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The Case for a Vegan World

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ArgumentsEdit

  1. Diets High in Fat, Especially Animal Fat, Greatly Increase The Risk of Breast Cancer
  2. Consumption of animal fat and the hormones contained within it, cause development changes in humans, e.g. Early Puberty
  3. Premarin, the hormone replacement treatment made from pregnant mares urine increases the risk of vaginal bleeding, uterine and breast cancer
  4. Milk increases the risk of Ovarian Cancer in Women
  5. A low fat Vegan diet rich in soy products with phytoestrogens can help prevent and deal with the symptoms of menopause because it will regulate eostrogen levels at a moderate level
  6. A low fat Vegan diet with plenty of fibre reduces period pain because it regulates eostrogen levels and the fibre will soak up excess oestrogen excreted by the liver
  7. Polychlorinated biphenyls and organochlorines cause Endomytriosis in humans, they commonly accumulate in the fat of animals humans use for food and in their milk. Fish consumption is an especial risk.
  8. Polychlorinated biphenyls and organochlorines are excreted from the bodies of nursing mothers through their breast milk, poisoning the infant.
  9. The consumption of dairy products increases the risk of ovarian cancer
  10. Meat eaters have higher risk of impotence
  11. The consumption of animal fats greatly increases the risk of prostate cancer because fats carry hormones such as dihydrotestosterone around the body and feed hormonal cancers. The consumption of certain plant derived substances can help to manage the disease when it appears (saw palmetto, cold pressed flax seed oil, Vitamins B and E)

ObjectionsEdit

  1. Organic Meat?

References for the ArgumentsEdit

  1. http://www.cancerproject.org/survival/cancer_facts/breast.php Armstrong B, Doll R. Environmental factors and cancer incidence and mortality in different countries, with special reference to dietary practices. Int J Cancer 1975;15:617-31. Hirayama T. Epidemiology of breast cancer with special reference to the role of diet. Prev Med 1978;7:173-95. Lands WEM, Hamazaki T, Yamazaki K, et al. Changing dietary patterns. Am J Clin Nutr 1990;51:991-3. Carroll KK, Braden LM. Dietary fat and mammary carcinogenesis. Nutrition and Cancer 1985;6:254-9. Rose DP, Boyar AP, Wynder EL. International comparisons of mortality rates for cancer of the breast, ovary, prostate, and colon, and per capita food consumption. Cancer 1986;58:2363-71. 83. Verreault R, Brisson J, Deschenes L, Naud F, Meyer F, Belanger L. Dietary fat in relation to prognostic indicators in breast cancer. J Natl Cancer Inst 1988;80:819-25. Newman SC, Miller AB, Howe CR. A study of the effect of weight and dietary fat on breast cancer survival time. Am J Epidemiol 1986;123:767-74. Holm LE, Callmer E, Hjalmar ML, Lidbrink E, Nilsson B, Skoog L. Dietary habits and prognostic factors in breast cancer. J Natl Cancer Inst 1989;81:1218-23. Donegan WL, Hartz AJ, Rimm AA. The association of body weight with recurrent cancer of the breast. Cancer 1978;41:1590-4. Schapira DV, Kumar NB, Lyman GH, Cox CE. Obesity and body fat distribution and breast cancer prognosis. Cancer 1991;67:523-8.

1A 15 November 2006: WOMEN who eat red meat more than once a day double the risk of getting the most common form of breast cancer, doctors have found. A study of pre-menopausal women examined the effect of diet on different types of breast cancer and found that those who ate the most meat - especially in processed forms such as hamburgers and sausages - were at the greatest risk of hormone-sensitive breast cancers. The natural female hormones oestrogen and progesterone are essential for a range of bodily functions but are also responsible for stimulating growth in 70 per cent of breast cancers - those known as hormone receptor positive. Eunyoung Cho, associate professor of medicine at Harvard Medical School, who led the study, said there were several reasons red meat triggered this type of breast cancer. They included the treatment of American beef cattle with hormones to speed up growth, carcinogens created when meat was cooked at high temperatures and the presence of a certain form of iron in meat. More than 90,600 pre-menopausal American nurses aged 26 to 46 filled in questionnaires about their diets between 1991 and 1999, according to Archives of Internal Medicine, which published the research. Twelve years after the start of the study researchers identified 1021 cases of breast cancer in the group. Women who ate more than 1½ servings of red meat a day (where a serving is defined as the main part of a dish) were 97 per cent more likely to have a hormone receptor positive breast cancer than those who ate three or fewer servings a week. The increased risk for those who said they had between three and five servings a week was 42 per cent. Women who had meat in processed form such as sausages, salami and mortadella more than three times a week were 2.3 times more likely to get a hormone receptor positive cancer than those who ate them less than once a month. Those who ate hamburgers between one and three times a week were 71 per cent more likely than those who did so less than once a month. There was little difference in the risk of hormone receptor positive breast cancer between those was ate unprocessed beef, pork or lamb between one and three times a week and those who did so less than once a month. Dr Cho checked to ensure that causes of breast cancer such as obesity, smoking, alcohol and family medical history were not the real causes of the increased risks. Telegraph, London

