The China Study References
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.
American Cancer Society. "Cancer Facts and Figures”1998." Atlanta, GA: American Cancer Society, 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.
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.
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.
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.
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. The nutrition of man. New York: F. A. Stokes, 1907.
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.
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.
Higginson J. "Present trends in cancer epidemiology." Proc. Can. Cancer Conf. 8 (1969):40–75.
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.
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.
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)
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.
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.
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.
Exceptions include those foods artificially stripped of their fat, such as non-fat milk.
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.
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
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.
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.
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.
Westman EC, Yancy WS, Edman JS, et al. "Carbohydrate Diet Program." Am. J. Med. 113(2002): 30–36.
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.
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.