Final China Study Response (HTML Version)

(For those who are brave, can’t view PDFs, or simply adore scrolling. Reference numbers should be clickable, as should some of the table of contents.)

“The China Study”:

A Formal Analysis and Response

Denise Minger
August 2, 2010


SECTION 1: Reiteration and Expansion of Criticisms

  1. Linkage of animal protein with cancer by way of cholesterol
  2. Misleading association of breast cancer with lipid intake and lipid intake with animal protein
  3. Supposition that plasma cholesterol increases liver cancer risk
  4. Misrepresentation of heart-protective effects of green vegetables, and the three-variable linkage between animal protein, apolipoprotein B, and cardiovascular disease
  5. Biased use of unadjusted univariate correlations to confer protective benefits of plant foods but not with animal foods
  6. Use of a three-variable chain to connect animal foods with “Western” diseases
  7. Unexplored role of blood glucose, insulin, and disease
  8. Dismissing relevant variables
  9. Errors in the extrapolation of casein to all animal protein

SECTION 2: Biological Models and Cited Papers

  1. Breast cancer
  2. Liver cancer
  3. Energy utilization
  4. Affluent-poverty diseases
  5. Summary

SECTION 3: Response to Points Raised by Campbell

  1. Wheat: confounded variable or legitimate concern?
  2. Selection of univariate correlations and confirmation bias
  3. Tuoli county and erroneous data
  4. Whole-food, plant-based diets versus whole-food diets with animal products




When I first embarked on an analysis of T. Colin Campbell’s The China Study, I did not anticipate the range or magnitude of responses it would invoke—reactions that have been at times controversial, at times impassioned, and at times downright heated, but above all else intellectually provocative. It seems “The China Study” is a book that, in many cases, is either intensely revered or vehemently criticized, and its ability to generate ongoing discussion signifies a deep-seated division in the scientific community.

I would like to thank Dr. Campbell for his cordial response to my critique, as well as for the time he has taken to elucidate his philosophy of nutrition and his approach to research. While I do not agree with some of his conclusions, I honor his contributions to the field of health and nutrition, and deeply admire his courage to promote an unpopular message amidst a research sector dominated by special interests and opposing views.

I propose that Campbell’s hypothesis is not altogether wrong but, more accurately, incomplete. While he has skillfully identified the importance of whole, unprocessed foods in achieving and maintaining health, his focus on wedding animal products with disease has come at the expense of exploring—or even acknowledging—the presence of other diet-disease patterns that may be stronger, more relevant, and ultimately more imperative for public health and nutritional research.

Having lit a proverbial fuse, I feel called and compelled to make the sum of my findings available to the public so that they may add, in whatever extent or direction, to the symphony of voices engaged in this discourse. My intent with this paper is not to discredit Campbell as a scientist, nor to promote or discourage a particular diet—but rather, to present new ways of looking at the China Study data and related research while highlighting the shortcomings in Campbell’s specific conclusions. I hope this information can be valuable to readers while—above all else—encouraging the use of independent, critical thought to advance our understanding of health.

Section 1:

Reiteration and Expansion of Criticisms

Although some of the following points have been discussed previously, they were largely dismissed as “reductionist.” Given Campbell’s preference to examine nutrition from a holistic perspective with less focus on individual components, his assessment is understandable, albeit inaccurate. I cite these points not to split nutritional hairs, but to reveal a consistent pattern of bias and misrepresentation as it relates to Campbell’s hypothesis.

Here, I present my original points once more with additional information and references to highlight their relevance.

1. An attempt to link animal protein with cancer by way of cholesterol—a chain of variables that exhibits several logical and statistical shortcomings.

In citing the China Study data, Campbell states that total cholesterol is “positively associated with most cancer mortality rates” and also “positively associated with animal protein intake.”[1] However, he provides no indication that he examined or accounted for the cancer-risk-raising variables associated with cholesterol, including schistosomiasis and hepatitis B infection.[2]

Additionally, per Campbell’s own assessment, cholesterol is only one of several variables that tend to cluster alongside Western-type diseases: The others include higher blood glucose levels, increased consumption of refined carbohydrates, higher beer intake, and industrial rather than agricultural employment[3],[4]—with the latter bringing changes in lifestyle and increased work hazards such as benzene exposure, an extensively studied cause of lung cancer, leukemia, and other lymphatic and hematopoietic malignancies in Chinese factory workers.[5],[6]

This entanglement of risk-raising factors casts doubt on the usefulness of cholesterol as an indicator of animal food consumption rather than of accompanying variables—especially considering the lack of a known biological mechanism that causes cholesterol to rise from increased protein consumption.

As previously mentioned, Campbell also fails to cite direct links between animal foods themselves and cancer, relying instead on biomarkers as a liaison. Since epidemiological data can only identify trends and not cause-and-effect sequences, and because some diseases intrinsically alter blood profiles, the assumption that higher cholesterol precedes disease is also unsubstantiated. To link specific foods or a category of foods with disease requires evidence that the foods themselves—independent of confounding factors—influence disease risk; the reliance on biomarkers that only partially relate to dietary items is too indirect to yield truly meaningful conclusions.