  1. Refs needed here
  2. http://www.pcrm.org/magazine/GM02Autumn/GM02Autumn08.html http://www.pcrm.org/health/prevmed/menopause.html Colditz GA, Stampfer MJ, Willett WC, et al. Type of postmenopausal hormone use and risk of breast cancer: 12-year follow-up from the Nurses’ Health Study. Cancer Causes and Control 1992;3:433-9. Yang CP, Daling JR, Band PR, Gallagher RP, White E, Weiss NS. Noncontraceptive hormone use and risk of breast cancer. Cancer Causes and Control 1992;3:475-9. Bergkvist L, Adami HO, Persson I, Hoover R, Schairer C. The risk of breast cancer after estrogen and estrogen-progestin replacement. N Engl J Med 1989;321:293-7.
  3. Refs needed here
  4. http://www.pcrm.org/health/prevmed/menopause.html http://www.pcrm.org/magazine/GM02Autumn/GM02Autumn08.html
  5. http://www.pcrm.org/magazine/GM02Autumn/GM02Autumn08.html http://www.pcrm.org/health/prevmed/menstrual_pain.html Merskey H, Bogduk N (eds). Classification of Chronic Pain, 2nd edition. Seattle: IASP Press, 1994, pp. 164-6. Chan WY. Prostaglandins and nonsteroidal antiinflammatory drugs in dysmenorrhea. Ann Rev Pharmacol Toxicol 1983;23:131-49. Ylikorkala O, Dawood MY. New concepts in dysmenorrhea. Am J Obstet Gynecol 1978;130:833-47. Prentice R, Thompson D, Clifford C, Gorbach S, Goldin B, Byar D. Dietary fat reduction and plasma estradiol concentration in healthy postmenopausal women. J Natl Cancer Inst 1990;82:129-34.
  6. http://www.pcrm.org/health/prevmed/endometriosis.html Ahlborg UG, Lipworth L, Titus-Ernstoff L, et al. Organochlorine compounds in relation to breast cancer, endometrial cancer, and endometriosis: an assessment of the biological and epidemiological evidence. Crit Rev Toxicol 1995;25:463-531. Moen MH, Magnus P. The familial risk of endometriosis. Acta Obstet Gynecol Scand 1993;72:560-4. Mangtani P, Booth M. Epidemiology of endometriosis. J Epidem Comm Health 1993;47:84-8. Dmowski WP. Immunological aspects of endometriosis. Int J Gynecol Obstet 1995;50 (Suppl 1):S3-10. Balasch J, Creus M, Fabregues F, et al. Visible and non-visible endometriosis at laparoscopy in fertile and infertile women and in patients with chronic pelvic pain: a prospective study. Human Repro 1996;11:387-91. Holloway M. An epidemic ignored: endometriosis linked to dioxin and immunologic dysfunction. Sci Am 1994;270:24-6. Koninckx PK, Braet P, Kennedy SH, Barlow DH. Dioxin pollution and endometriosis in Belgium. Human Reproduction 1994;9:1001-2. Hergenrather J, Hlady G, Wallace B, Savage E. Pollutants in breast milk of vegetarians. N Engl J Med 1981;304:792. Dawood MY. Considerations in selecting appropriate medical therapy for endometriosis. Int J Gynecol Obstet 1993;40(suppl):S29-S42. Revelli A, Modotti M, Ansaldi C, Massobrio M. Recurrent endometriosis: a review of biological and clinical aspects. Obstet Gynecol Survey 1995;50:747-54.
  7. http://www.pcrm.org/health/prevmed/endometriosis.html Ahlborg UG, Lipworth L, Titus-Ernstoff L, et al. Organochlorine compounds in relation to breast cancer, endometrial cancer, and endometriosis: an assessment of the biological and epidemiological evidence. Crit Rev Toxicol 1995;25:463-531. Koninckx PK, Braet P, Kennedy SH, Barlow DH. Dioxin pollution and endometriosis in Belgium. Human Reproduction 1994;9:1001-2. Hergenrather J, Hlady G, Wallace B, Savage E. Pollutants in breast milk of vegetarians. N Engl J Med 1981;304:792.
  8. http://www.pcrm.org/health/cancerproject/women.html Cramer DW, Harlow BL, Willett WC, et al. Galactose consumption and metabolism in relation to the risk of ovarian cancer. Lancet 1989;2:66-71.
  9. Refs needed here
