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In The China Study, T. Colin Campbell, PhD and Thomas M. Campbell II, MD detail the connection between nutrition and heart disease, diabetes, and cancer. Recognized as the most comprehensive nutritional study ever conducted on the relationship between diet and the risk of developing disease, The China Study cuts through the haze of misinformation and examines the source of nutritional confusion produced by government entities, lobbies, and opportunistic scientists. Our China Study Reference library provides links to the on-line abstracts of the studies used in each chapter.
Chapter 1

American Cancer Society. “Cancer Facts and Figures”1998.” Atlanta, GA: American Cancer Society, 1998.

Flegal KM, Carroll MD, Ogden CL, et al. “Prevalence and trends in obesity among U.S. adults, 1999–2000.” JAMA 288 (2002): 1723–1727.

National Center for Health Statistics. “Obesity still on the rise, new data show. The U.S. Department of Health and Human Services News Release.” October 10, 2003. Washington, DC: 2002. Accessed atwww.cdc.gov/nchs/releases/02news/obesityonrise.htm

Lin B-H, Guthrie J, and Frazao E. ”Nutrient Contribution of Food Away from Home.” In: E. Frazao (ed.), America’s Eating Habits: Changes and Consequences. Washington, DC: Economic Research Service, USDA, 1999. Cited on p. 138 in: Information Plus. Nutrition: a key to good health. Wylie, TX: Information Plus, 1999.

Mokdad AH, Ford ES, Bowman BA, et al. “Diabetes trends in the U.S.: 1990–1998.” Diabetes Care 23 (2000): 1278–1283.

Centers for Disease Control and Prevention. “National Diabetes Fact Sheet: National Estimates and General Information on Diabetes in the United States, Revised Edition.” Atlanta, GA: Centers for Disease Control and Prevention, 1998.

American Diabetes Association. “Economic consequences of diabetes mellit in the U.S. in 1997.”Diabetes Care 21 (1998): 296–309. Cited In: Mokdad AH, Ford ES, Bowman BA, et al. “Diabetes trends in the U.S.: 1990–1998.” Diabetes Care 23 (2000): 1278–1283.

American Heart Association. ”Heart Disease and Stroke Statistics—2003 Update.” Dallas, TX: American Heart Association, 2002.

Ornish D, Brown SE, Scherwitz LW, et al. “Can lifestyle changes reverse coronary heart disease?” Lancet 336 (1990): 129–133.

Esselstyn CB, Ellis SG, Medendorp SV, et al. ”A strategy to arrest and reverse coronary artery disease: a 5-year longitudinal study of a single physician’s practice.” J. Family Practice 41 (1995): 560–568.

Starfield B. “Is U.S. health really the best in the world?” JAMA 284 (2000): 483–485.

Anderson RN. “Deaths: leading causes for 2000.” National Vital Statistics Reports 50(16) (2002):

Phillips D, Christenfeld N, and Glynn L. “Increase in U.S. medication-error death between 1983 and 1993.” Lancet 351 (1998): 643–644.

U.S. Congressional House Subcommittee Oversight Investigation. “Cost and quality of health care: unnecessary surgery.” Washington, DC: 1976. Cited by: Leape, L. “Unnecessary surgery.” Ann. Rev. Publ. Health 13 (1992): 363–383.

Lazarou J, Pomeranz B, and Corey PN. “Incidence of adverse drug reactions in hospitalized patients.”JAMA 279 (1998): 1200–1205.

World Health Organization. Technical Report Series No. 425. “International Drug Monitoring: the Role of the Hospital.” Geneva, Switzerland: World Health Organization, 1966.

Health Insurance Association of America. Source Book of Health Insurance Data: 1999–2000.Washington, DC, 1999.

National Center for Health Statistics. Health, United States, 2000 with Adolescent Health Chartbook.Hyattsville, MD: National Center for Health Statistics, 2000.

Starfield B. Primary Care: Balancing Health Needs, Services, and Technology. New York, NY: Oxford University Press, 1998.

World Health Organization. World Health Report 2000: Press release. ”World Health Organization assesses the world’s health systems.” June 21, 2000. Geneva. Accessed at www.who.int

Coble YD. American Medical Association press release. “AMA decries rise in number of uninsured Americans.” September 30, 2003. Chicago, IL. Accessed at www.ama-assn.org/ama/pub/article/1617–8064.html

Campbell TC. “Present day knowledge on aflatoxin.” Phil J Nutr 20 (1967): 193–201.

Campbell TC, Caedo JP, Jr., Bulatao-Jayme J, et al. “Aflatoxin M1 in human urine.” Nature 227 (1970): 403–404.

This program was conducted in collaboration with the Philippine Department of Health and was funded by the United States Agency for International Development (USAID). USAID paid my full salary for six years and resulted in 110 “mother craft centers” distributed around much of the Philippines. Progress on this contract was prepared as monthly reports to USAID by Associate Dean C.W. Engel at Virginia Tech.

Hu J, Zhao X, Jia J, et al. “Dietary calcium and bone density among middle-aged and elderly women in China.” Am. J. Clin. Nutr. 58 (1993): 219–227.

Hu J, Zhao X, Parpia B, et al. “Dietary intakes and urinary excretion of calcium and acids: a cross-sectional study of women in China.” Am. J. Clin. Nutr. 58 (1993): 398–406.

Hu J, Zhao X, Parpia B, et al. “Assessment of a modified household food weighing method in a study of bone health in China.” European J. Clin. Nutr. 48 (1994): 442–452.

Potischman N, McCulloch CE, Byers T, et al. “Breast cancer and dietary and plasma concentrations of carotenoids and vitamin A.” Am. J. Clin. Nutr. 52 (1990): 909–915.

Potischman N, McCulloch CE, Byers T, et al. ”Associations between breast cancer, triglycerides and cholesterol.” Nutr. Cancer 15 (1991): 205–215.

Chen J, Campbell TC, Li J, et al. Diet, life-style and mortality in China. A study of the characteristics of 65 Chinese counties. Oxford, UK; Ithaca, NY; Beijing, PRC: Oxford University Press; Cornell University Press; People’s Medical Publishing House, 1990.

Campbell TC, and Chen J. “Diet and chronic degenerative diseases:perspectives from China.” Am. J. Clin. Nutr. 59 (Suppl.) (1994): 1153S–1161S.

Campbell TC. “The dietary causes of degenerative diseases: nutrients vs foods.” In: N. J. Temple and D. P. Burkitt (eds.), Western diseases: their dietary prevention and reversibility, pp. 119–152. Totowa, NJ: Humana Press, 1994.

Campbell TC, and Chen J. “Diet and chronic degenerative diseases: a summary of results from an ecologic study in rural China.” In: N. J. Temple and D. P. Burkitt (eds.), Western diseases: their dietary prevention and reversibility, pp. 67–118. Totowa, NJ: Humana Press, 1994.

Chittenden RH. Physiological economy in nutrition. New York: F.A. Stokes, 1904.

Chittenden RH. The nutrition of man. New York: F. A. Stokes, 1907.

Chapter 2

Stillings BR. “World supplies of animal protein.” In: J. W. G. Porter and B. A. Rolls (eds.), Proteins in Human Nutrition, pp. 11–33. London: Academic Press, 1973.

Campbell TC, Warner RG, and Loosli JK. “Urea and biuret for ruminants.” In: Cornell Nutri•tion Conference, Buffalo, NY, 1960, pp. 96–103.

Campbell TC, Loosli JK, Warner RG, et al. “Utilization of biuret by ruminants.” J. Animal Science 22 (1963): 139–145.

Autret M. “World protein supplies and needs. Proceedings of the Sixteenth Easter School in Agricultural Science, University of Nottingham, 1969.” In: R. A. Laurie (ed.), Proteins in Hu•man Food, pp. 3–19. Westport, CT.: Avi Publishing Company, 1970.

Scrimshaw NS, and Young VR. “Nutritional evaluation and the utilization of protein resourc•es.” In: C. E. Bodwell (ed.), Evaluation of Proteins for Humans, pp. 1–10. Westport, CT: The Avi Publishing Co., 1976.

Jalil ME, and Tahir WM. “World supplies of plant proteins.” In: J. W. G. Porter and B. A. Rolls (eds.), Proteins in Human Nutrition, pp. 35–46. London: Academic Press, 1973.

Blount WP. “Turkey “X” Disease.” Turkeys 9 (1961): 52, 55–58, 61, 77.

Sargeant K, Sheridan A, O’Kelly J, et al. “Toxicity associated with certain samples of ground•nuts.” Nature 192 (1961): 1096–1097.

Lancaster MC, Jenkins FP, and Philp JM. “Toxicity associated with certain samples of ground•nuts.” Nature 192 (1961): 1095–1096.

Wogan GN, and Newberne PM. “Dose-response characteristics of aflatoxin B1 carcinogenesis in the rat.” Cancer Res. 27 (1967): 2370–2376.

Wogan GN, Paglialunga S, and Newberne PM. “Carcinogenic effects of low dietary levels of aflatoxin B1 in rats.” Food Cosmet. Toxicol. 12 (1974): 681–685.

Campbell TC, Caedo JP, Jr., Bulatao-Jayme J, et al. “Aflatoxin M1 in human urine.” Nature 227 (1970): 403–404.

Madhavan TV, and Gopalan C. “The effect of dietary protein on carcinogenesis of aflatoxin.” Arch. Path. 85 (1968): 133–137.

Chapter 3

Natural Resources Defense Council. “Intolerable risk: pesticides in our children’s food.” New York: Natural Resources Defense Council, February 27, 1989.

Winter C, Craigmill A, and Stimmann M. “Food Safety Issues II. NRDC report and Alar.” UC Davis Environmental Toxicology Newsletter 9(2) (1989): 1.

Lieberman AJ, and Kwon SC. “Fact versus fears: a review of the greatest unfounded health scares of recent times.” New York: American Council on Science and Health, June, 1998.

Whelan EM, and Stare FJ. Panic in the pantry: facts and fallacies about the food you buy. Buffalo, NY: Prometheus Books, 1992.

U.S. Apple Association. “News release: synopsis of U.S. Apple Press Conference.” McLean, VA: U.S. Apple Association, February 25, 1999.

Cassens RG. Nitrite-cured meat: a food safety issue in perspective. Trumbull, CT: Food and Nutrition Press, Inc., 1990.

Lijinsky W,  and Epstein SS. “Nitrosamines as environmental carcinogens.” Nature 225 (1970): 21–23.

National Toxicology Program. “Ninth report on carcinogens, revised January 2001.” Wash•ington, DC: U.S. Department of Health and Human Services, Public Health Service, January, 2001. Accessed atehis.niehs.nih.gov/roc/toc9.html

International Agency for Cancer Research. IARC Monographs on the Evaluation of the Car•cinogenic Risk of Chemicals to Humans: Some N-Nitroso Compounds. Vol. 17 Lyon, France: International Agency for Research on Cancer, 1978.

Druckrey H, Janzowski R, and Preussmann R. “Organotrope carcinogene wirkungen bei 65 verschiedenen N-nitroso-verbindungen an BD-ratten.” Z. Krebsforsch. 69 (1967): 103–201.

Thomas C, and So BT. “Zur morphologie der durch N-nitroso-verbindungen erzeugten tumo•ren im oberen verdauungstrakt der ratte.” Arzneimittelforsch. 19 (1969): 1077–1091.

Eisenbrand G, Spiegelhalder B, Janzowski C, et al. “Volatile and non-volatile N-nitroso com•pounds in foods and other environmental media.” IARC Sci. Publi. 19 (1978): 311–324.

National Archives and Records Administration. “Code of Federal Regulations: Title 9, Ani•mals and Animal Products, Section 319.180 (9CFR319.180).” Washington, DC: Government Printing Office, 2001.

Kanfer S. October 2, 1972. “The decline and fall of the American hot dog.” Time: 86.

Newberne P. “Nitrite promotes lymphoma incidence in rats.” Science 204 (1979): 1079– 1081

Madhavan TV, and Gopalan C. “The effect of dietary protein on carcinogenesis of aflatoxin.” Arch. Path. 85 (1968): 133–137

If this defect becomes part of the first round of daughter cells, then this will be passed on to all subsequent generations of cells, with the potential to eventually become clinically detect•able cancer. However, this is an oversimplification of a very complex process. Perhaps two of the more significant omissions are the hypotheses that 1) more than one mutation may be required to initiate and promote cancer, and 2) not all genetic defects result in cancer.

Mgbodile MUK, and Campbell TC. “Effect of protein deprivation of male weanling rats on the kinetics of hepatic microsomal enzyme activity.” J. Nutr. 102 (1972): 53–60.

Hayes JR, Mgbodile MUK, and Campbell TC. “Effect of protein deficiency on the inducibility of the hepatic microsomal drug-metabolizing enzyme system. I. Effect on substrate interac•tion with cytochrome P-450.” Biochem. Pharmacol. 22 (1973): 1005–1014.

Mgbodile MUK, Hayes JR, and Campbell TC. “Effect of protein deficiency on the inducibility of the hepatic microsomal drug-metabolizing enzyme system. II. Effect on enzyme kinetics and electron transport system.” Biochem. Pharmacol. 22 (1973): 1125–1132.

Hayes JR, and Campbell TC. “Effect of protein deficiency on the inducibility of the hepatic microsomal drug-metabolizing enzyme system. III. Effect of 3-methylcholanthrene induction on activity and binding kinetics.” Biochem. Pharmacol. 23 (1974): 1721–1732.

Campbell TC. “Influence of nutrition on metabolism of carcinogens (Martha Maso Honor’s Thesis).” Adv. Nutr. Res. 2 (1979): 29–55.

Preston RS, Hayes JR, and Campbell TC. “The effect of protein deficiency on the in vivo bind•ing of aflatoxin B1 to rat liver macromolecules.” Life Sci. 19 (1976): 1191–1198.

Portman RS, Plowman KM, and Campbell TC. “On mechanisms affecting species susceptibil•ity to aflatoxin.” Biochim. Biophys. Acta 208 (1970): 487–495.

Prince LO, and Campbell TC. “Effects of sex difference and dietary protein level on the binding of aflatoxin B1 to rat liver chromatin proteins in vivo.” Cancer Res. 42 (1982): 5053– 5059.

Mainigi KD, and Campbell TC. “Subcellular distribution and covalent binding of aflatoxins as functions of dietary manipulation.” J Toxicol. Eviron. Health 6 (1980): 659–671.

Nerurkar LS, Hayes JR, and Campbell TC. “The reconstitution of hepatic microsomal mixed function oxidase activity with fractions derived from weanling rats fed different levels of protein.” J. Nutr. 108 (1978): 678–686.

Gurtoo HL, and Campbell TC. “A kinetic approach to a study of the induction of rat liver microsomal hydroxylase after pretreatment with 3,4-benzpyrene and aflatoxin B1.” Biochem. Pharmacol. 19 (1970): 1729–1735.

Adekunle AA, Hayes JR, and Campbell TC. “Interrelationships of dietary protein level, afla•toxin B1 metabolism, and hepatic microsomal epoxide hydrase activity.” Life Sci. 21 (1977): 1785–1792.

Mainigi KD, and Campbell TC. “Effects of low dietary protein and dietary aflatoxin on he•patic glutathione levels in F-344 rats.” Toxicol. Appl. Pharmacol. 59 (1981): 196–203.

Farber E, and Cameron R. “The sequential analysis of cancer development.” Adv. Cancer Res. 31 (1980): 125–226.

Foci response for the various charts in this chapter mostly reflect “% of liver volume,” which integrates “number of foci” and “size of foci,” both of which indicate tumor-forming ten•dency. So that the responses from individual experiments can be compared among each other, the data are adjusted to a common scale that reflects the response produced by a standard dose of aflatoxin and by feeding a 20% protein diet.

