(2):205-211, 1989.
5. Epstein, SS. Potential public health hazards of biosynthetic milk hormones.
International Journal of Health Services 20:73-84, 1990.
6. Kronfeld, DS. Safety of bovine growth hormone. Science 251:256-257, 1991.
7. U.S. General Accounting Office. rBGH. FDA Approval Should Be Withheld Until the Mastitis Issues is Resolved. 1992.
8. Mepham TB. Public health implications of bovine somatotropin use in dairying: discussion paper. Journal of the Royal Society of Medicine 85:736-739, 1992.
9. Millstone E, et al. Plagiarism or protecting public health? Nature 371:647-648, 1994.
10. U.S. General Accounting Office. Recombinant bovine growth hormone. FDA approval should be withheld until the mastitis issue is resolved. 1992.
11. Davis SR, et al. Effects of injecting growth hormone of thyroxine on milk production and blood plasma concentrations of insulin-like growth factors I and II in dairy cows.
Journal of Endocrinology 114:17-24, 1987.
12. Prosser CG, et al. Changes in concentrations of IGF-1 in milk during BGH treatment in the goat. Journal of Endocrinology 112 (March Supplement): Abstract 65, 1987.
13. McBride BW, et al. The influence of bovine growth hormone (somatotropin) on animals and their products. Research and Development in Agriculture 5:1-21, 1988. page 5
14. Francis GL, et al. Insulin-like growth factors 1 and 2 in bovine colostrum. Sequences and biological activities compared with those of a potent truncated form. Biochem J. 251:95-103, 1988.
15. Prosser CG, et al. Increased secretion of insulin-like growth factor-1 into Milk of cows treated with recombinantly derived bovine growth hormones. Journal of Dairy Research 56:17-26, 1989.
16. Juskevich JC & Guyer CG. Bovine growth hormone food safety evaluation.
Science 249:875-884, 1990.
17. National Institutes of Health. Technology Assessment Conference Statement on
Bovine Somatotropin. Journal of the American Medical Association 265:1423-1425, 1991.
18. Joint FAO/WHO Expert Committee on Food Additives (JECFA). Fortieth Report,
Geneva. June 9-18, 1992. Cited six unpublished industry studies confirming increased IGF-1 levels in rBGH milk. These included one by Monsanto (Schams et al, 1988) reporting a four-fold increase, and another (Miller et al, 1989) reporting a further 50% increase following pasteurization.
19. Epstein SS. BST and cancer. New Scientist U.K., October 29, 1994.
20. Mepham TB, et al. Safety of milk from cows treated with bovine somatotropin.
The Lancet 2:197, 1994
21. Mepham TB & Schofield PN. International Dairy Federation Nutrition Week, Paris, June 1995.
22. Epstein SS. Unlabeled milk from cows treated with biosynthetic growth hormones:
a case of regulatory abdication. International Journal of Health Services 261:173-185, 1996.
23. Furlanetto RW & DiCarlo JN. Somatotropin-C receptors and growth effects in human breast cells maintained in long-term tissue culture. Cancer Research 44:2122-2128, 1984.
24. Glimm DR, et al. Effect of bovine somatotropin in the distribution of immunoreactive insulin-like growth factor-1 in lactating bovine mammary tissue.
Journal of Dairy Science 71:2923-2935, 1988.
25. Reynolds RK, et al. Regulation of epidermal growth factor and insulin-like growth factors I receptors by estradiol and progesterone in normal and neoplastic endometrial cells cultures. Gynecology Oncology 38:396-406, 1990. page 6
26. Lippman A. Growth factors, receptors and breast cancer. National Institutes of Health Research 3:59-62, 1991.
27. Rosen N, et al. Insulin-like growth factors in human breast cancer. Breast Cancer Research Treatment 18 (Suppl):555-562, 1991.
28. Harris JR, et al. Breast Cancer. New England Journal of Medicine 7:473-480, 1992.
29. Pollak MN, et al. Tamoxifen reduced insulin-like growth factor-1 (IGF-1). Breast Cancer Research Treatment 22:91-100, 1992.
30. Lippman ME. The development of biological therapies for breast cancer. Science 259:631-632, 1993.
31. Pappa V, et al. Insulin-like growth facotr-1 receptors are over expressed and predict a low risk in human breast cancer. Cancer Research 53:3736-3740, 1993.
32. Bruning PF, et al. Insulin-like growth factor-binding protein 3 is decreased in early-stage operable pre-menopausal breast cancer. International Journal of Cancer 62(3):266-270, July 1995.
33. Epstein SS. Unlabeled milk from cows treated with biosynthetic growth hormones: a case of regulatory abdication. International Journal of Health Services 261:173-185, 1996.