2. The association of breast cancer with lipid intake—and lipid intake with animal protein consumption—as a means to link breast cancer with animal foods.

Although many of Campbell’s observations about breast cancer in rural China align with widely accepted risk factors, such as earlier menarche and greater exposure to hormones, Campbell relies on an intermediary variable (fat consumption) to forge a link that does not exist directly between animal foods and breast cancer. If an intermediary variable is introduced, a positive association can superficially emerge where the direct association is actually neutral or mildly negative. On page 86 of “The China Study,” Campbell suggests that in China, “the association between fat and breast cancer might really be telling us that as consumption of animal-based foods goes up, so does breast cancer”—an idea spawned from his observation that animal protein consumption correlates strongly with lipid intake. On the same page, he notes that the correlation between fat consumption and animal protein was “very high, at 70 – 84%”—with 70% expressing the linear relationship between animal protein and percentage of calories as fat, and 84% expressing the linear relationship between animal protein and total lipid intake.[7]

However, these figures—especially the persuasively high 84%—may be overestimated. Campbell has noted that the data for the county with the highest animal protein and fat intake, Tuoli, was “clearly not accurate on the 3 days that the data were being collected,” because “on those days, they were essentially eating as if it were a feast to impress the survey team.”[8] Further, Campbell states that Tuoli was “intentionally excluded from virtually all our analyses” because of its misleading values for meat intake.[9]

Tuoli County was not, however, excluded from the calculation for the association between animal protein consumption and lipid intake, which has a correlation of 0.84 or 84% only when using all 65 counties. A visual graph of the data reveals Tuoli’s strong influence in this correlation, as represented by the data point at the far right.

If the Tuoli data is ultimately unreliable and reflects a short-term “feast” of meat, its inclusion in the animal protein/lipid correlation may be erroneous. Since Campbell has provided no method for correcting the data nor indicated what more reliable values may be, omitting this county from the calculation may be warranted.

With the removal of Tuoli, the correlation between animal protein intake and total lipid intake drops from 0.84 to 0.52 (p<0.001). While still high and statistically significant, this correlation is low enough to undermine Campbell’s immediate implication of animal foods with breast cancer via lipid consumption.

More importantly, once the data set is corrected for Tuoli County, the correlation between plant oils and total fat intake rises drastically. Using all 65 counties, the variable “Oil intake other than rapeseed”—which includes soybean oil, corn oil, cottonseed oil, peanut oil, and sesame oil—has a non-significant linear correlation of 0.18,[10] and the variable “Rapeseed oil intake” correlates at 0.08.[11] When Tuoli is removed from calculation, these numbers rise to 0.42 (p<0.001) and 0.25 (p=0.514), respectively.

Using the data set with the flawed inclusion of Tuoli, Campbell cites a strong association between animal protein and lipid intake as a reason to implicate animal foods with breast cancer. Yet using the revised data set, animal foods do not contribute significantly more fat to total lipid intake than do plant oils. As a result, any association between breast cancer and dietary fat could be linked to either animal or plant-sourced foods, and there is no justification for indicting only animal products.

This may be particularly relevant because, according to one of Campbell’s publications, certain plant oils such as corn have carcinogenic properties; he notes that “Increased intake of corn oil has previously been shown to promote the development of L-azaserine-induced preneoplastic lesions in rats,”[12] a similar phenomenon to what his research demonstrated with casein.

Nonetheless, the association with lipid intake and breast cancer may not even be noteworthy. From his paper “Additional ecological evidence: lipids and breast cancer mortality among women age 55 and over in China,” Campbell et al conclude:

Although the result is consistent with a positive association between lipid intake and breast cancer risk, the observed association is weaker than the association previously observed. This finding provides only modest support for the possibility of a diet-breast cancer link.[13]

Neither the association between animal foods and lipid intake nor lipid intake and breast cancer, then, is particularly strong. This casts doubt on the accuracy of Campbell’s statement that the China Study data showed a “connection of breast cancer with dietary fat, [and] thus with animal-based foods.”[14]

Moreover, another variable may be more relevant than lipids when exploring the mechanisms behind breast cancer occurrence. Although Campbell emphasizes the importance of biological models and clinical research to corroborate epidemiological data, particularly univariate correlations, he does not examine the positive correlations between breast cancer and blood glucose or processed starch and sugar consumption in the China Study data,[15] even in light of research showing these associations may be highly relevant. Research spanning the previous decade has revealed a potential role of blood glucose levels in the development of breast cancer,[16] has linked hyperinsulinaemia with both early menarche and breast cancer,[17] and has shown that high insulin levels are a risk factor for breast cancer independent of estrogen.[18] Additional discussion of the relationship between blood glucose, insulin, and cancer is included under item 6.