Appleton BS, and Campbell TC. “Inhibition of aflatoxin-initiated preneoplastic liver lesions by low dietary protein.” Nutr. Cancer 3 (1982): 200–206.

Dunaif GE, and Campbell TC. “Relative contribution of dietary protein level and Aflatoxin B1 dose in generation of presumptive preneoplastic foci in rat liver.” J. Natl. Cancer Inst. 78 (1987): 365–369.

Youngman LD, and Campbell TC. “High protein intake promotes the growth of preneoplastic foci in Fischer #344 rats: evidence that early remodeled foci retain the potential for future growth.” J. Nutr. 121 (1991): 1454–1461.

Youngman LD, and Campbell TC. “Inhibition of aflatoxin B1-induced gamma-glutamyl transpeptidase positive (GGT+) hepatic preneoplastic foci and tumors by low protein diets: evidence that altered GGT+ foci indicate neoplastic potential.” Carcinogenesis 13 (1992): 1607–1613.

Dunaif GE, and Campbell TC. “Dietary protein level and aflatoxin B1-induced preneoplastic hepatic lesions in the rat.” J. Nutr. 117 (1987): 1298–1302.

Horio F, Youngman LD, Bell RC, et al. “Thermogenesis, low-protein diets, and decreased de•velopment of AFB1-induced preneoplastic foci in rat liver.” Nutr. Cancer 16 (1991): 31–41.

About 12% dietary protein is required to maximize growth rate, according to the National Research Council of the National Academy of Sciences.

Subcommittee on Laboratory Animal Nutrition. Nutrient requirements of laboratory animals. Second revised edition, number 10. Washington, DC: National Academy Press, 1972.

National Research Council. Recommended dietary allowances. Tenth edition. Washington, DC: National Academy Press, 1989.

Schulsinger DA, Root MM, and Campbell TC. “Effect of dietary protein quality on develop•ment of aflatoxin B1-induced hepatic preneoplastic lesions.” J. Natl. Cancer Inst. 81 (1989): 1241–1245.

Youngman LD. The growth and development of aflatoxin B1-induced preneoplastic lesions, tumors, metastasis, and spontaneous tumors as they are influenced by dietary protein level, type, and intervention. Ithaca, NY: Cornell University, Ph.D. Thesis, 1990.

Beasley RP. “Hepatitis B virus as the etiologic agent in hepatocellular carcinoma-epidemiologic considerations.” Hepatol. 2 (1982): 21S–26S.

Blumberg BS, Larouze B, London WT, et al. “The relation of infection with the hepatitis B agent to primary hepatic carcinoma.” Am. J. Pathol. 81 (1975): 669–682.

Chisari FV, Ferrari C, and Mondelli MU. “Hepatitis B virus structure and biology.” Microbiol. Pathol. 6 (1989): 311–325.

Hu J, Cheng Z, Chisari FV, et al. “Repression of hepatitis B virus (HBV) transgene and HBV-induced liver injury by low protein diet.” Oncogene 15 (1997): 2795–2801.

Cheng Z, Hu J, King J, et al. “Inhibition of hepatocellular carcinoma development in hepatitis B virus transfected mice by low dietary casein.” Hepatology 26 (1997): 1351–1354.

Hawrylewicz EJ, Huang HH, Kissane JQ, et al. “Enhancement of the 7,12-dimethylbenz(a)a nthracene (DMBA) mammary tumorigenesis by high dietary protein in rats.” Nutr. Reps. Int. 26 (1982): 793–806.

Hawrylewicz EJ. “Fat-protein interaction, defined 2-generation studies.” In: C. Ip, D. F. Birt, A. E. Rogers and C. Mettlin (eds.), Dietary fat and cancer, pp. 403–434. New York: Alan R. Liss, Inc., 1986.

Huang HH, Hawrylewicz EJ, Kissane JQ, et al. “Effect of protein diet on release of prolactin and ovarian steroids in female rats.” Nutr. Rpts. Int. 26 (1982): 807–820.

O’Connor TP, Roebuck BD, and Campbell TC. “Dietary intervention during the post-dosing phase of L-azaserine-induced preneoplastic lesions.” J Natl Cancer Inst 75 (1985): 955–957.

O’Connor TP, Roebuck BD, Peterson F, et al. “Effect of dietary intake of fish oil and fish protein on the development of L-azaserine-induced preneoplastic lesions in rat pancreas.” J Natl Cancer Inst 75 (1985): 959–962.

He Y. Effects of carotenoids and dietary carotenoid extracts on aflatoxin B1-induced mutagenesis and hepatocarcinogenesis. Ithaca, NY: Cornell University, PhD Thesis, 1990.

He Y, and Campbell TC. “Effects of carotenoids on aflatoxin B1-induced mutagenesis in S. typhimurium TA 100 and TA 98.” Nutr. Cancer 13 (1990): 243–253.

Chapter 4

Li J-Y, Liu B-Q, Li G-Y, et al. “Atlas of cancer mortality in the People’s Republic of China. Anaid for cancer control and research.” Int. J. Epid. 10 (1981): 127–133.

Higginson J. “Present trends in cancer epidemiology.” Proc. Can. Cancer Conf. 8 (1969):40–75.

Wynder EL, and Gori GB. “Contribution of the environment to cancer incidence: an epidemiologic exercise.” J. Natl. Cancer Inst. 58 (1977): 825–832.

Doll R, and Peto R. “The causes of cancer: Quantitative estimates of avoidable risks of cancer in the Unites States today.” J Natl Cancer Inst 66 (1981): 1192–1265.

Fagin D. News release. “Breast cancer cause still elusive study: no clear link between pollution,breast cancer on LI.” August 6, 2002. Newsday.com. Accessed athttp://www.newsday.com/news/local/longisland/ny-licanc062811887aug06.story?coll=ny%2Dtop%2Dheadlines

There were 82 mortality rates, but about a third of these rates were duplicates of the samedisease for different aged people.

Calorie intake in China is for a 65 kg adult male doing “light physical work.” Comparabledata for the American male is adjusted for a body weight of 65 kg.

SerVaas C. ”Diets that protected against cancers in China.” The Saturday Evening Post October1990: 26–28.

All the available disease mortality rates were arranged in a matrix so that it was possible to readily determine the relationship of each rate with every other rate. Each comparison was then assigned a plus or minus, depending on whether they were directly or inversely correlated. All plus correlations were assembled in one list and all minus correlations wereassembled in a second list. Each individual entry in either list was therefore positively relatedto entries in its own list but inversely related to diseases in the opposite list. Most, but not all,of these correlations were statistically significant.

Campbell TC, Chen J, Brun T, et al. “China: from diseases of poverty to diseases of affluence. Policy implications of the epidemiological transition.” Ecol. Food Nutr. 27 (1992): 133–144.

Chen J, Campbell TC, Li J, et al. Diet, life-style and mortality in China. A study of the characteristics of 65 Chinese counties. Oxford, UK; Ithaca, NY; Beijing, PRC: Oxford University Press;Cornell University Press; People’s Medical Publishing House, 1990.

Lipid Research Clinics Program Epidemiology Committee. “Plasma lipid distributions in selected North American Population. The Lipid Research Clinics Program Prevalence Study.”Circulation 60 (1979): 427–439.

Campbell TC, Parpia B, and Chen J. “Diet, lifestyle, and the etiology of coronary artery disease:The Cornell China Study.” Am. J. Cardiol. 82 (1998): 18T-21T.

These data are for villages SA, LC and RA for women and SA, QC and NB for men, as seen in the monograph (Chen, et al. 1990)

Sirtori CR, Noseda G, and Descovich GC. “Studies on the use of a soybean protein diet forthe management of human hyperlipoproteinemias.” In: M. J. Gibney and D. Kritchevsky(eds.), Current Topics in Nutrition and Disease, Volume 8: Animal and Vegetable Proteins in Lipid Metabolism and Atherosclerosis., pp. 135–148. New York, NY: Alan R. Liss, Inc., 1983.

Carroll KK. “Dietary proteins and amino acids - their effects on cholesterol metabolism.” In:M. J. Gibney and D. Kritchevsky (eds.), Animal and Vegetable Proteins in Lipid Metabolism and Atherosclerosis, pp. 9–17. New York, NY: Alan R. Liss, Inc., 1983.

Terpstra AHM, Hermus RJJ, and West CE. “Dietary protein and cholesterol metabolism in rabbits and rats.” In: M. J. Gibney and D. Kritchevsky (eds.), Animal and Vegetable Proteins in Lipid Metabolism and Athersclerosis, pp. 19–49. New York: Alan R. Liss, Inc., 1983.

Kritchevsky D, Tepper SA, Czarnecki SK, et al. “Atherogenicity of animal and vegetable protein. Influence of the lysine to arginine ratio.” Atherosclerosis 41 (1982): 429–431.

Dietary fat can be expressed as percent of total weight of the diet or as percent of total calories.Most commentators and researchers express fat as percent of total calories because we primarily consume food to satisfy our need for calories, not our need for weight. I will do the same throughout this book.

National Research Council. Diet, Nutrition and Cancer. Washington, DC: National Academy Press, 1982.

United States Department of Health and Human Services. The Surgeon General’s Report on Nutrition and Health. Washington, DC: Superintendant of Documents, U.S. Government Printing Office, 1988.

National Research Council, and Committee on Diet and Health. Diet and health: implications for reducing chronic disease risk. Washington, DC: National Academy Press, 1989.

Expert Panel. Food, nutrition and the prevention of cancer, a global perspective. Washington,DC: American Institute for Cancer Research/World Cancer Research Fund, 1997.

Exceptions include those foods artificially stripped of their fat, such as non-fat milk.

Armstrong D, and Doll R. “Environmental factors and cancer incidence and mortality in different countries, with special reference to dietary practices.” Int. J. Cancer 15 (1975):617–631.

U.S. Senate. “Dietary goals for the United States, 2nd Edition.” Washington, DC: U.S. Government Printing Office, 1977.

Committee on Diet Nutrition and Cancer. Diet, nutrition and cancer: directions for research.Washington, DC: National Academy Press, 1983.

There also were a number of other policy statements and large human studies that were begun at about this time that were to receive much public discussion and that were founded and/or interpreted in relation to dietary fat and these diseases. These included the initiationof the U.S. Dietary Guidelines report series begun in 1980, the Harvard Nurses’ Health Studyin 1984, the initial reports of the Framingham Heart Study in the 1960s, the Seven CountriesStudy of Ancel Keys, the Multiple Risk Factor Intervention Trial (MRFIT) and others.

Carroll KK, Braden LM, Bell JA, et al. “Fat and cancer.” Cancer 58 (1986): 1818–1825.

Drasar BS, and Irving D. “Environmental factors and cancer of the colon and breast.” Br. J.Cancer 27 (1973): 167–172.

Haenszel W, and Kurihara M. “Studies of Japanese Migrants: mortality from cancer and other disease among Japanese and the United States.” J Natl Cancer Inst 40 (1968): 43–68.

Higginson J, and Muir CS. “Epidemiology in Cancer.” In: J. F. Holland and E. Frei (eds.),Cancer Medicine, pp. 241–306. Philadelphia, PA: Lea and Febiger, 1973.

The correlation of fat intake with animal protein intake is 84% for grams of fat consumed and 70% for fat as a percent of calories.376 The China Study

Kelsey JL, Gammon MD, and Esther MJ. “Reproductive factors and breast cancer.” Epidemiol.Revs. 15 (1993): 36–47.

de Stavola BL, Wang DY, Allen DS, et al. “The association of height, weight, menstrual and reproductive events with breast cancer: results from two prospective studies on the island of Guernsey (United Kingdom).” Cancer Causes and Control 4 (1993): 331–340.

Rautalahti M, Albanes D, Virtamo J, et al. ”Lifetime menstrual activity—indicator of breast cancer risk.”(1993): 17–25

It was not possible to statistically detect an association of blood hormone levels with breast cancer risk within this group of women because their blood samples were taken at random times of their menstrual cycles and breast cancer rates were so low, thus minimizing the abilityto detect such an association, even when real.

Key TJA, Chen J, Wang DY, et al. “Sex hormones in women in rural China and in Britain.”Brit. J. Cancer 62 (1990): 631–636.

These biomarkers include plasma copper, urea nitrogen, estradiol, prolactin, testosterone and, inversely, sex hormone binding globulin, each of which has been known to be associated with animal protein intake from previous studies.

For the total dietary fiber (TDF), the averages for China and the U.S. were 33.3 and 11.1grams per day, respectively. The range of the county averages are 7.7–77.6 grams per day in China, compared with a range of 2.4–26.6 grams per day for the middle 90% of American males.

The correlation for plant protein was +0.53*** and for animal protein was +0.12.

In principle, using “cancer prevalence within families” as the outcome measurement more effectively controls for the various causes of cancer that associate with different kinds of cancer,thus permitting study of an isolated effect of the dietary factor.

Guo W, Li J, Blot WJ, et al. “Correlations of dietary intake and blood nutrient levels with esophageal cancer mortality in China.” Nutr. Cancer 13 (1990): 121–127.

The full effects of these fat-soluble antioxidants can be demonstrated only when antioxidan tconcentrations are adjusted for the levels of LDL for individual subjects. This was not known at the time of the survey, thus provisions were not made for this adjustment.

Kneller RW, Guo W, Hsing AW, et al. “Risk factors for stomach cancer in sixty-five Chinese counties.”Cancer Epi. Biomarkers Prev. 1 (1992): 113–118.

Information Plus. Nutrition: a key to good health. Wylie, TX: Information Plus, 1999.

Westman EC, Yancy WS, Edman JS, et al. “Carbohydrate Diet Program.” Am. J. Med. 113(2002): 30–36.

Atkins RC. Dr. Atkins’ New Diet Revolution. New York, NY: Avon Books, 1999.

Wright JD, Kennedy-Stephenson J, Wang CY, et al. “Trends in Intake of Energy and Macronutrients—United States, 1971–2000.” Morbidity and mortality weekly report 53 (February 6,2004): 80–82.

Noakes M, and Clifton PM. “Weight loss and plasma lipids.” Curr. Opin. Lipidol. 11 (2000):65–70.

Bilsborough SA, and Crowe TC. “Low-carbohydrate diets: what are the potential short- and long-term health implications?” Asia Pac. J. Clin. Nutr. 12 (2003): 396–404.

Stevens A, Robinson DP, Turpin J, et al. “Sudden cardiac death of an adolescent during dieting.” South. Med. J. 95 (2002): 1047–1049.

Patty A. “Low-carb fad claims teen’s life – Star diet blamed in death.” The Daily Telegraph(Sidney, Australia) November 2, 2002: 10.

Atkins, 1999. Page 275.

Atkins claims that an antioxidant cocktail can protect against heart disease, cancer and aging,a claim refuted by several large trials recently completed (see chapter 11).

Atkins, 1999. Page 103.

Bone J. “Diet doctor Atkins ‘obese’, had heart problems: coroner: Widow angrily denies that opponents’ claims that heart condition caused by controversial diet.” Ottawa Citizen February 11, 2004: A11.

Campbell TC. “Energy balance: interpretation of data from rural China.” Toxicological Sciences 52 (1999): 87–94.

Horio F, Youngman LD, Bell RC, et al. “Thermogenesis, low-protein diets, and decreased development of AFB1-induced preneoplastic foci in rat liver.” Nutr. Cancer 16 (1991): 31–41.

Krieger E, Youngman LD, and Campbell TC. “The modulation of aflatoxin (AFB1) induced preneoplastic lesions by dietary protein and voluntary exercise in Fischer 344 rats.” FASEB J.2 (1988): 3304 Abs.