34. LeRoith D. Insulin-like growth factors and cancer. Annals of Internal Medicine 122(1):54-59, January, 1995.
35. Bohlke K, et al. Insulin-like growth factor-1 in relation to premenopausal ductal carcinoma in situ of the breast. Epidemiology 9(5):570-573, 1998.
36. Del Giudice ME, et al. Insulin and related factors in premenopausal breast cancer risk. Breast Cancer Research and Treatment 47 (2):111-120, 1998.
37. Hankinson SE, et al. Circulating concentrations of insulin-like growth factor-1 and risk of breast cancer. The Lancet 351:1393-1396, 1998.
38. Agurs-Collins T, et al. Insulin-like growth factor-1 and breast cancer risk in post-menopausal American women. Proceedings of the American Association of Cancer Research 40:152, 1999.
39. Toniolo P, et al. Serum insulin-like growth factor-1 and breast cancer.
International Journal of Cancer 88(5):828-832, 2000.
40. Yu H & Rohan T. Role of the insulin-like growth factor family in cancer development and progression. Journal of the National Cancer Institute 92:1472-1484, 2000. page 7
41. Epstein SS. Re Role of the insulin-like growth factors in cancer development and progression. Journal of the National Cancer Institute 93(3):238, 2001.
42. Pines A, et al. Gastrointestinal tumors in acromegalic patients. Am J Gastroenterology 80:266-269, 1985.
43. Orme SM, et al. Cancer incidence and mortality in acromegaly: a retrospective cohort study. Journal of Endocrinology Supplement Number OC22, June 1996.
44. Epstein SS. Unlabeled milk from cows treated with biosynthetic growth hormones: a case of regulatory abdication. International Journal of Health Services 261:173-185, 1996.
45. Manousos O, et al. IGF-I and IGF-II in relation to colorectal cancer. International Journal of Cancer 83:15-17, 1999.
46. Ma J, et al. Prospective study of colorectal cancer risk in men and plasma levels of insulin-like growth factor-1 and IGF-1 binding protein-3. Journal of the National Cancer Institute 91:620-625, 1999.
47. Giovannucci E, et al. Plasma insulin-like growth factor-I and binding protein-3 and risk of colorectal cancer and adenoma in women. Proceedings of the American Association of Cancer Research 40:211, 1999.
48. Renehan AG, et al. Circulating insulin-like growth factor II and colorectal adenomas. Journal of Clinical Endocrinology & Metabolism 85(9):3402-3408, 2000.
49. Mantzoros CS, et al. Insulin-like growth factor 1 in relation to prostate cancer and benign prostatic hyperplasia. British Journal of Cancer 76:1115-1118, 1997.
50. Chan JM, et al. Plasma insulin-like growth factor-I and prostate cancer risk: a prospective study. Science 279:563-566, 1998.
51. Wolk A, et al. Insulin-like growth factor 1 and prostate cancer risk: a population-based, case-control study. Journal of the National Cancer Institute 90:911-915, 1998.
52. Signorello LB, et al. Insulin-like growth factor-binding protein-1 and prostate cancer.
Journal of the National Cancer Institute 91:1965-1967, 1999.
53. Stattin P, et al. Plasma insulin-like growth factor-binding proteins, and prostate
cancer risk: a prospective study. Journal of the National Cancer Institute 92:1910-1917, 2000.
54. Harman SM, et al. Serum levels of insulin-like growth factor I (IGF-1), IGF-II, IGF-binding protein-3, and prostate-specific antigen as predictors of clinical prostate cancer.
Journal of Clinical Endocrinology & Metabolism 85(11):4258-4265, 2000. page 8
55. Juul A, et al. The ratio between serum levels of IGF-1 and the IGF binding protein decreases with age in healthy patients and is increased in acromegalic patients. Clinical Endocrinology 41:85-93, 1994.
56. Tremble JM & McGregor AM. In Treating Acromegaly, editor Wass p. 5-12.
Journal of Endocrinology Ltd., Bristol, England, 1994.
57. Resnicoff M, et al. The insulin-like growth factor-I receptor protects tumor cells from apoptosis in vivo. Cancer Research 55(11):2463-2469, June 1,1995.
58. Epstein SS. Re: role of the insulin-like growth factor family in cancer development and progression. Journal of the National Cancer Institute 93(3):238, 2001
59. Milk Pricing in the United States. By Alden C. Manchester and Don P. Blayney.
Market and Trade Economics Division, Economic Research Service, U.S. Department
of Agriculture. Agriculture Information Bulletin No. 761.
60. Pennington JAT. Bowes and Churches Food Values of Portions Commonly Used, 17th ed. New York: Lippincott, 1998.
61. Ornish D, Brown SE, Scherwitz LW, Billings JH, Armstrong WT, Ports TA. Can lifestyle changes reverse coronary heart disease? Lancet 1990;336:129-33.