  10. http://www.pcrm.org/health/prevmed/prostate.html Kolonel LN. Nutrition and prostate cancer. Cancer Causes and Control 1996;7:83-94. Giovannucci E, Rimm EB, Colditz GA, et al. A prospective study of dietary fat and risk of prostate cancer. J Natl Cancer Inst 1993;85:1571-9. Whittemore AS, Kolonel LN, Wu AH, et al. Prostate cancer in relation to diet, physical activity, and body size in blacks, white, and Asians in the United States and Canada. J Natl Cancer 1995;87:652-61. Armstrong B, Doll R. Environmental factors and cancer incidence and mortality in different countries, with special reference to dietary practices. Int J Cancer 1975;15:617-31. Hirayama T. Epidemiology of prostate cancer with special reference to the role of diet. Natl Cancer Inst Monogr 1979;53:149-54. National Research Council. Diet, Nutrition, and Cancer. Washington, D.C.: National Academy Press, 1982. Phillips RL. Role of life-style and dietary habits in risk of cancer among Seventh-day Adventists. Cancer Research 1975;35:3513-22. Mills P, Beeson WL, Phillips RL, Fraser GE. Cohort study of diet, lifestyle, and prostate cancer in Adventist men. Cancer 1989;64:598-604. Breslow N, Chan CW, Dhom G, et al. Latent carcinoma of prostate at autopsy in seven areas. Int J Cancer 1977;20:680-8. Howie BJ, Shultz TD. Dietary and hormonal interrelationships among vegetarian Seventh-day Adventists and nonvegetarian men. Am J Clin Nutr 1985;42:127-34. Hamalainen EK, Adlercreutz H, Puska P, Pietinen P. Decrease of serum total and free testosterone during a low-fat high-fibre diet. J Steroid Biochem 1983;18:369-70. Hill PB, Wynder EL. Effect of a vegetarian diet and dexamethasone on plasma prolactin, testosterone and dehydroepiandrosterone in men and women. Cancer Lett 1979;7:273-82. Liang T, Liao S. Inhibition of steroid 5a-reductase by specific aliphatic unsaturated fatty acids. Biochem J 1992;285:557-62. Cohen P. Serum insulin-like growth factor-I levels and prostate cancer risk—interpreting the evidence. J Natl Cancer Inst 1998;90:876-9. Mantzoros CS, Tzonou A, Signorello LB, Stampfer M, Trichopoulos D, Adami HO. Insulin-like growth factor I in relation to prostate cancer and benign prostatic hyperplasia. Br J Cancer 1997;76:1115-8. Chan JM, Stampfer MJ, Giovannucci E, et al. Plasma insulin-like growth factor-I and prostate cancer risk: a prospective study. Science 1998;279:563-6. Wolk A, Mantzoros CS, Andersson SO, et al. Insulin-like growth factor I and prostate cancer risk: a population-based, case control study. J Natl Cancer Inst 1998;90:911-5. Lwamura M, Sluss PM, Casamento JB, Cockett ATK. Insulin-like growth factor I: action and receptor characterization in human prostate cancer cell lines. Prostate 1993;22:243-52. Culig Z, Hobisch A, Cronauer MV, et al. Androgen receptor activation in prostatic tumor cell lines by insulin-like growth factor-I, keratinocyte growth factor, and epidermal growth factor. Eur Urol 1995;27(suppl 2):45-7. World Cancer Research Fund/American Institute for Cancer Research. Food, Nutrition, and the Prevention of Cancer: A Global Perspective. American Institute for Cancer Research. Washington, D.C., 1997, p. 461. Cadogan J, Eastell R, Jones N, Barker ME. Milk intake and bone mineral acquisition in adolescent girls: randomised, controlled intervention trial. BMJ1997;315:1255-60. Heaney RP, McCarron DA, Dawson-Hughes B, et al. Dietary changes favorably affect bone remodeling in older adults. J Am Dietetic Asso 1999;99:1228-33. Kontessis PS, Trevisan R, Bossinakou I, et al. Renal, metabolic, and hormonal responses to proteins of different origin in normotensive, nonproteinuric type I diabetic patients. Diabetes Care 1995;18:1233-40. Araki H, Watanabe H, Mishina T, Nakao M. High-risk group for benign prostatic hypertrophy. Prostate 1983;4:253-64. Walker M. Serenoa repens extract (Saw palmetto) relief for benign prostatic hypertrophy (BPH). Townsend Letter for Doctors: 1991;2-3:107-10; Perlmutter D. LifeGuide. Naples, FL, LifeGuide Press, 1994.

References for the ObjectionsEdit

Examples and AnecdotesEdit

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