The cited associations of total animal and plant protein intakes are taken from manuscript under review.62. Campbell TC, Chen J, Liu C, et al. “Non-association of aflatoxin with primary liver cancer ina cross-sectional ecologic survey in the People’s Republic of China.” Cancer Res. 50 (1990):6882–6893.

Chapter 5

Adams CF. “How many times does your heart beat per year?” Accessed October 20, 2003.Accessed athttp://www.straightdope.com/classics/a1_088a.htm

National Heart, Lung, and Blood Institute. “Morbidity and Mortality: 2002 Chart Book on Cardiovascular,Lung, and Blood Diseases.” Bethesda, MD: National Institutes of Health, 2002.

American Heart Association. “Heart Disease and Stroke Statistics-2003 Update.” Dallas, TX:American Heart Association, 2002.

Braunwald E. “Shattuck lecture-cardiovascular medicine at the turn of the millenium: triumphs,concerns and opportunities.” New Engl. J. Med. 337 (1997): 1360–1369.

American Cancer Society. “Cancer Facts and Figures-1998.” Atlanta, GA: American Cancer Society, 1998.

Anderson RN. “Deaths: leading causes for 2000.” National Vital Statistics Reports 50(16)(2002):

Enos WE, Holmes RH, and Beyer J. “Coronary disease among United States soldiers killed in action in Korea.” JAMA 152 (1953): 1090–1093.

Esselstyn CJ. “Resolving the coronary artery disease epidemic through plant-based nutrition.” Prev. Cardiol. 4 (2001): 171–177.

Antman EM, and Braunwald E. “Acute myocardial infarction.” In: E. Braunwald (ed.), Heartdisease, a textbook of cardiovascular disease, Vol. II (Fifth Edition), pp. 1184–1288. Philadelphia:W.B. Saunders Company, 1997.

Esselstyn CJ. “Lecture: Reversing heart disease.” December 5, 2002. Ithaca, NY: Cornell University,2002.

Ambrose JA, and Fuster V. “Can we predict future acute coronary events in patients with stable coronary artery disease?” JAMA 277 (1997): 343–344.

Forrester JS, and Shah PK. “Lipid lowering versus revascularization: an idea whose time (fortesting) has come.” Circulation 96 (1997): 1360–1362.

Now named the National Heart, Lung, and Blood Institute of the National Institutes of Health in Bethesda, Maryland.

Gofman JW, Lindgren F, Elliot H, et al. “The role of lipids and lipoproteins in atherosclerosis.” Science 111 (1950): 166.

Kannel WB, Dawber TR, Kagan A, et al. “Factors of risk in the development of coronary heart disease”six-year follow-up experience.” Ann. Internal Medi. 55 (1961): 33–50.

Jolliffe N, and Archer M. “Statistical associations between international coronary heart disease death rates and certain environmental factors.” J. Chronic Dis. 9 (1959): 636–652.

Scrimgeour EM, McCall MG, Smith DE, et al. “Levels of serum cholesterol, triglyceride, HDL cholesterol, apolipoproteins A-1 and B, and plasma glucose, and prevalence of diastolic hypertension and cigarette smoking in Papua New Guinea Highlanders.” Pathology 21 (1989):46–50.

Campbell TC, Parpia B, and Chen J. “Diet, lifestyle, and the etiology of coronary artery disease:The Cornell China Study.” Am. J. Cardiol. 82 (1998): 18T-21T.

Kagan A, Harris BR, Winkelstein W, et al. ”Epidemiologic studies of coronary heart diseas eand stroke in Japanese men living in Japan, Hawaii and California.” J. Chronic Dis. 27 (1974):345–364.

Kato H, Tillotson J, Nichaman MZ, et al. “Epidemiologic studies of coronary heart disease and stroke in Japanese men living in Japan, Hawaii and California: serum lipids and diet.” Am. J. Epidemiol. 97 (1973): 372–385.

Morrison LM. “Arteriosclerosis.” JAMA 145 (1951): 1232–1236.

Morrison LM. “Diet in coronary atherosclerosis.” JAMA 173 (1960): 884–888.

Lyon TP, Yankley A, Gofman JW, et al. “Lipoproteins and diet in coronary heart disease.” California Med. 84 (1956): 325–328.

Gibney MJ, and Kritchevsky D, eds. Current Topics in Nutrition and Disease, Volume 8: Animal and Vegetable Proteins in Lipid Metabolism and Atherosclerosis. New York, NY: Alan R. Liss,Inc., 1983.

Sirtori CR, Noseda G, and Descovich GC. “Studies on the use of a soybean protein diet forthe management of human hyperlipoproteinemias.” In: M. J. Gibney and D. Kritchevsky(eds.), Current Topics in Nutrition and Disease, Volume 8: Animal and Vegetable Proteins in LipidMetabolism and Atherosclerosis., pp. 135–148. New York, NY: Alan R. Liss, Inc., 1983.

G.S. Myers, personal communication, cited by Groom, D. “Population studies of atherosclerosis.” Ann. Internal Med. 55(1961):51–62.

Centers for Disease Control. ”Smoking and Health: a national status report.” Morbidity and Mortality Weekly Report 35 (1986): 709–711.

Centers for Disease Control. “Cigarette smoking among adults”United States, 2000.” Morbidity and Mortality Weekly Report 51 (2002): 642–645.

Age-adjusted, ages 25–74.

Marwick C. “Coronary bypass grafting economics, including rehabilitation. Commentary.”Curr. Opin. Cardiol. 9 (1994): 635–640.

Page 1319 in Gersh BJ, Braunwald E, and Rutherford JD. “Chronic coronary artery disease.”In: E. Braunwald (ed.), Heart Disease: A Textbook of cardiovascular Medicine, Vol. 2(FifthEdition), pp. 1289–1365. Philadelphia, PA: W.B. Saunders, 1997.

Ornish D. “Avoiding revascularization with lifestyle changes: the Multicenter Lifestyle Demonstration Project.” Am. J. Cardiol. 82 (1998): 72T–76T.

Shaw PJ, Bates D, Cartlidge NEF, et al. “Early intellectual dysfunction following coronary bypass surgery.” Quarterly J. Med. 58 (1986): 59–68.

Cameron AAC, Davis KB, and Rogers WJ. “Recurrence of angina after coronary artery bypass surgery. Predictors and prognosis (CASS registry).” J. Am. Coll. Cardiol. 26 (1995): 895–899.

Page 1320 in Gersh BJ, Braunwald E, and Rutherford JD. “Chronic coronary artery disease.”In: E. Braunwald (ed.), Heart Disease: A Textbook of cardiovascular Medicine, Vol. 2(FifthEdition), pp. 1289–1365. Philadelphia, PA: W.B. Saunders, 1997.

Kirklin JW, Naftel DC, Blackstone EH, et al. “Summary of a consensus concerning death and ischemic events after coronary artery bypass grafting.” Circulation 79(Suppl 1) (1989):I81–I91.

Page 1368–9 in Lincoff AM, and Topol EJ. “Interventional catherization techniques.” In: E.Braunwald (ed.), Heart Disease: A Textbook of Cardiovascular Medicine, pp. 1366–1391.Philadelphia, PA: W.B. Saunders, 1997.

Hirshfeld JW, Schwartz JS, Jugo R, et al. “Restenosis after coronary angioplasty: a multivariatestatistical model to relate lesion and procedure variables to restenosis.” J. Am. Coll. Cardiol.18 (1991): 647–656.

Information Plus. Nutrition: a key to good health. Wylie, TX: Information Plus, 1999.

Naifeh SW. The Best Doctors in America, 1994–1995. Aiken, S.C.: Woodward & White, 1994.

Esselstyn CB, Jr. “Foreward: changing the treatment paradigm for coronary artery disease.” Am. J. Cardiol. 82 (1998): 2T-4T.

Esselstyn CB, Ellis SG, Medendorp SV, et al. “A strategy to arrest and reverse coronary artery disease: a 5-year longitudinal study of a single physician’s practice.” J. Family Practice 41(1995): 560–568.

Esselstyn CJ. “Introduction:more than coronary artery disease.” Am. J. Cardiol. 82 (1998):5T-9T.

The flow of blood is related to the fourth power of the radius. Thus, a reduction of seven percent is approximately related to a 30% greater blood flow, although it is not possible to obtain by calculation a more precise determination of this number.

Personal communication with Dr. Esselstyn, 9/15/03.

Ornish D, Brown SE, Scherwitz LW, et al. “Can lifestyle changes reverse coronary heart disease?”Lancet 336 (1990): 129–133.

Ratliff NB. “Of rice, grain, and zeal: lessons from Drs. Kempner and Esselstyn.” ClevelandClin. J. Med. 67 (2000): 565–566.

American Heart Association. “AHA Dietary Guidelines. Revision 2000: A Statement for Healthcare Professionals from the Nutrition Committee of the American Heart Association.”Circulation 102 (2000): 2296–2311.

National Cholesterol Education Program. ”Third report of the National Cholesterol Education Program (NCEP) expert panel on detection, evaluation and treatment of high blood cholesterol in adult (adult treatment panel III): executive summary.” Bethesda, MD: National Institutes of Health, 2001.

Castelli W. “Take this letter to your doctor.” Prevention 48 (1996): 61–64.

Schuler G, Hambrecht R, Schlierf G, et al. “Regular physical exercise and low-fat diet.” Circulation86 (1992): 1–11.

Chapter 6

Flegal KM, Carroll MD, Ogden CL, et al. “Prevalence and trends in obesity among U.S.adults, 1999–2000.” JAMA 288 (2002): 1723–1727.

Ogden CL, Flegal KM, Carroll MD, et al. “Prevalence and trends in overweight among U.S.children and adolescents.” JAMA 288 (2002): 1728–1732.

Dietz WH. “Health consequences of obesity in youth: childhood predictors of adult disease.” Pediatrics 101 (1998): 518–525.

Fontaine KR, and Barofsky I. “Obesity and health-related quality of life.” Obesity Rev. 2(2001): 173–182.

Colditz GA. “Economic costs of obesity and inactivity.” Med. Sci. Sports Exerc. 31 (1999):S663–S667.

Adcox S. “New state law seeks to cut down obesity.” Ithaca Journal Sept. 21, 2002: 5A.

Ellis FR, and Montegriffo VME. “Veganism, clinical findings and investigations.” Am. J. Clin.Nutr. 23 (1970): 249–255.

Berenson, G., Srinivasan, S., Bao, W., Newman,  W. P. r., Tracy, R. E., and Wattigney, W. A. ” Association between multiple cardiovascular risk factors and atherosclerosis to chidlren and young adults.  The Bogalusa heart Study.” New Engl. J. Med., 338: 1650-1656, 1998.

Key TJ, Fraser GE, Thorogood M, et al. “Mortality in vegetarians and nonvegetarians: de380tailed findings from a collaborative analysis of 5 prospective studies.” Am. J. Clin. Nutri.70(Suppl.) (1999): 516S–524S.

Bergan JG, and Brown PT. “Nutritional status of “new” vegetarians.” J. Am. Diet. Assoc. 76(1980): 151–155.

Appleby PN, Thorogood M, Mann J, et al. “Low body mass index in non-meat eaters: thepossible roles of animal fat, dietary fibre, and alcohol.” Int J. Obes. 22 (1998): 454–460.

Dwyer JT. ”Health aspects of vegetarian diets.” Am. J. Clin. Nutr. 48 (1988): 712–738.

Key TJ, and Davey G. “Prevalence of obesity is low in people who do not eat meat.” Brit. Med.Journ. 313 (1996): 816–817.

Shintani TT, Hughes CK, Beckham S, et al. “Obesity and cardiovascular risk interventionthrough the ad libitum feeding of traditional Hawaiian diet.” Am. J. Clin. Nutr. 53 (1991):1647S–1651S.

Barnard RJ. “Effects of life-style modification on serum lipids.” Arch. Intern. Med. 151 (1991):1389–1394.

McDougall J, Litzau K, Haver E, et al. “Rapid reduction of serum cholesterol and bloodpressure by a twelve-day, very low fat, strictly vegetarian diet.” J. Am. Coll. Nutr. 14 (1995):491–496.

Ornish D, Scherwitz LW, Doody RS, et al. “Effects of stress management training and dietary changes in treating ischemic heart disease.” JAMA 249 (1983): 54–59.

Shintani TT, Beckham S, Brown AC, et al. “The Hawaii diet: ad libitum high carbohydrate,low fat multi-cultural diet for the reduction of chronic disease risk factors: obesity, hypertension,hypercholesterolemia, and hyperglycemia.” Hawaii Med. Journ. 60 (2001): 69–73.

Nicholson AS, Sklar M, Barnard ND, et al. “Toward improved management of NIDDM: a randomized,controlled, pilot intervention using a lowfat, vegetarian diet.” Prev. Med. 29 (1999):87–91.

Ornish D, Scherwitz LW, Billings JH, et al. “Intensive lifestyle changes for reversal of coronary heart disease.” JAMA 280 (1998): 2001–2007.

Astrup A, Toubro S, Raben A, et al. “The role of low-fat diets and fat substitutes in body weight management: what have we learned from clinical studies?” J. Am. Diet. Assoc. 97(suppl)(1997): S82–S87.

Duncan KH, Bacon JA, and Weinsier RL. “The effects of high and low energy density diets on satiety, energy intake, and eating time of obese and nonobese subjects.” Am. J. Clin. Nutr. 37(1983): 763–767.

Heaton KW. “Food fibre as an obstacle to energy intake.” Lancet (1973): 1418–1421.

Levin N, Rattan J, and Gilat T. “Energy intake and body weight in ovo-lacto vegetarians.” J.Clin. Gastroenterol. 8 (1986): 451–453.

Campbell TC. “Energy balance: interpretation of data from rural China.” Toxicological Sciences52 (1999): 87–94.

Poehlman ET, Arciero PJ, Melby CL, et al. ”Resting metabolic rate and postprandial thermogenesis in vegetarians and non vegetarians.” Am. J. Clin. Nutr. 48 (1988): 209–213.

The study by Poehlman et al. showed high oxygen consumption and higher resting metabolicrate but was badly misinterpreted by the authors. We had very similar results with experimentalrats.

Fogelholm M, and Kukkonen-Harjula K. “Does physical activity prevent weight gain—a systematic review.” Obesity Rev. 1 (2000): 95–111.

Ravussin E, Lillioja S, Anderson TE, et al. “Determinants of 24-hour energy expenditure in man. Methods and results using a respiratory chamber.” J. Clin. Invest. 78 (1986): 1568–1578.

Thorburn AW, and Proietto J. “Biological determinants of spontaneous physical activity.” Obesity Rev. 1 (2000): 87–94.

Krieger E, Youngman LD, and Campbell TC. “The modulation of aflatoxin(AFB1) induced preneoplastic lesions by dietary protein and voluntary exercise in Fischer 344 rats.” FASEB J.2 (1988): 3304 Abs.

Heshka S, and Allison DB. “Is obesity a disease?” Int. J. Obesity Rel. Dis. 25 (2001): 1401–1404.

Kopelman PG, and Finer N. “Reply: is obesity a disease?” Int J. Obes. 25 (2001): 1405–1406.

Campbell TC. “Are your genes hazardous to your health?” Nutrition Advocate 1 (1995): 1–2,8.

Campbell TC. “Genetic seeds of disease: How to beat the odds.” Nutrition Advocate 1 (1995):1–2, 8.

Campbell TC. “The ‘Fat Gene’ Dream Machine.” Nutrition Advocate 2 (1996): 1–2.

Chapter 7

Mokdad AH, Ford ES, Bowman BA, et al. “Diabetes trends in the U.S.: 1990–1998.” Diabetes Care 23 (2000): 1278–1283.

Centers for Disease Control and Prevention. “National Diabetes Fact Sheet: General Information and National Estimates on Diabetes in the United States, 2000.” Atlanta, GA: Centers for Disease Control and Prevention.