62. Cramer DW, Harlow BL, Willet WC. Galactose consumption and metabolism in relation to the risk of ovarian cancer. Lancet 1989;2:66-71.
63. Outwater JL, Nicholson A, Barnard N. Dairy products and breast cancer: the IGF-1, estrogen, and bGH hypothesis. Medical Hypothesis 1997;48:453-61.
64. Chan JM, Stampfer MJ, Giovannucci E, et al. Plasma insulin-like growth factor-1 and prostate cancer risk: a prospective study. Science 1998;279:563-5.
65. World Cancer Research Fund. Food, Nutrition, and the Prevention of Cancer: A Global Perspective. American Institute of Cancer Research. Washington, D.C.: 1997.
66. Cadogan J, Eastell R, Jones N, Barker ME. Milk intake and bone mineral acquisition in adolescent girls: randomised, controlled intervention trial. BMJ1997;315:1255-69.
67. Scott FW. Cow milk and insulin-dependent diabetes mellitus: is there a relationship? Am J Clin Nutr 1990;51:489-91.
68. Karjalainen J, Martin JM, Knip M, et al. A bovine albumin peptide as a possible trigger of insulin-dependent diabetes mellitus. N Engl J Med 1992;327:302-7.
69. Feskanich D, Willet WC, Stampfer MJ, Colditz GA. Milk, dietary calcium, and bone fractures in women: a 12-year prospective study. Am J Public Health 1997;87:992-7.
70. Cumming RG, Klineberg RJ. Case-control study of risk factors for hip fractures in the elderly. Am J Epidemiol 1994;139:493-505.
71. Huang Z, Himes JH, McGovern PG. Nutrition and subsequent hip fracture risk among a national cohort of white women. Am J Epidemiol 1996;144:124-34.
72. Cummings SR, Nevitt MC, Browner WS, et al. Risk factors for hip fracture in white women. N Engl J Med 1995;332:767-73.
73. Finn SC. The skeleton crew: is calcium enough? J Women’s Health 1998;7(1):31-6.
74. Nordin CBE. Calcium and osteoporosis. Nutrition 1997;3(7/8):664-86.
75. Reid DM, New SA. Nutritional influences on bone mass. Proceed Nutr Soc 1997;56:977-87.
76. Tucker KL, Hannan MR, Chen H, Cupples LA, Wilson PWF, Kiel DP. Potassium, magnesium, and fruit and vegetable intakes are associated with greater bone mineral density in elderly men and women. Am J Clin Nutr 1999;69:727-36.
77. Prince R, Devine A, Dick I, et al. The effects of calcium supplementation (milk powder or tablets) and exercise on bone mineral density in postmenopausal women. J Bone Miner Res 1995;10:1068-75.
78. The Cornell-China-Oxford Project. The China Study- Dr. T .Colin Campbell 2006
Tuesday, March 6, 2007
Arsenic Levels High in Chickens
Arsenic in Chicken
After reviewing 5000 chicken samples, researchers from the National Institutes of Health and the USDA's Food Safety Inspection Service recently reported alarmingly high levels of arsenic contamination in the flesh of broiler chickens[1] These government researchers found that the amount of arsenic in chicken greatly exceeded the Environmental Protection Agency's new upper safety limit of arsenic allowed in drinking water. In fact, the amount of arsenic found in chicken was 6 to 9 times that allowed by the EPA. A "bucket" of Kentucky Fried Chicken would be expected to have up to almost fifty times the amount of arsenic allowed in a glass of water.[2]
How did the arsenic get into the chickens? The poultry industry fed it to them. Most broiler chickens (which constitute 99% of the chicken meat that people eat) are fed arsenic in the United States[3,4] Although fish and shellfish also present significant dietary sources of arsenic,[6] according to the Food and Drug Administration arsenic compounds are extensively added to the feed of animals--particularly chickens and pigs--to make them grow faster.[5] The animals Americans eat are so heavily infested with internal parasites that adding arsenic to the feed can result in a "stunning" increase in growth rates.[7]
Dr. Ellen Silbergeld, a researcher from the Johns Hopkins School of Public Health, said the poultry industry's practice of using arsenic compounds in its feed is something that has not been studied. "It's an issue everybody is trying to pretend doesn't exist," she said.[8] "Arsenic acted as a growth stimulant in chickens -- develops the meat faster -- and since then, the poultry industry has gone wild using this ingredient," says Donald Herman, a Mississippi agricultural consultant and former Environmental Protection Agency researcher who has studied this use of arsenic for a decade. "And they've tried everything to refrain it from becoming public knowledge,".[9]
The poultry industry argues that the organic form of arsenic given to chickens isn't toxic.[10] "This study appears to be much ado about nothing," says Richard Lobb, the public relations Director of the National Chicken Council. He says the less toxic form of arsenic is "used responsibly and safely by poultry producers."[11] The researchers, however, found not only elevated levels of organic arsenic in chicken meat, they found elevated levels of the highly toxic inorganic form typically used only in insecticides and weed killers.[12] And cooking the muscles of these animals may create additional toxic arsenic by-products.[13]
Inorganic arsenic is considered one of the prominent environmental causes of cancer mortality in the world.[14] Arsenic is a human carcinogen linked to liver, lung, skin, kidney, bladder and prostate cancers. It can also cause neurological, cardiovascular, gastrointestinal and immune system abnormalities. Diabetes has also been linked to arsenic exposure.[15]
The feeding of arsenic to chickens in the U.S. releases hundreds of tons of arsenic into the environment every year in the form of poultry manure which is spread on fields as fertilizer.[16] In fact there's currently a coalition of families suffering serious health conditions suing chicken producers like Tyson after research showed cancer rates as much as 50 times above the national average in communities neighboring factory farmed poultry operations.
