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17. lf 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 detect­able 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.
18. 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.
19. 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 interac­tion with cytochrome P-450." Biochem. Pharmacol. 22 (1973): 1005-1014.
20. Mgbodile MUK, Hayes JR, and Campbell TC. "Effect of protein deficiency on the inducibility of the hepatic microsomal drug-metabolizing enzyme system. 11. Effect on enzyme kinetics and electron transport system." Biochem. Pharmacol. 22 (1973): 1125-1132.
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23. Preston RS, HayesJR, and Campbell TC. "The effect of protein deficiency on the in vivo bind­ing of aflatoxin B1 to rat liver macromolecules." Life Sci. 19 (1976): 1191-1198.
24. Portman RS, Plowman KM, and Campbell TC. "On mechanisms affecting species susceptibil­ity to anatoxin." Biochim. Biophys. Acta 208 (1970): 487-495.
25. Prince LO, and Campbell TC. "Effects of sex difference and dietary protein level on the binding of af\atoxin B1 to rat liver chromatin proteins in vivo." Cancer Res. 42 (1982): 5053-5059.
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28. 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.
29. Adekunle AA, Hayes JR. and Campbell TC. "Interrelationships of dietary protein level, afla­toxin B1 metabolism, and hepatic microsomal epoxide hydrase activity." Life Sci. 21 (1977): 1785-1792.
30. Mainigi KD, and Campbell TC. "Effects of low dietary protein and dietary af!atoxin on he­patic glutathione levels in F-344 rats." Toxicol. Appl. Phannacol. 59 (1981): 196-203.
31. Farber E, and Cameron R. "The sequential analysis of cancer development." Adv. Cancer Res. 31 (1980): 125-226.
32. 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 ten­dency. 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 af!atoxin and by feeding a 20% protein diet.
33. Appleton BS, and Campbell TC. "Inhibition of aflatoxin-initiated preneoplastic liver lesions by low dietary protein." Nutr. Cancer 3 (1982): 200-206.
34. Dunaif GE, and Campbell TC. "Relative contribution of dietary protein level and Aflatoxin B dose in generation of presumptive preneoplastic foci in rat liver."]. Natl. Cancer Inst. 78 1
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35. 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."]. Nutr. 121 (1991): 1454-1461.
36. Youngman LD, and Campbell TC. "Inhibition of aflatoxin El-induced gamrna-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.
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39. About 12% dietary protein is required to maximize growth rate, according to the National Research Council of the National Academy of Sciences.
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43. Youngman LD. The growth and dev elopment of ajlatoxin Bl-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.
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Глава 4
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6. There were 82 mortality rates, but about a third of these rates were duplicates of the same disease for different aged people.
7. Calorie intake in China is for a 65 kg adult male doing "light physical work." Comparable data for the American male is adjusted for a body weight of 65 kg.
8. SerVaas C. "Diets that protected against cancers in China." The Saturday Evening Post October 1990: 26-28.
9. 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 were assembled in a second list. Each individual entry in either list was therefore positively related to entries in its own list but inversely related to diseases in the opposite list. Most, but not all, of these correlations were statistically significant.
10. Campbell TC, Chen], Brun T, et al. "China: from diseases of poverty to diseases of affiuence. Policy implications of the epidemiological transition." Ecol. Food Nutr. 27 (1992): 133-144.
11. Chen], Campbell TC, LiJ, 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.
12. 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.
13. Campbell TC, Parpia B, and Chen]. "Diet, lifestyle, and the etiology of coronary artery dis­ease: The Cornell China Study." Am.]. Cardiol. 82 (1998): 18T-21T.
14. 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)
15. Sirtori CR, Nosed.a G, and Descovich GC. "Studies on the use of a soybean protein diet for the 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.
16. Carroll KK. "Dietary proteins and amino acids---their effects on cholesterol metabolism." In:
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18. 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.
19. 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.
20. National Research Council. Diet, Nutrition and Cancer. Washington, DC: National Academy Press, 1982.
21. United States Department of Health and Human Services. The Surgeon General???? Report on Nutrition and Health. Washington, DC: Superintendant of Documents, U.S. Government Printing Office, 1988.
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23. Expert Panel. Food, nutrition and the prevention of cancer, a global perspective. Washington, DC: American Institute for Cancer Research/World Cancer Research Fund, 1997.
24. Exceptions include those foods artificially stripped of their fat, such as non-fat milk.
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26. U.S. Senate. "Dietary goals for the United States, 2nd Edition." Washington, DC: U.S. Gov­ernment Printing Office, 1977.
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28. 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 initiation of the U.S. Dietary Guidelines report series begun in 1980, the Harvard Nurses' Health Study in 1984, the initial reports of the Framingham Hean Study in the 1960s, the Seven Countries Study of Ancel Keys, the Multiple Risk Factor Intervention Trial (MRFIT) and others.
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32. Higginson J, and Muir CS. "Epidemiology in Cancer." ln: J. E Holland and E. Frei (eds.), Cancer Medicine, pp. 241-306. Philadelphia, PA: Lea and Febiger, 1973.
33. 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.
34. Kelsey JL, Gammon MD, and Esther MJ. "Reproductive factors and breast cancer." Epidemiol. Revs. 15 (1993): 36-47.
35. 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 Cawes and Control 4 (1993): 331-340.
36. Rautalahti M, Albanes D, Virtamo J, et al. "Lifetime menstrual activity-indicator of breast cancer risk." (1993): 17-25
37. 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 abil­ity to detect such an association, even when real.
38. Key TJA, Chen J, Wang DY, et al. "Sex hormones in women in rural China and in Britain." Brit.]. Cancer 62 (1990): 631-636.
39. 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.
40. For the total dietary fiber (TDF), the averages for China and the U.S. were 33.3 and 11.1 grams 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.
41. The correlation for plant protein was +0.53*** and for animal protein was +0.12.
42. 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.
43. 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.
44. The full effects of these fat-soluble antioxidants can be demonstrated only when antioxidant concentrations 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.
45. Kneller RW, Guo W, Hsing AW, et al. "Risk factors for stomach cancer in sixty-five Chinese counties." Cancer Epi. Biomarhers Prev. 1 (1992): 113-118.
46. Information Plus. Nutrition: a hey to good health. Wylie, TX: Information Plus, 1999.
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48. Atkins RC. Dr. Atkins' New Diet Revolution. New York, NY: Avon Books, 1999.
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51. Bilsborough SA, and Crowe TC. "Low-carbohydrate diets: what are the potential short- and long-term health implications?" Asia Pac.]. Clin. Nutr. 12 (2003): 396--404.
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53. Patty A. "Low-carb fad claims teen's life - Star diet blamed in death." The Daily Telegraph (Sidney, Australia) November 2, 2002: 10.
54. Atkins, 1999. Page 275.
55. 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).
56. Atkins, 1999. Page 103.
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