Griffin KL. “New lifestyles: new lifestyles, hope for kids with diabetes.” (Scroll to #19 on page) Milwaukee Journal Sentinel 22 July 2002: 1G.

American Diabetes Association. “Type 2 diabetes in children and adolescents.” Diabetes Care23 (2000): 381–389.

Himsworth HP. “Diet and the incidence of diabetes mellitus.” Clin. Sci. 2 (1935): 117–148.

West KM, and Kalbfleisch JM. “Glucose tolerance, nutrition, and diabetes in Uruguay, Venezuela,Malaya, and East Pakistan.

 Diabetes 15 (1966): 9–18.

West KM, and Kalbfleisch JM. “Influence of nutritional factors on prevalence of diabetes.” Diabetes 20 (1971): 99–108.

Fraser GE. “Associations between diet and cancer, ischemic heart disease, and all-cause mortality in non-Hispanic white California Seventh-day Adventists.” Am. J. Clin. Nutr. 70(Suppl.)(1999): 532S–538S.

Snowdon DA, and Phillips RL. “Does a vegetarian diet reduce the occurrence of diabetes?”Am. J. Publ. Health 75 (1985): 507–512.

Tsunehara CH, Leonetti DL, and Fujimoto WY. “Diet of second generation Japanese-American men with and without non-insulin-dependent diabetes.” Am. J. Clin. Nutri. 52 (1990):731–738.

Marshall J, Hamman RF, and Baxter J. “High-fat, low-carbohydrate diet and the etiology of non-insulin-dependent diabetes mellitus: the San Luis Valley Study.” Am. J. Epidemiol. 134(1991): 590–603.

Kittagawa T, Owada M, Urakami T, et al. “Increased incidence of non-insulin-dependent diabetes melitus among Japanese schoolchildren correlates with an increased intake of animal protein and fat.” Clin. Pediatr. 37 (1998): 111–116.

Trowell H. “Diabetes mellitus death-rates in England and Wales 1920–1970 and food supplies.”Lancet 2 (1974): 998–1002.

Meyer KA, Kushi LH, Jacobs DR, Jr., et al. “Carbohydrates, dietary fiber, and incident Type 2diabetes in older women.” Am. J. Clin. Nutri. 71 (2000): 921–930.

Anderson JW. “Dietary fiber in nutrition management of diabetes.” In: G. Vahouny, V. and D.Kritchevsky (eds.), Dietary Fiber: Basic and Clinical Aspects, pp. 343–360. New York: PlenumPress, 1986.

Anderson JW, Chen WL, and Sieling B. “Hypolipidemic effects of high-carbohydrate, highfiberdiets.”Metabolism 29 (1980): 551–558.

Story L, Anderson JW, Chen WL, et al. “Adherence to high-carbohydrate, high-fiber diets:long-term studies of non-obese diabetic men.” Journ. Am. Diet. Assoc. 85 (1985): 1105–1110.

Barnard RJ, Lattimore L, Holly RG, et al. “Response of non-insulin-dependent diabetic patients to an intensive program of diet and exercise.” Diabetes Care 5 (1982): 370–374.

Barnard RJ, Massey MR, Cherny S, et al. “Long-term use of a high-complex-carbohydrate,high-fiber, low-fat diet and exercise in the treatment of NIDDM patients.” Diabetes Care 6 (1983): 268–273.

Anderson JW, Gustafson NJ, Bryant CA, et al. “Dietary fiber and diabetes: a comprehensive review and practical application.” J. Am. Diet. Assoc. 87 (1987): 1189–1197.

Jenkins DJA, Wolever TMS, Bacon S, et al. “Diabetic diets: high carbohydrate combined with high fiber.”Am. J. Clin. Nutri. 33 (1980): 1729–1733.

Diabetes Prevention Program Research Group. “Reduction in the incidence of Type 2 diabetes with lifestyle intervention or Metformin.” New Engl. J. Med. 346 (2002): 393–403.

Tuomilehto J, Lindstrom J, Eriksson JG, et al. “Prevention of Type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance.” New Engl. J. Med. 344(2001): 1343–1350.

Chapter 8

Estrogen present in its free, unbound form.

Estrogen activity is due to more than one analogue, but usually refers to estradiol. I will use thegeneral term “estrogen” to include all steroid and related female hormones whose effects parallelestradiol activity. A small amount of testosterone in women also shows the same effect.

Wu AH, Pike MC, and Stram DO. “Meta-analysis: dietary fat intake, serum estrogen levels,and the risk of breast cancer.” J. Nat. Cancer Inst. 91 (1999): 529–534.

Bernstein L, and Ross RK. “Endogenous hormones and breast cancer risk.” Epidemiol. Revs.15 (1993): 48–65.

Pike MC, Spicer DV, Dahmoush L, et al. “Estrogens, progestogens, normal breast cell proliferation,and breast cancer risk.” Epidemiol. Revs. 15 (1993): 17–35.

Bocchinfuso WP, Lindzey JK, Hewitt SC, et al. “Induction of mammary gland development in estrogen receptor-alpha knockout mice.” Endocrinology 141 (2000): 2982–2994.

Atwood CS, Hovey RC, Glover JP, et al. “Progesterone induces side-branching of the ductal epithelium in the mammary glands of peripubertal mice.” J. Endocrinol. 167 (2000): 39–52.

Rose DP, and Pruitt BT. “Plasma prolactin levels in patients with breast cancer.” Cancer 48(1981): 2687–2691.

Dorgan JF, Longcope C, Stephenson HE, Jr., et al. “Relation of prediagnostic serum estrogenand androgen levels to breast cancer risk.” Cancer Epidemiol Biomarkers Prev 5 (1996):533–539.

Dorgan JF, Stanczyk FZ, Longcope C, et al. “Relationship of serum dehydroepiandrosterone(DHEA), DHEA sulfate, and 5-androstene-3 beta, 17 beta-diol to risk of breast cancer in postmenopausal women.”Cancer Epidemiol Biomarkers Prev 6 (1997):

Thomas HV, Key TJ, Allen DS, et al. “A prospective study of endogenous serum hormone concentrations and breast cancer risk in post-menopausal women on the island of Guernsey.”Brit. J. Cancer 76 (1997): 410–405.

Hankinson SE, Willett W, Manson JE, et al. ”Plasma sex steroid hormone levels and risk ofbreast cancer in postmenopausal women.” J. Nat. Cancer Inst. 90 (1998): 1292–1299.

Rosenthal MB, Barnard RJ, Rose DP, et al. “Effects of a high-complex-carbohydrate, low-fat,low-cholesterol diet on levels of serum lipids and estradiol.” Am. J. Med. 78 (1985): 23–27.

Adlercreutz H. “Western diet and Western diseases: some hormonal and biochemical mechanisms and associations.” Scand. J. Clin. Lab. Invest. 50(Suppl.201) (1990): 3–23.

Heber D, Ashley JM, Leaf DA, et al. “Reduction of serum estradiol in postmenopausal women given free access to low-fat high-carbohydrate diet.” Nutrition 7 (1991): 137–139.

Rose DP, Goldman M, Connolly JM, et al. “High-fiber diet reduces serum estrogen concentrations in premenopausal women.” Am. J. Clin. Nutr. 54 (1991): 520–525.

Rose DP, Lubin M, and Connolly JM. “Efects of diet supplementation with wheat bran onserum estrogen levels in the follicular and luteal phases of the menstrual cycle.” Nutrition 13(1997): 535–539.

Tymchuk CN, Tessler SB, and Barnard RJ. “Changes in sex hormone-binding globulin, insulin,and serum lipids in postmenopausal women on a low-fat, high-fiber diet combined with exercise.” Nutr. Cancer 38 (2000): 158–162.

Key TJA, Chen J, Wang DY, et al. “Sex hormones in women in rural China and in Britain.”Brit. J. Cancer 62 (1990): 631–636.

Prentice R, Thompson D, Clifford C, et al. “Dietary fat reduction and plasma estradiol concentration in healthy postmenopausal women.” J. Natl. Cancer Inst. 82 (1990): 129–134.

Boyar AP, Rose DP, and Wynder EL. “Recommendations for the prevention of chronic disease:the application for breast disease.” Am. J. Clin. Nutr. 48(3 Suppl) (1988): 896–900.

Nandi S, Guzman RC, and Yang J. “Hormones and mammary carcinogenesis in mice, rats andhumans: a unifying hypothesis.” Proc. National Acad. Sci 92 (1995): 3650–3657.

Peto J, Easton DF, Matthews FE, et al. “Cancer mortality in relatives of women with breastcancer, the OPCS study.” Int. J. Cancer 65 (1996): 275–283.

Colditz GA, Willett W, Hunter DJ, et al. “Family history, age, and risk of breast cancer. Prospective data from the Nurses’ Health Study.” JAMA 270 (1993): 338–343.

National Human Genome Research Institute. “Learning About Breast Cancer.” Accessed at http://www.genome.gov/10000507#ql

Futreal PA, Liu Q, Shattuck-Eidens D, et al. “BRCA1 mutations in primary breast and ovarian carcinomas.” Science 266 (1994): 120–122.

Miki Y, Swensen J, Shatttuck-Eidens D, et al. “A strong candidate for the breast and ovarian cancer susceptibility gene BRCA1.” Science 266 (1994): 66–71.

Wooster R, Bignell G, Lancaster J, et al. “Identification of the breast cancer susceptibility gene BRCA2.”Nature 378 (1995): 789–792.

Tavtigian SV, Simard J, Rommens J, et al. ”The complete BRCA2 gene and mutations in chromosome13q-linked kindreds.” Nat. Genet. 12 (1996): 333–337.

Ford D, Easton D, Bishop DT, et al. “Risks of cancer in BRCA1 mutation carriers.” Lancet 343(1994): 692–695.

Antoniou A, Pharoah PDP, Narod S, et al. ”Average risks of breast and ovarian cancer associated jjjwith BRCA1 or BRCA2 mutations detected in case series unselected for family history: acombined analysis of 22 studies.” Am. J. Hum. Genet. 72 (2003): 1117–1130.

Newman B, Mu H, Butler LM, et al. “Frequency of breast cancer attributable to BRCA1 in apopulation-based series of American women.” JAMA 279 (1998): 915–921.

Peto J, Collins N, Barfoot R, et al. “Prevalence of BRCA1 and BRCA2 gene mutations in patientswith early-onset breast cancer.” J. Nat. Cancer Inst. 91 (1999): 943–949.

Tabar L, Fagerberg G, Chen HH, et al. ”Efficacy of breast cancer screening by age. New resultsfrom the Swedish Two-County Trial.” Cancer 75 (1995): 2507–2517.

Bjurstram N, Bjorneld L, Duffy SW, et al. “The Gothenburg Breast Cancer Screening Trial:first results on mortality, incidence, and mode of detection for women ages 39–49 years at randomization.” Cancer 80 (1997): 2091–2099.

Frisell J, Lidbrink E, Hellstrom L, et al. “Follow-up after 11 years: update of mortality results in the Stockholm mammographic screening trial.” Breast Cancer Res. Treat 1997 45 (1997):263–270.

Greenlee RT, Hill-Harmon MB, Murray T, et al. “Cancer statistics, 2001.” CA Cancer J. Clin.51 (2001): 15–36.

Cairns J. “The treatment of diseases and the War against Cancer.” Sci. Am. 253 (1985):31–39.

Cuzick J, and Baum M. ”Tamoxifen and contralateral breast cancer.” Lancet 2 (1985): 282.

Cuzick J, Wang DY, and Bulbrook RD. ”The prevention of breast cancer.” Lancet 1 (1986):83–86.

Fisher B, Costantino JP, Wickerham DL, et al. “Tamoxifen for prevention of breast cancer:report of the National Surgical Adjuvant Breast and Bowel Project P-1 Study.” J. Nat. CancerInst. 90 (1998): 1371–1388.

Freedman AN, Graubard BI, Rao SR, et al. “Estimates of the number of U.S. women who could benefit from tamoxifen for breast cancer chemoprevention.” J. Nat. Cancer Inst. 95(2003): 526–532.

Powles T, Eeles R, Ashley S, et al. “Interim analysis of the incidence of breast cancer in the Royal Marsden Hospital tamoxifen randomised chemoprevention trial.” Lancet 352 (1998):98–101.

Veronesi U, Maisonneuve P, Costa A, et al. “Prevention of breast cancer with tamoxifen: preliminary findings from the Italian randomised trial among hysterectomised women.” Lancet352 (1998): 93–97.

Cuzick J. “A brief review of the current breast cancer prevention trials and proposals for future trials.”Eur J Cancer 36 (2000): 1298–1302.

Cummings SR, Eckert S, Krueger KA, et al. ”The effect of raloxifene on risk of breast cancer in postmenopausal women: results from the MORE randomized trial.” JAMA 281 (1999):2189–2197.

Dorgan JF, Hunsberger S, A., McMahon RP, et al. ”Diet and sex hormones in girls: findings from a randomized controlled clinical trial.” J. Nat. Cancer Inst. 95 (2003): 132–141.

Ornish D, Scherwitz LW, Billings JH, et al. “Intensive lifestyle changes for reversal of coronary heart disease.” JAMA 280 (1998): 2001–2007.

Esselstyn CB, Ellis SG, Medendorp SV, et al. “A strategy to arrest and reverse coronary artery disease: a 5-year longitudinal study of a single physician’s practice.” J. Family Practice 41(1995): 560–568.

Hildenbrand GLG, Hildenbrand LC, Bradford K, et al. “Five-year survival rates of melanoma patients treated by diet therapy after the manner of Gerson: a retrospective review.” AlternativeTherapies in Health and Medicine 1 (1995): 29–37.

Youngman LD, and Campbell TC. “Inhibition of aflatoxin B1-induced gamma-glutamyltranspeptidase positive (GGT+) hepatic preneoplastic foci and tumors by low protein diets:evidence that altered GGT+ foci indicate neoplastic potential.” Carcinogenesis 13 (1992):1607–1613.

Ronai Z, Gradia S, El-Bayoumy K, et al. “Contrasting incidence of ras mutations in rat mammaryand mouse skin tumors induced by anti-benzo[c]phenanthrene-3,4-diol-1,2-epoxide.” Carcinogensis 15 (1994): 2113–2116.

Jeffy BD, Schultz EU, Selmin O, et al. “Inhibition of BRCA-1 expression by benzo[a]pyreneand diol epoxide.” Mol. Carcinogenesis 26 (1999): 100–118.

Gammon MD, Santella RM, Neugut AI, et al. “Environmental toxins and breast cancer on Long Island. I. Polycyclic aromatic hydrocarbon DNA adducts.” Cancer Epidemiol BiomarkersPrev 11 (2002): 677–685.

Gammon MD, Wolff MS, Neugut AI, et al. “Environmental toxins and breast cancer on LongIsland. II. Organchlorine compound levels in blood.” Cancer Epidemiol Biomarkers Prev 11(2002): 686–697.

Humphries KH, and Gill S. “Risks and benefits of hormone replacement therapy: the evidence speaks.”Canadian Med. Assoc. Journ. 168 (2003): 1001–1010.

Writing Group for the Women’s Health Initiative Investigators. “Risks and benefits of estrogen plus progest in in healthy postmenopausal women: principal results from the Women’s Health Initiative Randomized Controlled Trial.” JAMA 288 (2002): 321–333.

Hulley S, Grady D, Bush T, et al. ”Randomized trial of estrogen plus progestin for secondary prevention of coronary heart disease in postmenopausal women. Heart and Estrogen/progestin Replacement Study (HERS) Research Group.” JAMA 280 (1998): 605–613.

While this finding is not statistically significant, its consistency with the WHI finding is striking.

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Kinzler KW, and Vogelstein B. ”Lessons from Heredity. Colorectal Cancer.” Cell 87 (1996):159–170.