The February 2004 Medical Letter on the CDC & FDA concludes "Chicken consumption may contribute significant amounts of arsenic to total arsenic exposure of the U.S. population..." Levels of arsenic in chicken are so high that other sources may have to be monitored carefully to prevent undue toxic exposure among the population.[17]
1 Environmental Health Perspectives 112(2004):18.
2 One KFC bucket contains 3 legs, 3 breasts, 3 wings and 3 thighs [http://cspinet.org/new/pdf/letter_to_ftc.pdf] weighing a total of 1176 grams [http://www.yum.com/nutrition/documents/kfc_nutrition.pdf] containing up to 108.5 mcg of inorganic arsenic [Environmental Health Perspectives 112(2004):18] exceeding to EPA limit on an 8oz. glass of water by a factor of 48.4 [EPA 815- Z- 01- 001].
3 Momplaisir, G. M; C. G. Rosal; E. M. Heithmar ˆíArsenic Speciation Methods for Studying the Environmental Fate of Organoarsenic Animal- Feed Additives,ˆì U. S. EPA, NERL- Las Vegas, 2001; (TIM No. 01- 11)
4 Medical Letter on the CDC & FDA February 1, 2004
5 Momplaisir, G. M; C. G. Rosal; E. M. Heithmar ˆíArsenic Speciation Methods for Studying the Environmental Fate of Organoarsenic Animal- Feed Additives,ˆì U. S. EPA, NERL- Las Vegas, 2001; (TIM No. 01- 11)
6 Ibid.
7 Texas Lawyer, January 23, 1995
8 Daily Times (Salisbury, MD) January 4, 2004
9 Texas Lawyer, January 23, 1995
10 Daily Times (Maryland) 11 January 2004.
11 Health Day News 19 January 2004.
12 Environmental Health Perspectives 112(2004):18.
13 Hanaoka, K., Goessler, W., Ohno, H., Irgolic, K. J., and Kaise, T., (2001). Formation of toxic arsenical in roasted muscles of marine animals, Appl. Organometal. Chem., 15: 61- 66.
14 Smith, A.H., C. Hopenhayn-Rich, M.L. Bates, H.M. Goeden, I. HertzPicciotto, H.M. Duggan, R. Wood, M.J. Kosnett, and M.T. Smith. 1992. Cancer risks from arsenic in drinking water. Environmental Health Perspectives 97, 259-267.
15 Momplaisir, G. M; C. G. Rosal; E. M. Heithmar ˆíArsenic Speciation Methods for Studying the Environmental Fate of Organoarsenic Animal- Feed Additives,ˆì U. S. EPA, NERL- Las Vegas, 2001; (TIM No. 01- 11)
