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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.

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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.

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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.

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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.

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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.

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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)

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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.

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

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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.

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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.

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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.

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

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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.

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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.

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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.

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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.

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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.

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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.

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

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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.

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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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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.

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

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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.

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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.

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

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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.

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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.

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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.