Ferlay J, Bray F, Pisani P, et al. GLOBOCAN 2000: Cancer Incidence, mortality and prevalence worldwide, Version 1.0. Lyon, France: IARCPress, 2001.

Limited version of Ferlay et al. document available at www.dep.iarc.fr/globocan/globocan.htm, last updated on 03/02/2001.

Expert Panel. Food, nutrition and the prevention of cancer, a global perspective. Washington,DC: American Institute for Cancer Research/World Cancer Research Fund, 1997.

Armstrong D, and Doll R. ”Environmental factors and cancer incidence and mortality in different countries, with special reference to dietary practices.” Int. J. Cancer 15 (1975):617–631.

Burkitt DP. “Epidemiology of cancer of the colon and the rectum.” Cancer 28 (1971): 3–13.

Jansen MCJF, Bueno-de-Mesquita HB, Buzina R, et al. “Dietary fiber and plant foods in relation to colorectal cancer mortality: The Seven Countries Study.” Int. J. Cancer 81 (1999):174–179.

Whiteley LO, and Klurfeld DM. “Are dietary fiber-induced alterations in colonic epithelialcell proliferation predictive of fiber’s effect on colon cancer?” Nutr. Cancer 36 (2000): 131–149.

Most of these associations were not statistically significant, but the consistency of the inverse association between fiber and colorectal cancer was impressive.

Campbell TC, Wang G, Chen J, et al. “Dietary fiber intake and colon cancer mortality in The People’s Republic of China.” In: D. Kritchevsky, C. Bonfield and J. W. Anderson (eds.),Dietary Fiber, pp. 473–480. New York, NY: Plenum Publishing Corporation, 1990.

Trock B, Lanza E, and Greenwald P. “Dietary fiber, vegetables, and colon cancer: critical review and meta-analysis of the epidemiologic evidence.” J. Nat. Cancer Inst. 82 (1990):650–661.

Howe GR, Benito E, Castelleto R, et al. “Dietary intake of fiber and decreased risk of cancers of the colon and rectum: evidence from the combined analysis of 13 case-control studies.” J.Nat. Cancer Inst. 84 (1992): 1887–1896.

Bingham SA, Day NE, Luben R, et al. “Dietary fibre in food and protection against colorectal cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC): an observational study.” Lancet 361 (2003): 1496–1501.

O’Keefe SJD, Ndaba N, and Woodward A. “Relationship between nutritional status, dietary intake patterns and plasma lipoprotein concentrations in rural black South Africans.” Hum.Nutr. Clin. Nutr. 39 (1985): 335–341.

Sitas F. “Histologically diagnosed cancers in South Africa, 1988.” S. African Med. J. 84 (1994):344–348.

O’Keefe SJD, Kidd M, Espitalier-Noel G, et al. “Rarity of colon cancer in Africans is associated with low animal product consumption, not fiber.” Am. J. Gastroenterology 94 (1999):1373–1380.

McKeown-Eyssen G. “Epidemiology of colorectal cancer revisited: are serum triglycerides and/or plasma glucose associated with risk?” Cancer Epidemiol Biomarkers Prev 3 (1994):687–695.

Giovannucci E. “Insulin and colon cancer.” Cancer Causes and Control 6 (1995): 164–179.

Bruce WR, Giacca A, and Medline A. “Possible mechanisms relating diet and risk of colon cancer.”Cancer Epidemiol Biomarkers Prev 9 (2000): 1271–1279.

Kono S, Honjo S, Todoroki I, et al. “Glucose intolerance and adenomas of the sigmoid colon in Japanese men (Japan).” Cancer Causes and Control 9 (1998): 441–446.

Schoen RE, Tangen CM, Kuller LH, et al. “Increased blood glucose and insulin, body size,and incident colorectal cancer.” J. Nat. Cancer Inst. 91 (1999): 1147–1154.

Bruce WR, Wolever TMS, and Giacca A. “Mechanisms linking diet and colorectal cancer: the possible role of insulin resistance.” Nutr. Cancer 37 (2000): 19–26.

Lipkin M, and Newmark H. “Development of clinical chemoprevention trials.” J. Nat. Cancer Inst. 87 (1995): 1275–1277.

Holt PR, Atillasoy EO, Gilman J, et al. “Modulation of abnormal colonic epithelial cell proliferationand differentiation by low-fat dairy foods. A randomized trial.” JAMA 280 (1998):1074–1079.

Mobarhan S. “Calcium and the colon: recent findings.” Nutr. Revs. 57 (1999): 124–126.

Alberts DS, Ritenbuagh C, Story JA, et al. “Randomized, double-blinded, placebo-controlled study of effect of wheat bran fiber and calcium on fecal bile acids in patients with resected adenomatous colon polyps.” J. Nat. Cancer Inst. 88 (1996): 81–92.

Chen J, Campbell TC, Li J, et al. Diet, life-style and mortality in China. A study of the characteristics of 65 Chinese counties. Oxford, UK; Ithaca, NY; Beijing, PRC: Oxford University Press;Cornell University Press; People’s Medical Publishing House, 1990.

Jass JR. “Colon cancer: the shape of things to come.” Gut 45 (1999): 794–795.

Burt RW. “Colon cancer screening.” Gastroenterology 119 (2000): 837–853.

Winawer SJ, Zauber AG, Ho MN, et al. “Prevention of colorectal cancer by colonoscopic polypectomy.”New Engl. J. Med. 329 (1993): 1977–1981.

Pignone M, Rich M, Teutsch SM, et al. ”Screening for colorectal cancer in adults at average risk: a summary of the evidence for the U.S. Preventive Services Task Force.” Ann. InternalMed. 137 (2002): 132–141.

Scott RJ, and Sobol HH. “Prognostic implications of cancer susceptibility genes: Any news?” Recent Results in Cancer Research 151 (1999): 71–84.

Lee ML, Wang R-T, Hsing AW, et al. “Case-control study of diet and prostate cancer in China.” Cancer Causes and Control 9 (1998): 545–552.

Villers A, Soulie M, Haillot O, et al. “Prostate cancer screening (III): risk factors, natural history,course without treatment.” Progr. Urol. 7 (1997): 655–661.

Stanford JL. “Prostate cancer trends 1973–1995.” Bethesda, MD: SEER Program, NationalCancer Institute, 1998.

Chan JM, and Giovannucci EL. “Dairy products, calcium, and vitamin D and risk of prostate cancer.”Epidemiol. Revs. 23 (2001): 87–92.

Giovannucci E. “Dietary influences of 1,25 (OH)2 vitamin D in relation to prostate cancer: a hypothesis.”Cancer Causes and Control 9 (1998): 567–582.

Chan JM, Stampfer MJ, Ma J, et al. “Insulin-like growth factor-I (IGF-I) and IGF bindingprotein-3 as predictors of advanced-stage prostate cancer.” J Natl Cancer Inst 94 (2002):1099–1109.

Doi SQ, Rasaiah S, Tack I, et al. ”Low-protein diet suppresses serum insulin-like growth factor-1 and decelerates the progresseion of growth hormone-induced glomerulosclerosis.” Am.J. Nephrol. 21 (2001): 331–339.

Heaney RP, McCarron DA, Dawson-Hughes B, et al. “Dietary changes favorably affect bond remodeling in older adults.” J. Am. Diet. Assoc. 99 (1999): 1228–1233.

Allen NE, Appleby PN, Davey GK, et al. “Hormones and diet: low insulin-like growth factor-Ibut normal bioavailable androgens in vegan men.” Brit. J. Cancer 83 (2000): 95–97.

Cohen P, Peehl DM, and Rosenfeld RG. “The IGF axis in the prostate.” Horm. Metab. res. 26(1994): 81–84.

Chapter 9

Mackay IR. “Tolerance and immunity.” Brit. Med. Journ. 321 (2000): 93–96.

Jacobson DL, Gange SJ, Rose NR, et al. “Short analytical review. Epidemiology and estimated population burden of selected autoimmune diseases in the United States.” Clin. Immunol. Immunopath.84 (1997): 223–243.

Davidson A, and Diamond B. “Autoimmune diseases.” New Engl. J. Med. 345 (2001): 340–350.

Aranda R, Sydora BC, McAllister PL, et al. “Analysis of intestinal lymphocytes in mousecolitis mediated by transfer of CD4+, CD45RBhigh T cells to SCID recipients.” J. Immunol. 158(1997): 3464–3473.

Folgar S, Gatto EM, Raina G, et al. “Parkinsonism as a manifestation of multiple sclerosis.” Movement Disorders 18 (2003): 108–113.

Cantorna MT. “Vitamin D and autoimmunity: is vitamin D status an environmental factor affecting autoimmune disease prevalence?” Proc. Soc. Exp. Biol. Med. 223 (2000): 230–233.

DeLuca HF, and Cantorna MT. “Vitamin D: its role and uses in immunology.” FASEB J. 15(2001): 2579–2585.

Winer S, Astsaturov I, Cheung RK, et al. “T cells of multiple sclerosis patients target acommon environmental peptide that causes encephalitis in mice.” J. Immunol. 166 (2001):4751–4756.

Davenport CB. “Multiple sclerosis from the standpoint of geographic distribution and race.”Arch. Neurol. Pschiatry 8 (1922): 51–58.

Alter M, Yamoor M, and Harshe M. “Multiple sclerosis and nutrition.” Arch. Neurol. 31(1974): 267–272.

Carroll M. “Innate immunity in the etiopathology of autoimmunity.” Nature Immunol. 2(2001): 1089–1090.

Karjalainen J, Martin JM, Knip M, et al. “A bovine albumin peptide as a possible trigger of insulin-dependent Diabetes Mellitus.” New Engl. Journ. Med. 327 (1992): 302–307.

Akerblom HK, and Knip M. “Putative environmental factors and Type 1 diabetes.” Diabetes/Metabolism Revs.

(1998): 31–67.14. Naik RG, and Palmer JP. “Preservation of beta-cell function in Type 1 diabetes.” Diabetes Rev.7 (1999): 154–182.

Virtanen SM, Rasanen L, Aro A, et al. ”Infant feeding in Finnish children less than 7 yr of age with newly diagnosed IDDM. Childhood diabetes in Finland Study Group.” Diabetes Care 14(1991): 415–417.

Savilahti E, Akerblom HK, Tainio V-M, et al. “Children with newly diagnosed insulin dependent diabetes mellitus have increased levels of cow’s milk antibodies.” Diabetes Res. 7 (1988):137–140.

Yakota A, Yamaguchi T, Ueda T, et al. “Comparison of islet cell antibodies, islet cell surfactantibodies and anti-bovine serum albumin antibodies in Type 1 diabetes.” Diabetes Res. Clin.Pract. 9 (1990): 211–217.

Hammond-McKibben D, and Dosch H-M. “Cow’s milk, bovine serum albumin, and IDDM:can we settle the controversies?” Diabetes Care 20 (1997): 897–901.

Akerblom HK, Vaarala O, Hyoty H, et al. ”Environmental factors in the etiology of Type 1diabetes.” Am. J. Med. Genet. (Semin. Med. Genet.) 115 (2002): 18–29.

Gottlieb MS, and Root HF. “Diabetes mellitus in twins.” Diabetes 17 (1968): 693–704.388

Barnett AH, Eff C, Leslie RDG, et al. “Diabetes in identical twins: a study of 200 pairs.” Diabetologia20 (1981): 87–93.

Borch-Johnsen K, Joner G, Mandrup-Poulsen T, et al. “Relation between breast feedingand incidence rates of insulin-dependent diabetes mellitus: a hypothesis.” Lancet 2 (1984):1083–1086.

Perez-Bravo F, Carrasco E, Gutierrez-Lopez MD, et al. “Genetic predisposition and environmental factors leading to the development of insulin-dependent diabetes mellitus in Chilean children.” J. Mol. Med. 74 (1996): 105–109.

Kostraba JN, Cruickshanks KJ, Lawler-Heavner J, et al. “Early exposure to cow’s milk and solid foods in infancy, genetic predisposition, and risk of IDDM.” Diabetes 42 (1993): 288–295.

Pyke DA. “The genetic perspective: putting research into practice.” In: Diabetes 1988, Amsterdam,1989, pp. 1227–1230.

Kaprio J, Tuomilehto J, Koskenvuo M, et al. ”Concordance for Type 1 (insulin-dependent)and Type 2 (non-insulin-dependent) diabetes mellitus in a population-based cohort of twins in Finland.” Diabetologia 35 (1992): 1060–1067.

Dahl-Jorgensen K, Joner G, and Hanssen KF. “Relationship between cow’s milk consumption and incidence of IDDM in childhood.” Diabetes Care 14 (1991): 1081–1083.

The proportion of Type 1 diabetes due to the consumption of cow’s milk, the r2 value, is 96%.

LaPorte RE, Tajima N, Akerblom HK, et al. “Geographic differences in the risk of insulin dependent diabetes mellitus: the importance of registries.” Diabetes Care 8(Suppl. 1) (1985):101–107.

Bodansky HJ, Staines A, Stephenson C, et al. “Evidence for an environmental effect in the aetiology of insulin dependent diabetes in a transmigratory population.” Brit. Med. Journ. 304(1992): 1020–1022.

Burden AC, Samanta A, and Chaunduri KH. “The prevalence and incidence of insulin-dependent diabetes in white and Indian children in Leicester city (UK).” Int. J. Diabetes Dev.Countries 10 (1990): 8–10.

Elliott R, and Ong TJ. “Nutritional genomics.” Brit. Med. Journ. 324 (2002): 1438–1442.

Onkamo P, Vaananen S, Karvonen M, et al. “Worldwide increase in incidence of Type 1 diabetes—the analysis of the data on published incidence trends.” Diabetologia 42 (1999):1395–1403.

Gerstein HC. “Cow’s milk exposure and Type 1 diabetes mellitus: a critical overview of the clinical literature.” Diabetes Care 17 (1994): 13–19.

Kimpimaki T, Erkkola M, Korhonen S, et al. “Short-term exclusive breastfeeding predisposes young children with increased genetic risk of Type 1 diabetes to progressive beta-cell autoimmunity.” Diabetologia 44 (2001): 63–69.

Virtanen SM, Laara E, Hypponen E, et al. ”Cow’s milk consumption, HLA-DQB1 genotype,and Type 1 diabetes.” Diabetes 49 (2000): 912–917.

Monetini L, Cavallo MG, Stefanini L, et al. “Bovine beta-casein antibodies in breast- and bottle-fed infants: their relevance in Type 1 diabetes.” Diabetes Metab. Res. Rev. 17 (2001):51–54.

Norris JM, and Pietropaolo M. “Review article. Controversial topics series: milk proteins and diabetes.” J. Endocrinol. Invest. 22 (1999): 568–580.

Reingold SC. ”Research Directions in Multiple Sclerosis.” National Multiple Sclerosis Society,November 25, 2003. Accessed at http://www.nationalmssociety.org/%5CBrochures-Research.asp

Ackermann A. “Die multiple sklerose in der Schweiz.” Schweiz. med. Wchnschr. 61 (1931):1245–1250.

Swank RL. “Multiple sclerosis: correlation of its incidence with dietary fat.” Am. J. Med. Sci.220 (1950): 421–430.

Dip JB. “The distribution of multiple sclerosis in relation to the dairy industry and milk consumption.”New Zealand Med. J. 83 (1976): 427–430.

McDougall JM. 2002. Multiple sclerosis stopped by McDougall/Swank Program.www.nealhendrickson.com/McDougall/McDnewannouncementSwank021112.htm. Accessed Nov.16, 2002.

McLeod JG, Hammond SR, and Hallpike JF. “Epidemiology of multiple sclerosis in Australia.With NSW and SA survey results.” Med. J. Austr 160 (1994): 117–122.