16 Ibid.
17 Medical Letter on the CDC & FDA February 1, 2004
After reviewing 5000 chicken samples, researchers from the National Institutes of Health and the USDA's Food Safety Inspection Service recently reported alarmingly high levels of arsenic contamination in the flesh of broiler chickens[1] These government researchers found that the amount of arsenic in chicken greatly exceeded the Environmental Protection Agency's new upper safety limit of arsenic allowed in drinking water. In fact, the amount of arsenic found in chicken was 6 to 9 times that allowed by the EPA. A "bucket" of Kentucky Fried Chicken would be expected to have up to almost fifty times the amount of arsenic allowed in a glass of water.[2]
How did the arsenic get into the chickens? The poultry industry fed it to them. Most broiler chickens (which constitute 99% of the chicken meat that people eat) are fed arsenic in the United States[3,4] Although fish and shellfish also present significant dietary sources of arsenic,[6] according to the Food and Drug Administration arsenic compounds are extensively added to the feed of animals--particularly chickens and pigs--to make them grow faster.[5] The animals Americans eat are so heavily infested with internal parasites that adding arsenic to the feed can result in a "stunning" increase in growth rates.[7]
Dr. Ellen Silbergeld, a researcher from the Johns Hopkins School of Public Health, said the poultry industry's practice of using arsenic compounds in its feed is something that has not been studied. "It's an issue everybody is trying to pretend doesn't exist," she said.[8] "Arsenic acted as a growth stimulant in chickens -- develops the meat faster -- and since then, the poultry industry has gone wild using this ingredient," says Donald Herman, a Mississippi agricultural consultant and former Environmental Protection Agency researcher who has studied this use of arsenic for a decade. "And they've tried everything to refrain it from becoming public knowledge,".[9]
The poultry industry argues that the organic form of arsenic given to chickens isn't toxic.[10] "This study appears to be much ado about nothing," says Richard Lobb, the public relations Director of the National Chicken Council. He says the less toxic form of arsenic is "used responsibly and safely by poultry producers."[11] The researchers, however, found not only elevated levels of organic arsenic in chicken meat, they found elevated levels of the highly toxic inorganic form typically used only in insecticides and weed killers.[12] And cooking the muscles of these animals may create additional toxic arsenic by-products.[13]
Inorganic arsenic is considered one of the prominent environmental causes of cancer mortality in the world.[14] Arsenic is a human carcinogen linked to liver, lung, skin, kidney, bladder and prostate cancers. It can also cause neurological, cardiovascular, gastrointestinal and immune system abnormalities. Diabetes has also been linked to arsenic exposure.[15]
The feeding of arsenic to chickens in the U.S. releases hundreds of tons of arsenic into the environment every year in the form of poultry manure which is spread on fields as fertilizer.[16] In fact there's currently a coalition of families suffering serious health conditions suing chicken producers like Tyson after research showed cancer rates as much as 50 times above the national average in communities neighboring factory farmed poultry operations.
The February 2004 Medical Letter on the CDC & FDA concludes "Chicken consumption may contribute significant amounts of arsenic to total arsenic exposure of the U.S. population..." Levels of arsenic in chicken are so high that other sources may have to be monitored carefully to prevent undue toxic exposure among the population.[17]
1 Environmental Health Perspectives 112(2004):18.
2 One KFC bucket contains 3 legs, 3 breasts, 3 wings and 3 thighs [http://cspinet.org/new/pdf/letter_to_ftc.pdf] weighing a total of 1176 grams [http://www.yum.com/nutrition/documents/kfc_nutrition.pdf] containing up to 108.5 mcg of inorganic arsenic [Environmental Health Perspectives 112(2004):18] exceeding to EPA limit on an 8oz. glass of water by a factor of 48.4 [EPA 815- Z- 01- 001].
3 Momplaisir, G. M; C. G. Rosal; E. M. Heithmar ˆíArsenic Speciation Methods for Studying the Environmental Fate of Organoarsenic Animal- Feed Additives,ˆì U. S. EPA, NERL- Las Vegas, 2001; (TIM No. 01- 11)
4 Medical Letter on the CDC & FDA February 1, 2004
5 Momplaisir, G. M; C. G. Rosal; E. M. Heithmar ˆíArsenic Speciation Methods for Studying the Environmental Fate of Organoarsenic Animal- Feed Additives,ˆì U. S. EPA, NERL- Las Vegas, 2001; (TIM No. 01- 11)
6 Ibid.
7 Texas Lawyer, January 23, 1995
8 Daily Times (Salisbury, MD) January 4, 2004
9 Texas Lawyer, January 23, 1995
10 Daily Times (Maryland) 11 January 2004.
11 Health Day News 19 January 2004.
12 Environmental Health Perspectives 112(2004):18.
13 Hanaoka, K., Goessler, W., Ohno, H., Irgolic, K. J., and Kaise, T., (2001). Formation of toxic arsenical in roasted muscles of marine animals, Appl. Organometal. Chem., 15: 61- 66.
14 Smith, A.H., C. Hopenhayn-Rich, M.L. Bates, H.M. Goeden, I. HertzPicciotto, H.M. Duggan, R. Wood, M.J. Kosnett, and M.T. Smith. 1992. Cancer risks from arsenic in drinking water. Environmental Health Perspectives 97, 259-267.