Lawrence JS, Behrend T, Bennett PH, et al. ”Geographical studies of rheumatoid arthritis.”Ann. Rheum. Dis. 25 (1966): 425–432.

Keen H, and Ekoe JM. “The geography of diabetes mellitus.” Brit. Med. Journ. 40 (1984):359–365.

Swank RL. “Effect of low saturated fat diet in early and late cases of multiple sclerosis.” Lancet336 (1990): 37–39.

Swank RL. “Treatment of multiple sclerosis with low fat diet.” A.M.A. Arch. Neurol. Psychiatry69 (1953): 91–103.

Swank RL, and Bourdillon RB. “Multiple sclerosis: assessment of treatment with modified low fat diet.”J. Nerv. Ment. Dis. 131 (1960): 468–488.

Swank RL. “Multiple sclerosis: twenty years on low fat diet.” Arch. Neurol. 23 (1970): 460–474.

Agranoff BW, and Goldberg D. “Diet and the geographical distribution of multiple sclerosis.”Lancet 2(7888) (November 2 1974): 1061–1066.

Malosse D, Perron H, Sasco A, et al. ”Correlation between milk and dairy product consumption and multiple sclerosis prevalence: a worldwide study.” Neuroepidemiology 11 (1992):304–312.

Malosse D, and Perron H. “Correlation analysis between bovine populations, other farm animals,house pets, and multiple sclerosis prevalence.” Neuroepidemiology 12 (1993): 15–27.

Lauer K. ”Diet and multiple sclerosis.” Neurology 49(suppl 2) (1997): S55–S61.

Swank RL, Lerstad O, Strom A, et al. ”Multiple sclerosis in rural Norway. Its geographic distribution and occupational incidence in relation to nutrition.” New Engl. J. Med. 246 (1952):721–728.

Dalgleish AG. ”Viruses and multiple sclerosis.” Acta Neurol. Scand. Suppl. 169 (1997): 8–15.

McAlpine D, Lumsden CE, and Acheson ED. Multiple sclerosis: a reappraisal. Edinburgh and London: E&S Livingston, 1965.

Alter M, Liebowitz U, and Speer J. “Risk of multiple sclerosis related to age at immigration to Israel.”Arch. Neurol. 15 (1966): 234–237.

Kurtzke JF, Beebe GW, and Norman JE, Jr. “Epidemiology of multiple sclerosis in U.S. veterans:1. Race, sex, and geographic distribution.” Neurology 29 (1979): 1228–1235.

Ebers GC, Bulman DE, Sadovnick AD, et al. “A population-based study of multiple sclerosis in twins.”New Engl. J. Med. 315 (1986): 1638–1642.

Acheson ED, Bachrach CA, and Wright FM. “Some comments on the relationship of the distribution of multiple sclerosis to latitude solar radiation and other variables.” Acta PsychiatricaNeurologica Scand. 35 (Suppl.147) (1960): 132–147.

Warren S, and Warren KG. “Multiple sclerosis and associated diseases: a relationship to diabetes mellitus.” J. Canadian Sci. Neurol. 8 (1981): 35–39.

Wertman E, Zilber N, and Abransky O. “An association between multiple sclerosis and Type1 diabetes mellitus.” J. Neurol. 239 (1992): 43–45.

Marrosu MG, Cocco E, Lai M, et al. “Patients with multiple sclerosis and risk of Type 1 diabetesmellitus in Sardinia, Italy: a cohort study.” Lancet 359 (2002): 1461–1465.

Buzzetti R, Pozzilli P, Di Mario U, et al. “Multiple sclerosis and Type 1 diabetes.” Diabetologia45 (2002): 1735–1736.

Lux WE, and Kurtzke JF. ”Is Parkinson’s disease acquired? Evidence from a geographic comparison with multiple sclerosis.” Neurology 37 (1987): 467–471.

Prahalad S, Shear ES, Thompson SD, et al. “Increased Prevalence of Familial Autoimmunity in Simplex and Multiplex Families with Juvenile Rheumatoid Arthritis.” Arthritis Rheumatism46 (2002): 1851–1856.

Cantorna MT, Munsick C, Bemiss C, et al. ”1,25-Dihydroxycholecalciferol Prevents and Ameliorates Symptoms of Experimental Murine Inflammatory Bowel Disease.” J. Nutr. 130(2000): 2648–2652.

Cantorna MT, Woodward WD, Hayes CE, et al. “1,25-Dihydroxyvitamin D3 is a positive regulator for the two anti-encephalitogenic cytokines TGF-B1 and IL-4.” J Immunol. 160 (1998):5314–5319.

Cantorna MT, Humpal-Winter J, and DeLuca HF. ”Dietary calcium is a major factor in 1,25-dihydroxycholecalciferol suppression of experimental autoimmune encephalomyelitis in mice.” J. Nutr. 129 (1999): 1966–1971.

Multiple Sclerosis International Federation. “Alternative Therapies.” November 25,2003. Accessed at www.msif.org/en/symptoms_treatments/treatment_overview/alternative.html

Chapter 10

Frassetto LA, Todd KM, Morris C, Jr., et al. ”Worldwide incidence of hip fracture in elderly women: relation to consumption of animal and vegetable foods.” J. Gerontology 55 (2000):M585–M592.

Abelow BJ, Holford TR, and Insogna KL. ”Cross-cultural association between dietary animalprotein and hip fracture: a hypothesis.” Calcif. Tissue Int. 50 (1992): 14–18.

Wachsman A, and Bernstein DS. “Diet and osteoporosis.” Lancet May 4, 1968 (1968): 958–959.

Barzel U.S.. ”Acid loading and osteoporosis.” J. Am. Geriatr. Soc. 30 (1982): 613.

Sherman HC. ”Calcium requirement for maintenance in man.” J. Biol. Chem. 39 (1920):21–27.

Animal protein includes more of the sulphur-containing amino acids. When digested and metabolized, these amino acids produce the acid-forming sulphate ion, which must be excreted by the kidney. A recent report showed a remarkable 84% correlation between animal protein consumption and urinary acid excretion of sulphate.

Brosnan JT, and Brosnan ME. “Dietary protein, metabolic acidosis, and calcium balance.” In:H. H. Draper (ed.), Advances in Nutritional Research, pp. 77–105. New York: Plenum Press,1982.

Frassetto LA, Todd KM, Morris RC, Jr., et al. “Estimation of net endogenous noncarbonicacid production in humans from diet potassium and protein contents.” Am. J. Clin. Nutri. 68(1998): 576–583.

Margen S, Chu J-Y, Kaufmann NA, et al. “Studies in calcium metabolism. I. The calciuretic effect of dietary protein.” Am. J. Clin. Nutr. 27 (1974): 584–589.

Hegsted M, Schuette SA, Zemel MB, et al. “Urinary calcium and calcium balance in young men as affected by level of protein and phosphorus intake.” J. Nutr. 111 (1981): 553–562.

Kerstetter JE, and Allen LH. ”Dietary protein increases urinary calcium.” J. Nutr. 120 (1990):134–136.

Westman EC, Yancy WS, Edman JS, et al. “Carbohydrate Diet Program.” Am. J. Med. 113(2002): 30–36.

Sellmeyer DE, Stone KL, Sebastian A, et al. ”A high ratio of dietary animal to vegetable protein increases the rate of bone loss and the risk of fracture in postmenopausal women.” Am.J. Clin. Nutr. 73 (2001): 118–122.

Hegsted DM. ”Calcium and osteoporosis.” J. Nutr. 116 (1986): 2316–2319.

Heaney RP. “Protein intake and bone health: the influence of belief systems on the conduct of nutritional science.” Am. J. Clin. Nutr. 73 (2001): 5–6.

Cummings SR, and Black D. “Bone mass measurements and risk of fracture in Caucasianwomen: a review of findings for prospective studies.” Am. J. Med. 98(Suppl 2A) (1995):2S–24S.

Marshall D, Johnell O, and Wedel H. ”Meta-analysis of how well measures of bone mineral density predict occurrence of osteoporotic fractures.” Brit. Med. Journ. 312 (1996): 1254–1259.

Lips P. “Epidemiology and predictors of fractures associated with osteoporosis.” Am. J. Med.103(2A) (1997): 3S–11S.

Lane NE, and Nevitt MC. “Osteoarthritis, bone mass, and fractures: how are they related?”Arthritis Rheumatism 46 (2002): 1–4.

Lucas FL, Cauley JA, Stone RA, et al. ”Bone mineral density and risk of breast cancer: differences by family history of breast cancer.” Am. J. Epidemiol. 148 (1998): 22–29.

Cauley JA, Lucas FL, Kuller LH, et al. “Bone mineral density and risk of breast cancer in older women: the study of osteoporotic fractures.” JAMA 276 (1996): 1404–1408.

Mincey BA. “Osteoporosis in women with breast cancer.” Curr. Oncol. Rpts. 5 (2003): 53–57.

Riis BJ. “The role of bone loss.” Am. J. Med. 98(Suppl 2A) (1995): 2S–29S.

Ho SC. ”Body measurements, bone mass, and fractures: does the East differ from the West?” Clin. Orthopaed. Related Res. 323 (1996): 75–80.

Aspray TJ, Prentice A, Cole TJ, et al. ”Low bone mineral content is common but osteoporotic fractures are rare in elderly rural Gambian women.” J. Bone Min. Res. 11 (1996):1019–1025.

Tsai K-S. “Osteoporotic fracture rate, bone mineral density, and bone metabolism in Taiwan.”J. Formosan Med. Assoc. 96 (1997): 802–805.

Wu AH, Pike MC, and Stram DO. “Meta-analysis: dietary fat intake, serum estrogen levels,and the risk of breast cancer.” J. Nat. Cancer Inst. 91 (1999): 529–534.

UCLA Kidney Stone Treatment Center. “Kidney Stones—Index.” March, 1997. Accessed at http://www.radsci.ucla.edu:8000/gu/stones/kidneystone.htm

Stamatelou KK, Francis ME, Jones CA, et al. “Time trends in reported prevalence of kidney stones.”Kidney Int. 63 (2003): 1817–1823.

This genetically rare type of kidney stone results from an inability of the kidney to reabsorb cysteine, an amino acid.

Ramello A, Vitale C, and Marangella M. “Epidemiology of nephrolothiasis.” J. Nephrol.13(Suppl 3) (2000): S65–S70.

Robertson WG, Peacock M, and Hodgkinson A. “Dietary changes and the incidence of urinary calculi in the U.K. between 1958 and 1976.” Chron. Dis. 32 (1979): 469–476.

Robertson WG, Peacock M, Heyburn PJ, et al. “Risk factors in calcium stone disease of the urinary tract.” Brit. J. Urology 50 (1978): 449–454.

Robertson WG. “Epidemiological risk factors in calcium stone disease.” Scand. J. Urol.Nephrol. Suppl. 53 (1980): 15–30.

Robertson WG, Peacock M, Heyburn PJ, et al. “Should recurrent calcium oxalate stone formers become vegetarians?” Brit. J. Urology 51 (1979): 427–431.

This information was shown in Dr. Robertson’s seminar in Toronto.

Robertson WG. “Diet and calcium stones.” Miner Electrolyte Metab. 13 (1987): 228–234.

Cao LC, Boeve ER, de Bruijn WC, et al. “A review of new concepts in renal stone research.”Scanning Microscopy 7 (1993): 1049–1065.

Friedman DS, Congdon N, Kempen J, et al. ”Vision problems in the U.S.: prevalence of adult vision impairment and age-related eye disease in America.” Bethesda, MD: Prevent Blindness in America. National Eye Institute, 2002.

Foote CS. Photosensitized oxidation and singlet oxygen: consequences in biological systems. Vol.2 New York: Academic Press, 1976.

Seddon JM, Ajani UA, Sperduto RD, et al. “Dietary carotenoids, vitamins A, C, and E, and advanced age-related macular degeneration.” JAMA 272 (1994): 1413–1420.

Eye Disease Case-Control Study Group. “Antioxidant status and neovascular age-related macular degeneration.” Arch. Ophthalmol. 111 (1993): 104–109

The other four food groups were broccoli, carrot, sweet potato, and winter squash, showing disease reductions of 53%, 28%, 33% and 44%, respectively. Each reduction was only approaching or was marginally statistically significant.

Berman ER. Biochemistry of the eye. (Perspectives in vision research). New York, N.Y.: Plenum Publishing Corporation, 1991.

Lyle BJ, Mares-Perlman JA, Klein BEK, et al. “Antioxidant Intake and Risk of Incident Age-related Nuclear Cataracts in the Beaver Dam Eye Study.” Am. J. Epidemiol. 149 (1999):801–809.

Bates CJ, Chen SJ, Macdonald A, et al. “Quantitation of vitamin E and a carotenoid pigment in cataracterous human lenses, and the effect of a dietary supplement.” Int. J. Vitam. Nutr. Res.66 (1996): 316–321.

Varma SD, Beachy NA, and Richards RD. ”Photoperoxidation of lens lipids: prevention by vitamin E.”Photochem. Photobiol. 36 (1982): 623–626.

Talan J. “Alzheimer’s diagnoses can be two years late.” Ithaca Journal: 8A.

Petersen RC, Smith GE, Waring SC, et al. “Mild cognitive impairment.” Arch. Neurol. 56(1999): 303–308.

Kivipelto M, Helkala E-L, Hanninen T, et al. ”Midlife vascular risk factors and late-life mildcognitive impairment. A population based study.” Neurology 56 (2001): 1683–1689.

Breteler MMB, Claus JJ, Grobbee DE, et al. “Cardiovascular disease and distribution of cognitive function in elderly people: the Rotterdam Study.” Brit. Med. Journ. 308 (1994):1604–1608.

Haan MN, Shemanski L, Jagust WJ, et al. “The role of APOE e4 in modulating effects of other risk factors for cognitive decline in elderly persons.” JAMA 282 (1999): 40–46.

Sparks DL, Martin TA, Gross DR, et al. “Link between heart disease, cholesterol, and Alzheimer’s Disease: a review.” Microscopy Res. Tech. 50 (2000): 287–290.

Slooter AJ, Tang MX, van Duijn CM, et al. “Apolipoprotein E e4 and risk of dementia with stroke. A population based investigation.” JAMA 277 (1997): 818–821.

Messier C, and Gagnon M. ”Glucose regulation and cognitive functions: relation to Alzheimer’s disease and diabetes.” Behav. Brain Res. 75 (1996): 1–11.

Ott A, Stolk RP, Hofman A, et al. “Association of diabetes mellitus and dementia: the Rotterdam Study.”Diabetologia 39 (1996): 1392–1397.

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Launer LJ, Masaki K, Petrovitch H, et al. “The association between midlife blood pressure levels and late-life cognitive function.” JAMA 274 (1995): 1846–1851.

White, L., Petrovitch, H., Ross, G. W., Masaki, K. H., Abbot, R. D., Teng, E. L., Rodriquez, B. L., Blanchette, P. L., Havlik, R., Wergowske, G., Chiu, D., Foley, D. J., Murdaugh, C., and Curb, J D. ”Prevalence of dementia in older Japanese-American men in Hawaii.  The Honolulu-Asia Aging Study.” JAMA, 276: 955-960, 1996.

Hendrie HC, Ogunniyi A, Hall KS, et al. “Incidence of dementia and Alzheimer Disease in communities: Yoruba residing in Ibadan, Nigeria and African Americans residing in Indianapolis,Indiana.” JAMA 285 (2001): 739–747.

Chandra V, Pandav R, Dodge HH, et al. “Incidence of Alzheimer’s disease in a rural community in India: the Indo-U.S. Study.” Neurology 57 (2001): 985–989.

Grant WB. “Dietary links to Alzheimer’s Disease: 1999 Update.” J. Alzheimer’s Dis 1 (1999):197–201.

Grant WB. “Incidence of dementia and Alzheimer disease in Nigeria and the United States.”JAMA 285 (2001): 2448.

This recently published study is more interesting than the others because vitamin E was measured in a way that is more discriminating by considering the fact that vitamin E is carried inthe blood fat. That is, a high level of blood vitamin E may, at times, be due to high levels of blood fat.

The effects of vitamin C and selenium in a study by Perkins (Am. J. Epidemiol. 150 (1999):37–44) were not statistically significant in a logistic regression model, according to the authors. I disagree with their conclusion because the inverse “dose-response” trend (high antioxidant blood levels, less memory loss) was impressive and clearly significant. The authors failed to address this finding in their analysis.

Ortega RM, Requejo AM, Andres P, et al. “Dietary intake and cognitive function in a group of elderly people.” Am. J. Clin. Nutr. 66 (1997): 803–809.

Perrig WJ, Perrig P, and Stahelin HB. “The relation between antioxidants and memory performance in the old and very old.” J. Am. Geriatr. Soc. 45 (1997): 718–724.

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Jama JW, Launer LJ, Witteman JCM, et al. “Dietary antioxidants and cognitive function ina population-based sample of older persons: the Rotterdam Study.” Am. J. Epidemiol. 144(1996): 275–280.

Martin A, Prior R, Shukitt-Hale B, et al. ”Effect of fruits, vegetables or vitamin E-rich diet onvitamins E and C distribution in peripheral and brain tissues: implications for brain function.”J. Gerontology 55A (2000): B144–B151.

Joseph JA, Shukitt-Hale B, Denisova NA, et al. ”Reversals of age-related declines in neuronal signal transduction, cognitive, and motor behavioral deficits with blueberry, spinach, or strawberry dietary supplementation.” J. Neurosci. 19 (1999): 8114–8121.

Gillman MW, Cupples LA, Gagnon D, et al. “Protective effect of fruits and vegetables on development of stroke in men.” JAMA 273 (1995): 1113–1117.

Kalmijn S, Launer LJ, Ott A, et al. “Dietary fat intake and the risk of incident dementia in the Rotterdam Study.” Ann. Neurol. 42 (1997): 776–782.

Alzheimer’s trend was not statistically significant, perhaps due to the small number of disease cases.

Clarke R, Smith D, Jobst KA, et al. “Folate, vitamin B12, and serum total homocysteine levelsin confirmed Alzheimer disease.” Arch. Neurol. 55 (1998): 1449–1455.

McCully KS. “Homocysteine theory of arteriosclerosis: development and current status.” In:A. M. Gotto, Jr. and R. Paoletti (eds.), Athersclerosis reviews, Vol. 11, pp. 157–246. New York:Raven Press, 1983.

There is a potential snag in this logic, however. Homocysteine levels are regulated in part by B vitamins, most notably folic acid and vitamin B12, and people who are deficient in these vitamins may have higher homocysteine levels. People who do not consume animal-basedfoods are at risk for having low B12 levels, and thus high homocysteine levels. However, as described in chapter eleven, this has more to do with our separation from nature, and not adeficiency of plant-based diets.

Part III

1. http://www.southbeachdiet.com, accessed 4/26/04

Chapter 11

Atkins RC. Dr. Atkins’ New Diet Revolution. New York, NY: Avon Books, 1999.

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Omenn GS, Goodman GE, Thornquist MD, et al. “Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease.” New Engl. J. Med. 334 (1996):1150–1155.

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Morris CD, and Carson S. “Routine vitamin supplementation to prevent cardiovascular disease:a summary of the evidence for the U.S. Preventive Services Task Force.” Ann. InternalMed. 139 (2003): 56–70.

Kolata G. ”Vitamins: more may be too many (Science Section).” The New York Times April 29,2003: 1, 6.

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Holden JM, Eldridge AL, Beecher GR, et al. ”Carotenoid content of U.S. foods: an update of the database.” J. Food Comp. Anal. 12 (1999): 169–196.

The exact food listings in the database were: Ground Beef, 80% lean meat/20% fat, raw; Pork,fresh, ground, raw; Chicken, broilers or fryers, meat and skin, raw; Milk, dry, whole; Spinach,raw; Tomatoes, red, ripe, raw, year-round average; Lima Beans, large, mature seeds, raw; Peas,green, raw; Potatoes, russet, flesh and skin, raw.

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Shermer M. “Skeptical sayings. Wit and wisdom from skeptics past and present.” Skeptic 9(2002): 28.

I’ve never really liked putting such specific cutoff points on initiation, promotion and progression of chronic disease, because these cutoff points for each stage of chronic disease arecompletely arbitrary. What’s important to know is that a chronic disease can be with U.S. formost of our lives, and if it progresses, it will do so in a very fluid, continuous manner.

Hildenbrand GLG, Hildenbrand LC, Bradford K, et al. “Five-year survival rates of melanoma patients treated by diet therapy after the manner of Gerson: a retrospective review.” Alternative Therapies in Health and Medicine 1 (1995): 29–37.

McDougall JA. McDougall’s Medicine, A Challenging Second Opinion. Piscataway, NJ: NewCentury Publishers, Inc., 1985.

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Swank RL. “Effect of low saturated fat diet in early and late cases of multiple sclerosis.” Lancet 336 (1990): 37–39.

Chapter 12
N/A
Chapter 13

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Chapter 14

National Research Council. Diet, Nutrition and Cancer. Washington, DC: National Academy Press, 1982.

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Marchione M. “Taking the long view; for 25 years, Harvard’s Nurses’ Health Study has sought answers to women’s health questions.” Milwaukee Journal-Sentinel July 16, 2001: 01G.

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Chen J, Campbell TC, Li J, et al. Diet, life-style and mortality in China. A study of the characteristics of 65 Chinese counties. Oxford, UK; Ithaca, NY; Beijing, PRC: Oxford University Press;Cornell University Press; People’s Medical Publishing House, 1990.

Hu FB, Stampfer MJ, Manson JE, et al. “Dietary protein and risk of ischemic heart disease in women.” Am. Journ. Clin. Nutr. 70 (1999): 221–227.

Holmes MD, Hunter DJ, Colditz GA, et al. “Association of dietary intake of fat and fatty acids with risk of breast cancer.” JAMA 281 (1999): 914–920.

U.S. Department of Agriculture. “Agriculture Fact Book.” Washington, DC: U.S. Department of Agriculture, 1998. cited in: Information Plus Nutrition: a key to good health. Wylie, TX:Information Plus, 1999.

While the average percentage of calories derived from fat has gone down slightly, averagedaily fat intake, in grams, has stayed the same or has gone up.

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Henderson MM, Kushi LH, Thompson DJ, et al. ”Feasibility of a randomized trial of a lowfatdiet for the prevention of breast cancer: dietary compliance in the Women’s Health Trial Vanguard Study.” Prev. Med. 19 (1990): 115–133.

Self S, Prentice R, Iverson D, et al. “Statistical design of the Women’s Health Trial.” Controlled Clin. Trials 9 (1988): 119–136.

Armstrong D, and Doll R. “Environmental factors and cancer incidence and mortality indifferent countries, with special reference to dietary practices.” Int. J. Cancer 15 (1975):617–631.

Campbell TC. “The dietary causes of degenerative diseases: nutrients vs foods.” In: N. J.Temple and D. P. Burkitt (eds.), Western diseases: their dietary prevention and reversibility, pp.119–152. Totowa, NJ: Humana Press, 1994.

White E, Shattuck AL, Kristal AR, et al. “Maintenance of a low-fat diet: follow-up of the Women’s Health Trial.” Cancer Epi. Biom. Prev. 1 (1992): 315–323.

Willett WC, Hunter DJ, Stampfer MJ, et al. “Dietary fat and fiber in relation to risk of breast cancer. An 8-year follow-up.” J. Am. Med. Assoc. 268 (1992): 2037–2044.

Willett W. “Dietary fat and breast cancer.” Toxicol. Sci. 52[Suppl] (1999): 127–146.

Hunter DJ, Spiegelman D, Adami H-O, et al. “Cohort studies of fat intake and the risk of breast cancer—a pooled analysis.” New Engl. J. Med. 334 (1996): 356–361.

Missmer SA, Smith-Warner SA, Spiegelman D, et al. “Meat and dairy consumption and breastcancer: a pooled analysis of cohort studies.” Int. J. Epidemiol. 31 (2002): 78–85.

Rockhill B, Willett WC, Hunter DJ, et al. “Physical activity and breast cancer risk in a cohort of young women.” J. Nat. Cancer Inst. 90 (1998): 1155–1160.

Smith-Warner SA, Spiegelman D, Adami H-O, et al. “Types of dietary fat and breast cancer: a pooled analysis of cohort studies.” Int. J. Cancer 92 (2001): 767–774.

Hunter DJ, Morris JS, Stampfer MJ, et al. “A prospective study of selenium status and breast cancer risk.” JAMA 264 (1990): 1128–1131.

Smith-Warner SA, Spiegelman D, Yaun S-S, et al. “Intake of fruits and vegetables and risk of breast cancer: a pooled analysis of cohort studies.” JAMA 285 (2001): 769–776.

Mukamal KJ, Conigrave KM, Mittleman MA, et al. “Roles of drinking pattern and type of alcohol consumed in coronary heart disease in men.” New Engl. J. Med. 348 (2003): 109–118.

Tanasescu M, Hu FB, Willett WC, et al. “Alcohol consumption and risk of coronary heart disease among men with Type 2 diabetes mellitus.” J. Am. Coll. Cardiol. 38 (2001): 1836–1842.

Smith-Warner SA, Spiegelman D, Yaun S-S, et al. “Alcohol and breast cancer in women. A pooled analysis of cohort studies.” JAMA 279 (1998): 535–540.

He K, Rimm EB, Merchant A, et al. “Fish consumption and risk of stroke in men.” JAMA 288(2002): 3130–3136.

Albert CM, Hennekens CH, O’Donnell CJ, et al. “Fish consumption and risk of sudden cardiac death.”JAMA 279 (1998): 23–28.

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Hu FB, Stampfer MJ, Rimm EB, et al. ”A prospective study of egg consumption and risk of cardiovascular disease in men and women.” JAMA 281 (1999): 1387–1394.

Hu FB, Manson JE, and Willett WC. “Types of dietary fat and risk of coronary heart disease:a critical review.” J. Am. Coll. Nutr. 20 (2001): 5–19.

Mitchell S. “Eggs might reduce breast cancer risk.” United Press International Feb. 21, 2003.

Steinmetz, K. A. and Potter, J. J. “Egg consumption and cancer of the colon and rectum.” Eur. J. Cancer Prev., 3: 237-245, 1994.

Giovannucci E, Rimm EB, Stampfer MJ, et al. “Intake of fat, meat, and fiber in relation to risk of colon cancer in men.” Cancer Res. 54 (1994): 2390–2397.

Fuchs CS, Giovannucci E, Colditz GA, et al. “Dietary fiber and the risk of colorectal cancer and adenoma in women.” New Engl. J. Med. 340 (1999): 169–176.

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Boyd NF, Martin LJ, Noffel M, et al. “A meta-analysis of studies of dietary-fat and breast cancer risk.”Brit. J. Cancer 68 (1993): 627–636.

Campbell TC. “Animal protein and ischemic heart disease.” Am. J. Clin. Nutr. 71 (2000):849–850.

Hu FB, and Willett W. “Reply to TC Campbell.” Am. J. Clin. Nutr. 71 (2000): 850.

Morris CD, and Carson S. “Routine vitamin supplementation to prevent cardiovascular disease:a summary of the evidence for the U.S. Preventive Services Task Force.” Ann. InternalMed. 139 (2003): 56–70.

U.S. Preventive Services Task Force. “Routine vitamin supplementation to prevent cancer andcardiovascular disease: recommendations and rationale.” Ann. Internal Med. 139 (2003): 51–55.

Chapter 15

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Ntambi JM, Choi Y, Park Y, et al. “Effect of conjugated linoleic acid (CLA) on immune responses, body composition and stearoyl-CoA desaturase.” Can. J. Appl. Physiol. 27 (2002): 617–627.

Ip C, Chin SF, Scimeca JA, et al. “Mammary cancer prevention by conjugated dienoic derivative of linoleic acid.” Cancer Res. 51 ([1991): 6118–6124.

Ip C, Cheng J, Thompson HJ, et al. "Retention of conjugated linoleic acid in the mammary gland is associated with tumor inhibition during the post-initiation phase of carcinogenesis." Carcinogensis 18 (1997): 755–759.

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Ip C, Dong Y, Thompson HJ, et al. "Control of rat mammary epithelium proliferation by conjugated linoleic acid." Nutr. Cancer 39 (2001): 233–238.

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Chapter 16

Food and Nutrition Board, and Institute of Medicine. “Dietary reference intakes for energy,carbohydrates, fiber, fat, fatty acids, cholesterol, protein, and amino acids (macronutrients).” Washington, DC: The National Academy Press, 2002. Accessed at www.nap.edu/catalog/10490.html

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The RDA has been expressed as a singular quantity of protein, as 0.8 grams of protein per kilogram of body weight. Assuming a daily intake of 2,200 calories for a 70 kg person, this 0.8 grams is equivalent to about 10–11% of total calories: 70 kg X 0.8 gm/kg X 4 cal/gm X 1/2200 cal X 100 = 10.2%.

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Calculated from NIH Disease Funding Table: Special Areas of Interest. See previous reference.

National Cancer Institute. “FY 1999 Questions and Answers provided for the record for the FY 1999 House Appropriations Subcommitee.” July 15, 2003. Accessed at www3.cancer.gov/admin/fmb/1999QAs.htm.

National Cancer Institute. FY 2001 Congressional Justification. Accessed March 2, 2004. Available from http://www3.cancer.gov/admin/fmb/index.html.

Angell M. “The pharmaceutical industry—to whom is it accountable?” New Engl. J. Med. 342 (2000): 1902–1904.

National Cancer Institute. FY 2004 Congressional Justification. Accessed 2003. Available from www3.cancer.gov/admin/fmb/index/html.

Demas A. Food Education in the Elementary Classroom as a Means of Gaining Acceptance of Diverse Low Fat Foods in the School Lunch Program [PhD Dissertation]. Ithaca, NY: Cornell University, 1995:325pp.

Chapter 17

Austoker J. ”The ‘treatment of choice’: breast cancer surgery 1860–1985.” Soc. Soc. Hist. Med. Bull.(London) 37 (1985): 100–107.

Naifeh SW. The Best Doctors in America, 1994–1995. Aiken, S.C.: Woodward & White, 1994.

McDougall JA, and McDougall MA. The McDougall Plan. Clinton, NJ: New Win Publishing, Inc., 1983.

Committee on Nutrition in Medical Education. “Nutrition Education in U.S. Medical Schools.”Washington, DC: National Academy of Sciences, 1985.

White PL, Johnson OC, and Kibler MJ. “Council on Foods and Nutrition, American Medical Association—its relation to physicians.” Postgraduate Med. 30 (1961): 502–507.

Lo C. “Integrating nutrition as a theme throughout the medical school curriculum.” Am. J. Clin. Nutr. 72(Suppl) (2000): 882S–889S.

Pearson TA, Stone EJ, Grundy SM, et al. “Translation of nutrition science into medical education: the Nutrition Academic Award Program.” Am. J. Clin. Nutr. 74 (2001): 164–170.

Kassler WJ. ”Appendix F: Testimony of the American Medical Student Association.” Washington, DC: National Academy of Sciences, 1985.

Zeisel SH, and Plaisted CS. “CD-ROMs for Nutrition Education.” J. Am. Coll. Nutr. 18 (1999): 287.