15 Momplaisir, G. M; C. G. Rosal; E. M. Heithmar ˆíArsenic Speciation Methods for Studying the Environmental Fate of Organoarsenic Animal- Feed Additives,ˆì U. S. EPA, NERL- Las Vegas, 2001; (TIM No. 01- 11)
16 Ibid.
17 Medical Letter on the CDC & FDA February 1, 2004
Rocket Fuel in Milk Could Harm Children
Rocket Fuel in Milk
The headline in the San Francisco Chronicle pretty much summed it up: "Rocket fuel found in milk in California: Not clear if amount imperils children."[1]
For decades the Pentagon has been contaminating the drinking water of hundreds of U.S. communities across at least 43 states with ammonium perchlorate, the main explosive component of solid missile fuel.[2]Utah, where NASA and the military test their rockets, recently saw a local news broadcast wherein grocery store milk samples were randomly tested and all turned up alarming levels of perchlorate. Not surprisingly, the Bush Administration, despite the fact that every milk sample taken in Bush's home state of Texas was also found to be perchlorate contaminated,[3] attempted once again this year[4] to exempt chemical companies and military contractors like Lockheed Martin and Morton Thiokol from cleaning up this toxic waste which, as Senator Barbara Boxer noted, is "endangering the health of millions of Americans."[5]
Perchlorate leaches into the irrigation water used to grow feed crops for cattle who can then concentrate this agent into their milk. Testing milk off California grocery store shelves for the first time, the Environmental Working Group (EWG) recently found that infants and children may be exposed to more of this toxic chemical than is considered safe by the U.S. Environmental Protection Agency (EPA)[6] and other independent scientific bodies.[7] The average 1-year-old in Southern California, for example, is estimated to be getting twice the EPA's "provisional daily safe dose." The EWG also unearthed previously unreleased tests done by the California Food and Agriculture Department that found an average level of perchlorate contamination in California milk over 5 times the EPA safety standard. Cheese, yogurt and other dairy products are likely to be as contaminated as milk.[8]
Scientists know that at the levels that were found in milk, perchlorate can affect a baby's ability to make essential thyroid hormones.[9,10] What we don't know is if the disruptions in thyroid hormone levels caused by milk would be enough to cause the lowered IQ, mental retardation, loss of hearing and speech, and motor skill deficits seen in thyroid deficient fetuses, infants, and children.
The spokesperson for the state's $4.5 billion dairy industry agrees with the California Ag department that there is a "paucity of science" as to the potential effects of children drinking rocket fuel chemicals.[11]Government and industry both admit, though, that there could be some risk, but that moms and kids should NOT stop drinking milk because of all its "calcium, protein and minerals."[12] Is that the choice our children get? Rocket fuel or malnutrition? Pouring fortified SOY milk on one's cereal, kids can get comparable amounts of protein and calcium and even more minerals--without the toxic waste.Rice milk, almond milk, oatmilk, hazelnut milk and soy, are available in stores everywhere. You don't have to be a rocket scientist to figure out the healthier choice.
1 San Francisco Chronicle 22 June 2004.
2 http://www.ewg.org/issues/perchlorate/20030715/index.php
3 http://www.ewg.org/issues/perchlorate/20030919/index.php
4 http://www.ewg.org/issues/perchlorate/20040420/index.php
5 http://www.ewg.org/issues/perchlorate/20030401/index.php
6 Environmental Protection Agency (EPA). 2002. Perchlorate Environmental Contamination. NCEA-1-0503.
7 Massachusetts Department Of Environmental Protection (MADEP). 2004a. Perchlorate Toxicological Profile And Health Assessment (Final Draft). Office of Research and Standards. May 2004. Available at http://www.mass.gov/dep/brp/dws/percinfo.htm
8 Los Angeles Times 22 June 2004
9 Journal of Occupational and Environmental Medicine 42(2000):777.
10 [24] Schwartz, J. 2001. Gestational exposure to perchlorate is associated with measures of decreased thyroid function in a population of California neonates [thesis]. Berkeley, CA: University of California.
11 Associated Press 22 June 2004.
12 Los Angeles Times 22 June 2004.
The headline in the San Francisco Chronicle pretty much summed it up: "Rocket fuel found in milk in California: Not clear if amount imperils children."[1]
For decades the Pentagon has been contaminating the drinking water of hundreds of U.S. communities across at least 43 states with ammonium perchlorate, the main explosive component of solid missile fuel.[2]Utah, where NASA and the military test their rockets, recently saw a local news broadcast wherein grocery store milk samples were randomly tested and all turned up alarming levels of perchlorate. Not surprisingly, the Bush Administration, despite the fact that every milk sample taken in Bush's home state of Texas was also found to be perchlorate contaminated,[3] attempted once again this year[4] to exempt chemical companies and military contractors like Lockheed Martin and Morton Thiokol from cleaning up this toxic waste which, as Senator Barbara Boxer noted, is "endangering the health of millions of Americans."[5]
Perchlorate leaches into the irrigation water used to grow feed crops for cattle who can then concentrate this agent into their milk. Testing milk off California grocery store shelves for the first time, the Environmental Working Group (EWG) recently found that infants and children may be exposed to more of this toxic chemical than is considered safe by the U.S. Environmental Protection Agency (EPA)[6] and other independent scientific bodies.[7] The average 1-year-old in Southern California, for example, is estimated to be getting twice the EPA's "provisional daily safe dose." The EWG also unearthed previously unreleased tests done by the California Food and Agriculture Department that found an average level of perchlorate contamination in California milk over 5 times the EPA safety standard. Cheese, yogurt and other dairy products are likely to be as contaminated as milk.[8]
Scientists know that at the levels that were found in milk, perchlorate can affect a baby's ability to make essential thyroid hormones.[9,10] What we don't know is if the disruptions in thyroid hormone levels caused by milk would be enough to cause the lowered IQ, mental retardation, loss of hearing and speech, and motor skill deficits seen in thyroid deficient fetuses, infants, and children.