Two or three reputable agencies have also sponsored this program, but I suspect that the administrators of these agencies felt it necessary to associate with a project in medical education for their own purposes, regardless of the dubious list of other organizations.

http://www.med.unc.edu/nutr/nim/FAQ.htm.

Weinsier RL, Boker JR, Brooks CM, et al. “Nutrition training in graduate medical (residency) education: a survey of selected training programs.” Am. J. Clin. Nutr. 54 (1991): 957–962.

Young EA. “National Dairy Council Award for Excellence in Medical/Dental Nutrition Education Lecture, 1992: perspectives on nutrition in medical education.” Am. J. Clin. Nutr. 56 (1992): 745–751.

Kushner RF. “Will there be a tipping point in medical nutrition education?” Am. J. Clin. Nutr. 77 (2003): 288–291.

Angell M. “Is academic medicine for sale?” New Engl. J. Med. 342 (2000): 1516–1518.

Moynihan R. “Who pays for the pizza? Redefining the relationships between doctors and drug companies 1: Entanglement.” Brit. Med. Journ. 326 (2003): 1189–1192.

Moynihan R. “Who pays for the pizza? Redefining the relationships between doctors and drug companies. 2. Disentanglement.” Brit. Med. Journ. 326 (2003): 1193–1196.

Avorn J, Chen M, and Hartley R. “Scientific versus commercial sources of influence on the prescribing behavior of physicians.” Am. J. Med. 73 (1982): 4–8.

Lurie N, Rich EC, Simpson DE, et al. “Pharmaceutical representatives in academic medical centers: interaction with faculty and housestaff.” J. Gen. Intern. Med. 5 (1990): 240–243.

Steinman MA, Shlipak MG, and McPhee SJ. “Of principles and pens: attitudes and practices of medicine housestaff toward pharmaceutical industry promotions.” Am. J. Med. 110 (2001): 551–557.

Lexchin J. “Interactions between physicians and the pharmaceutical industry: what does the literature say?” Can.. Med. Assoc. J. 149 (1993): 1401–1407.

Lexchin J. ”What information do physicians receive from pharmaceutical representatives?” Can. Fam. Physician 43 (1997): 941–945.

Baird P. ”Getting it right: industry sponsorship and medical research.” Can. Med. Assoc. Journ. 168 (2003): 1267–1269.

Smith R. “Medical journals and pharmaceutical companies: uneasy bedfellows.” Brit. Med. Journ. 326 (2003): 1202–1205.

Chopra SS. “Industry funding of clinical trials: benefit or bias?” JAMA 290 (2003): 113–114.

Healy D. “In the grip of the python: conficts at the university-industry interface.” Sci. Engineering Ethics 9 (2003): 59–71.

Olivieri NF. “Patients’ health or company profits? The commericalization of academic research.” Sci. Engineering Ethics 9 (2003): 29–41.

Johnson L. “Schools report research interest conflicts.” The Ithaca Journal October 24, 2002: 3A.

Agovino T. “Prescription use by children multiplying, study says.” The Ithaca Journal Sept. 19, 2002: 1A.

Associated Press. “Survey: many guidelines written by doctors with ties to companies.” The Ithaca Journal Feb. 12, 2002

Weiss R. “Correctly prescribed drugs take heavy toll; millions affected by toxic reactions.” The Washington Post Apr. 15, 1998: A01.

Lasser KE, Allen PD, Woolhandler SJ, et al. “Timing of new black box warnings and withdrawals for prescription medications.” JAMA 287 (2002): 2215–2220.

Lazarou J, Pomeranz B, and Corey PN. “Incidence of adverse drug reactions in hospitalized patients.”JAMA 279 (1998): 1200–1205.

Chapter 18

Macilwain G. The General Nature and Treatment of Tumors. London, UK: John Churchill, 1845.

Williams H. The Ethics of Diet. A Catena of Authorities Deprecatory of the Practice of Flesh-Eating. London: F. Pitman, 1883.

U.S. Census Bureau.U.S. Popclock ProjectionMarch, 2004. Accessed at http://www.census.gov/cgi-bin/popclock.

Centers for Disease Control. “Prevalence of adults with no known risk factors for coronary heart disease-behavioral risk factor surveillance system, 1992.” Morbidity and mortality weekly report 43 (February 4, 1994): 61–63,69.

Kaufman DW, Kelly JP, Rosenberg L, et al. “Recent patterns of medication use in the ambulatory adult population of the United States: the Slone survey.” J. Am. Med. Assoc. 287 (2002): 337–344.

Flegal KM, Carroll MD, Ogden CL, et al. ”Prevalence and trends in obesity among U.S.adults, 1999–2000.” JAMA 288 (2002): 1723–1727.

American Heart Association. ”High blood cholesterol and other lipids—statistics.” March, 2004. Accessed at http://www.americanheart.org/presenter.jhtml?identifier=2016.

Wolz M, Cutler J, Roccella EJ, et al. ”Statement from the National High Blood Pressure Education Program: prevalence of hypertension.” Am. J. Hypertens. 13 (2000): 103–104.

Lucas JW, Schiller JS, and Benson V. “Summary health statistics for U.S. Adults: National Health Interview Survey, 2001.” National Center for Health Statistics. Vital Health Stat. 10(218). 2004.

Robbins J. The Food Revolution. Berkeley, California: Conari Press, 2001.

I strongly recommend reading John Robbins’ “The Food Revolution,” which convincingly details the connection between your diet and the environment.

World Health Organization. “The World Health Report 1997: Press Release. Human and social costs of chronic diseases will rise unless confronted now, WHO Director-General says.” Geneva, Switzerland: World Health Organization, 1997. Accessed at www.who.int/whr2001/2001/archives/1997/presse.htm.

Blood flow is related to the fourth power of the radius of the cross-section of the vessel. A surprisingly small increase in the opening of the artery makes a huge difference in the all important blood flow.

Vegetarian Resource Group. “How Many Vegetarians Are There?” March, 2004. Accessed atwww.vrg.org/journal/vj2003issue3/vj2003issue3poll.htm.

Herman-Cohen V. “Vegan revolution.” Ithaca Journal (reprinted from LA Times) Aug 11, 2003:12A.

Sabate J, Duk A, and Lee CL. ”Publication trends of vegetarian nutrition articles in biomedical literature, 1966–1995.” Am. J. Clin. Nutr. 70(Suppl) (1999): 601S–607S.

Appendix A

Boyd JN, Misslbeck N, Parker RS, et al. “Sucrose enhanced emergence of aflatoxin B1 (AFB1)-induced GGt positive rat hepatic cell foci.” Fed. Proc. 41 (1982): 356 Abst.

Tannenbaum A, and Silverstone H. “Nutrition in relation to cancer.” Adv. Cancer Res. 1 (1953): 451–501.

Youngman LD. The growth and development of aflatoxin B1-induced preneoplastic lesions, tumors, metastasis, and spontaneous tumors as they are influenced by dietary protein level, type, and intervention.Ithaca, NY: Cornell University, Ph.D. Thesis, 1990.

Youngman LD, and Campbell TC. “Inhibition of aflatoxin B1-induced gamma-glutamyltranspeptidase positive (GGT+) hepatic preneoplastic foci and tumors by low protein diets: evidence that altered GGT+ foci indicate neoplastic potential.” Carcinogenesis 13 (1992): 1607–1613.

Horio F, Youngman LD, Bell RC, et al. “Thermogenesis, low-protein diets, and decreased development of AFB1-induced preneoplastic foci in rat liver.” Nutr. Cancer 16 (1991): 31–41.

Bell RC, Levitsky DA, and Campbell TC. “Enhanced thermogenesis and reduced growth rates do not inhibit GGT+ hepatic preneoplastic foci development.” FASEB J. 6 (1992): 1395 Abs.

Miller DS, and Payne PR. “Weight maintenance and food intake.” J. Nutr. 78 (1962): 255–262.

Stirling JL, and Stock MJ. “Metabolic origins of thermogenesis by diet.” Nature 220 (1968):801–801.

Donald P, Pitts GC, and Pohl SL. ”Body weight and composition in laboratory rats: effects of diets with high or low protein concentrations.” Science 211 (1981): 185–186.

Rothwell NJ, Stock MJ, and Tyzbir RS. “Mechanisms of thermogenesis induced by low protein diets.”Metabolism 32 (1983): 257–261.

Rothwell NJ, and Stock MJ. “Influence of carbohydrate and fat intake on diet-induced thermogenesis and brown fat activity in rats fed low protein diets.” J Nutr 117 (1987): 1721–1726.

Krieger E, Youngman LD, and Campbell TC. “The modulation of aflatoxin(AFB1) induced preneoplastic lesions by dietary protein and voluntary exercise in Fischer 344 rats.” FASEB J.
2 (1988): 3304 Abs.

Appendix B

Chen J, Campbell TC, Li J, et al. Diet, life-style and mortality in China. A study of the characteristics of 65 Chinese counties. Oxford, UK; Ithaca, NY; Beijing, PRC: Oxford University Press; Cornell University Press; People’s Medical Publishing House, 1990.

There were eight-two mortality rates, but about a third of these rates were duplicates of the same disease for people of different ages.

This also means that very little or no useful information is obtained by including the values of all the individuals in the county. There is only one disease rate for each county; thus it is only necessary to have one number for any of the variables being compared with the disease rate.

Piazza A. Food consumption and nutritional status in the People’s Republic of China. London: Westview Press, 1986.

Messina M, and Messina V. The Dietitian’s Guide to Vegetarian Diets. Issues and Applications.Gaithersburg, MD: Aspen Publishers, Inc., 1996.

Appendix C

Holick MF. In: M. E. Shils, J. A. Olson, M. Shike and e. al (eds.), Modern nutrition in health and disease, 9th ed., pp. 329–345. Baltimore, MD: Williams and Wilkins, 1999.

Barger-Lux MJ, Heaney R, Dowell S, et al. “Vitamin D and its major metabolites: serum levels after graded oral dosing in healthy men.” Osteoporosis Int. 8 (1998): 222–230.

The biological half-life of storage vitamin D is 10–19 days, the time it takes for half of it to disappear.

Colston KW, Berger U, and Coombes RC. “Possible role for vitamin D in controlling breast cancer cell proliferation.” Lancet 1 (1989): 188–191.

Nieves J, Cosman F, Herbert J, et al. “High prevalence of vitamin D deficiency and reduced bone mass in multiple sclerosis.” Neurology 44 (1994): 1687–1692.

Al-Qadreh A, Voskaki I, Kassiou C, et al. “Treatment of osteopenia in children with insulin dependent diabetes mellitus: the effect of 1-alpha hydroxyvitamin D3.” Eur. J. Pediatr. 155 (1996): 15–17.

Cantorna MT, Hayes CE, and DeLuca HF. “1,25-Dihydroxyvitamin D3 reversibly blocks the progression of relapsing encephalomyelitis, a model of multiple sclerosis.” Proc. National Acad. Sci 93 (1996): 7861–7864.

Rozen F, Yang X-F, Huynh H, et al. “Antiproliferative action of vitamin D-related compounds and insulin-like growth factor-binding protein 5 accumulation.” J. Nat. Cancer Inst. 89 (1997): 652–656.

Cosman F, Nieves J, Komar L, et al. “Fracture history and bone loss in patients with MS.” Neurology 51 (1998): 1161–1165.

Giovannucci E, Rimm E, Wolk A, et al. “Calcium and fructose intake in relation to risk of prostate cancer.”Cancer Res. 58 (1998): 442–447.

Peehl DM, Krishnan AV, and Feldman D. “Pathways mediating the growth-inhibitory action of vitamin D in prostate cancer.” J. Nutr. 133(Suppl) (2003): 2461S–2469S.

Zella JB, McCary LC, and DeLuca HF. “Oral administration of 1,25-dihydroxyvitamin D3 completely protects NOD mice from insulin-dependent diabetes mellitus.” Arch. Biochem Biophys. 417 (2003): 77–80.

Davenport CB. “Multiple sclerosis from the standpoint of geographic distribution and race.” Arch. Neurol. Pschiatry 8 (1922): 51–58.

Alter M, Yamoor M, and Harshe M. “Multiple sclerosis and nutrition.” Arch. Neurol. 31 (1974): 267–272.

Van der Mei IA, Ponsonby AL, Blizzard L, et al. “Regional variation in multiple sclerosis prevalence in Australia and its association with ambivalent ultraviolet radiaion.” Neuroepidemiology 20 (2001): 168–174.

McLeod JG, Hammond SR, and Hallpike JF. “Epidemiology of multiple sclerosis in Australia. With NSW and SA survey results.” Med. J. Austr 160 (1994): 117–122.

Holick MF. “Vitamin D: a millenium perspective.” J. Cell. Biochem. 88 (2003): 296–307.

MacLaughlin JA, Gange W, Taylor D, et al. “Cultured psoriatic fibroblasts from involved and uninvolved sites have a partial, but not absolute resistance to the proliferation-inhibtion activity of 1,25-dihydroxyvitamin Ds.” Proc. National Acad. Sci 52 (1985): 5409–5412.

Goldberg P, Fleming MC, and Picard EH. “Multiple sclerosis: decreased relapse rate through dietary supplementation with calcium, magnesium and vitamin D.” Med. Hypoth. 21 (1986): 193–200.

Andjelkovic Z, Vojinovic J, Pejnovic N, et al. “Disease modifying and immunomodulatory effects of high dose 1a(OH)D3 in rheumatoid arthritis patients.” Clin. Exp. Rheumatol. 17 (1999): 453–456.

Hypponen E, Laara E, Reunanen A, et al. “Intake of vitamin D and risk of Type 1 diabetes: a birth-cohort study.” Lancet 358 (2001): 1500–1503.

Breslau NA, Brinkley L, Hill KD, et al. “Relationship of animal protein-rich diet to kidney stone formation and calcium metabolism.” J. Clin. Endocrinol. Metab. 66 (1988): 140–146.

Langman CB. “Calcitriol metabolism during chronic metabolic acidosis.” Semin. Nephrol. 9 (1989): 65–71.

Chan JM, Giovannucci EL, Andersson S-O, et al. “Dairy products, calcium, phosphorus, vitamin D, and risk of prostate cancer (Sweden).” Cancer Causes and Control 9 (1998): 559–566.

Byrne PM, Freaney R, and McKenna MJ. “Vitamin D supplementation in the elderly: review of safety and effectiveness of different regimes.” Calcified Tissue Int. 56 (1995): 518–520.

Agranoff BW, and Goldberg D. ”Diet and the geographical distribution of multiple sclerosis.” Lancet 2(7888) (November 2 1974): 1061–1066.

Akerblom HK, Vaarala O, Hyoty H, et al. “Environmental factors in the etiology of Type 1 diabetes.” Am. J. Med. Genet. (Semin. Med. Genet.) 115 (2002): 18–29.

Chan JM, Stampfer MJ, Ma J, et al. “Insulin-like growth factor-I (IGF-I) and IGF binding protein-3 as predictors of advanced-stage prostate cancer.” J Natl Cancer Inst 94 (2002): 1099–1109.

Cohen P, Peehl DM, and Rosenfeld RG. ”The IGF axis in the prostate.” Horm. Metab. res. 26 (1994): 81–84.

Doi SQ, Rasaiah S, Tack I, et al. “Low-protein diet suppresses serum insulin-like growth factor-1 and decelerates the progression of growth hormone-induced glomerulosclerosis.” Am. J. Nephrol. 21 (2001): 331–339.

Heaney RP, McCarron DA, Dawson-Hughes B, et al. “Dietary changes favorably affect bond remodeling in older adults.” J. Am. Diet. Assoc. 99 (1999): 1228–1233.

Allen NE, Appleby PN, Davey GK, et al. “Hormones and diet: low insulin-like growth factor-I but normal bioavailable androgens in vegan men.” Brit. J. Cancer 83 (2000): 95–97.