The spokesperson for the state's $4.5 billion dairy industry agrees with the California Ag department that there is a "paucity of science" as to the potential effects of children drinking rocket fuel chemicals.[11]Government and industry both admit, though, that there could be some risk, but that moms and kids should NOT stop drinking milk because of all its "calcium, protein and minerals."[12] Is that the choice our children get? Rocket fuel or malnutrition? Pouring fortified SOY milk on one's cereal, kids can get comparable amounts of protein and calcium and even more minerals--without the toxic waste.Rice milk, almond milk, oatmilk, hazelnut milk and soy, are available in stores everywhere. You don't have to be a rocket scientist to figure out the healthier choice.
1 San Francisco Chronicle 22 June 2004.
2 http://www.ewg.org/issues/perchlorate/20030715/index.php
3 http://www.ewg.org/issues/perchlorate/20030919/index.php
4 http://www.ewg.org/issues/perchlorate/20040420/index.php
5 http://www.ewg.org/issues/perchlorate/20030401/index.php
6 Environmental Protection Agency (EPA). 2002. Perchlorate Environmental Contamination. NCEA-1-0503.
7 Massachusetts Department Of Environmental Protection (MADEP). 2004a. Perchlorate Toxicological Profile And Health Assessment (Final Draft). Office of Research and Standards. May 2004. Available at http://www.mass.gov/dep/brp/dws/percinfo.htm
8 Los Angeles Times 22 June 2004
9 Journal of Occupational and Environmental Medicine 42(2000):777.
10 [24] Schwartz, J. 2001. Gestational exposure to perchlorate is associated with measures of decreased thyroid function in a population of California neonates [thesis]. Berkeley, CA: University of California.
11 Associated Press 22 June 2004.
12 Los Angeles Times 22 June 2004.
Monday, March 5, 2007
Hotdogs and Cured Meats Linked to Chlidhood Brain Tumors
Childhood Brain Tumors and Maternal Diet
Cancer is second only to accidents as a leading cause of death for our children these days. Brain tumors are the most common solid form of pediatric cancer. The development of childhood brain tumors is a chief reason why pregnant women no longer get X-rayed. Evidence has been building, though, that the mother's diet during pregnancy also plays a significant role.
Nitrites are found naturally in cigarette smoke and are artificially added to cured meats like bacon and bologna. They increase the shelf life of lunch meats, but seem to decrease the human life of those that consume them. They also may cause brain tumors.
A recent review of ten major epidemiological studies found that eight of them showed significant associations between maternal intake of cured meats during pregnancy and the risk of giving birth to a baby that would develop a brain tumor, usually within the first 5 years of life. Mothers eating lots of foods like sausages, ham, hot dogs, etc. had up to 6 times higher risk. The nitrites in meat under extreme chemical conditions (like in the acidity of the stomach) react with amides like creatine and creatinine (also found in meat) to create potent carcinogens called nitrosamides. The researcher suspect that the "nitrosamides formed endogenously in the mother's stomach could also be transported transplacentally to the brain of the embryo or fetus, passing the blood brain barrier, and resulting in brain tumor development in the child."[18]
In terms of other dietary factors, most of the studies that measured fruit and vegetable intake found (not surprisingly) that both fruit and vegetable intake during pregnancy seemed protective. Not all plant foods were found protective, though. A study published last month from the Children's Hospital of Philadelphia, found that unhealthy plant foods like french fries may also increase risk.[19] But otherwise, fruits and vegetables were found protective across a wide variety of tumors. One study published Summer 2005, for example, found that fruits and vegetable consumption even proved protective against retinoblastoma, a rare form of brain tumor that forms on the back of the eye and for which treatment typically requires the removal of one or both of the child's eyes.[20]
[18] Dietrich M, et al. 2005. A review: dietary and endogenously formed N-nitroso compounds and risk of childhood brain tumors. Cancer Causes and Control 16(2005):619-35.
[19] Bunin GR. Maternal diet during pregnancy and its association with medulloblastoma in children. Cancer Causes and Control (2005) 16:877-91.
[20] Orjuela MA, et al. 2005. Fruit and vegetable intake during pregnancy and risk for development of sporadic retinoblastoma. Cancer, Epidemiology, Biomarkers and Prevention 14(6):1433-40.
Cancer is second only to accidents as a leading cause of death for our children these days. Brain tumors are the most common solid form of pediatric cancer. The development of childhood brain tumors is a chief reason why pregnant women no longer get X-rayed. Evidence has been building, though, that the mother's diet during pregnancy also plays a significant role.
Nitrites are found naturally in cigarette smoke and are artificially added to cured meats like bacon and bologna. They increase the shelf life of lunch meats, but seem to decrease the human life of those that consume them. They also may cause brain tumors.
A recent review of ten major epidemiological studies found that eight of them showed significant associations between maternal intake of cured meats during pregnancy and the risk of giving birth to a baby that would develop a brain tumor, usually within the first 5 years of life. Mothers eating lots of foods like sausages, ham, hot dogs, etc. had up to 6 times higher risk. The nitrites in meat under extreme chemical conditions (like in the acidity of the stomach) react with amides like creatine and creatinine (also found in meat) to create potent carcinogens called nitrosamides. The researcher suspect that the "nitrosamides formed endogenously in the mother's stomach could also be transported transplacentally to the brain of the embryo or fetus, passing the blood brain barrier, and resulting in brain tumor development in the child."[18]
In terms of other dietary factors, most of the studies that measured fruit and vegetable intake found (not surprisingly) that both fruit and vegetable intake during pregnancy seemed protective. Not all plant foods were found protective, though. A study published last month from the Children's Hospital of Philadelphia, found that unhealthy plant foods like french fries may also increase risk.[19] But otherwise, fruits and vegetables were found protective across a wide variety of tumors. One study published Summer 2005, for example, found that fruits and vegetable consumption even proved protective against retinoblastoma, a rare form of brain tumor that forms on the back of the eye and for which treatment typically requires the removal of one or both of the child's eyes.[20]
[18] Dietrich M, et al. 2005. A review: dietary and endogenously formed N-nitroso compounds and risk of childhood brain tumors. Cancer Causes and Control 16(2005):619-35.
[19] Bunin GR. Maternal diet during pregnancy and its association with medulloblastoma in children. Cancer Causes and Control (2005) 16:877-91.
[20] Orjuela MA, et al. 2005. Fruit and vegetable intake during pregnancy and risk for development of sporadic retinoblastoma. Cancer, Epidemiology, Biomarkers and Prevention 14(6):1433-40.
Dairy and Prostate Cancer
Prostate Cancer and Milk
Prostate cancer is now the single most common cancer among men in the United States and is on the rise in almost every country in the world as they adopt a more meat and dairy centered diet.[4] Does drinking cow milk really increase a man's risk for developing this killer cancer, though? Yes, according to a meta-analysis of 11 independent studies published summer 2004. Milk-drinking men seem to have about a 70% greater chance of developing cancer of the prostate. In fact the case against milk is so strong and consistent that even if 50 new studies came out all failing to show any link between milk and prostate cancer, the balance of evidence would still indict milk as a significant cancer risk factor.[5]
Although the butterfat in dairy may play a role, the researchers blame the hormones in milk as the likely culprit. "Because commercial milk is mainly produced by pregnant cows in developed countries," the researchers claim, "it contains considerable amounts of estrogen." Combined with other growth hormones in the milk designed to make a calf gain 100 pounds in 50 days,[6] cow milk may promote the growth of hormone-sensitive cancers.
Milk is for babies.
[4] European Journal of Cancer 37(2001):S4
[5] Nutrition and Cancer 48(2004):22
[6] NorthEast DairyBusiness August 2002:24
Prostate cancer is now the single most common cancer among men in the United States and is on the rise in almost every country in the world as they adopt a more meat and dairy centered diet.[4] Does drinking cow milk really increase a man's risk for developing this killer cancer, though? Yes, according to a meta-analysis of 11 independent studies published summer 2004. Milk-drinking men seem to have about a 70% greater chance of developing cancer of the prostate. In fact the case against milk is so strong and consistent that even if 50 new studies came out all failing to show any link between milk and prostate cancer, the balance of evidence would still indict milk as a significant cancer risk factor.[5]
Although the butterfat in dairy may play a role, the researchers blame the hormones in milk as the likely culprit. "Because commercial milk is mainly produced by pregnant cows in developed countries," the researchers claim, "it contains considerable amounts of estrogen." Combined with other growth hormones in the milk designed to make a calf gain 100 pounds in 50 days,[6] cow milk may promote the growth of hormone-sensitive cancers.
Milk is for babies.
[4] European Journal of Cancer 37(2001):S4
[5] Nutrition and Cancer 48(2004):22
[6] NorthEast DairyBusiness August 2002:24
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