The animal food/breast cancer hypothesis is directly testable in the China Study data, given the records for total animal protein consumption as well as amount and frequency of meat intake, fish intake, dairy intake, and egg intake. Yet despite his stated hypothesis that animal-based foods correspond with increased breast cancer rates, Campbell provides no indication of excavating a direct link through any of his analyses.

3. The claim that animal products and plasma cholesterol increase rates of liver cancer in high-risk populations.

Stratified data shows that high-risk areas for liver cancer have a nearly neutral association with animal food intake, and inverse associations with meat, eggs, and dairy.[19] Of all animal food variables, only fish and fish protein are strongly correlated with liver cancer[20]—an issue Campbell et al address in the publication “Fish consumption, blood docosahexaenoic acid and chronic diseases in Chinese rural populations”:

[It] is not difficult to visualise the reason for the link with liver cancer [and fish consumption]. The coastal, estuarine and lacustrine regions with the high fish and sea food intakes are also those with the highest humidities. Storage of food in regions of high humidity is known to encourage the spread and growth of hepatitis B virus and Aspergillus flavus which produces aflatoxin, both are major causes of primary carcinoma of the liver.[21]

Moreover, an identifiable relationship between cholesterol and liver cancer does not prove causality. Although Campbell implies that elevated cholesterol levels increase liver cancer risk, the inverse may be true: Hypercholesterolemia has been identified as a complication of liver cancer,[22] often in conjunction with hypoglycaemia and hypercalcaemia.[23]

4. The incomplete statement that cardiovascular disease is inversely associated with green vegetable consumption, and the three-variable linkage between animal protein intake, apolipoprotein B (apo-B), and cardiovascular disease.

In his 1998 publication “Diet, lifestyle, and the etiology of coronary artery disease: the Cornell China Study,” Campbell states that coronary artery disease mortality rates were “inversely associated with the frequency of intake of green vegetables (r = -0.43, p<0.01)”[24] in rural Chinese populations—a statement cited elsewhere as a significant finding of the China Study.[25]

Although frequency of green vegetable consumption does boast a strong inverse correlation with heart disease in the unadjusted data, the actual amount of green vegetables consumed has a weak positive correlation (r = 0.05)[26]—a paradox Campbell does not mention or seem to explore. Had Campbell examined this discrepancy closer, he would notice the strong regional patterns associated with frequency of green vegetable consumption, including humidity (r = 0.68, p<0.001), heat (r = 0.61, p<0.001), elevation (r = -0.48, p<0.001), and latitude (r = -0.60, p<0.001),[27] all of which suggest this variable serves as a geographical marker and thus is likely associated with other regional risk factors and protective factors for disease.

While Campbell has noted he prefers to view nutritional patterns in the aggregate rather than individually, the “green vegetable paradox,” as I’ve termed it, is representative of similar and repeated oversights, potentially weakening his hypothesis as a whole. When referring to the China Study data, Campbell cites misleading figures when they endorse plant food consumption—without first completing the analytical steps necessary to prove their accuracy and eliminate confounding. Likewise, he consistently omits similar correlations that indicate a neutral or protective effect between animal foods and disease, even when those trends, too, seem to form an overarching pattern.

Furthermore, Campbell cites a chain of three variables to implicate animal protein with coronary heart disease: He notes that animal protein associates with the low-density lipoprotein fraction apo-B, that apo-B associates with increased mortality from coronary artery disease, and therefore concludes that animal protein associates with heart disease.[28] Although the first two statements are correct in isolation, the leap to the latter is unsupported by logic and contradicted by the China Study data.

While Campbell found it appropriate to cite an unadjusted correlation for frequency of green vegetable intake, had he done the same for animal food variables, he would find only neutral or inverse correlations between cardiovascular disease and:

  • amount of meat consumed (r = -0.28)*
  • frequency of meat consumption (r = -0.15)
  • amount of fish consumed (r = -0.15)
  • frequency of fish consumption (r = -0.14)
  • amount of eggs consumed (r = -0.13)
  • frequency of egg consumption (r = -0.14)
  • animal protein intake (r = 0.01)
  • fish protein intake (r = -0.11)[29]

* When Tuoli county is omitted, this correlation becomes r = -0.36, p<0.05. Other listed correlations do not significantly change.

The only animal food with a positive (though still not significant) correlation with heart disease is dairy, both in amount (r = 0.06 for full data set; r = 0.12 adjusted for Tuoli) and frequency (r = 0.11 for full data set; 0.12 adjusted for Tuoli).[30] However, considering dairy is generally only consumed in three counties, the accuracy of these correlations is difficult to determine.

Non-dairy animal foods do not consistently correlate with shared geographical features,[31] vegetable consumption,[32] or plasma antioxidants,[33] thus minimizing the possibility of common protective factors masking their true effect on heart disease. In light of this—and given Campbell’s interest in finding “overarching” themes in nutrition—it seems curious he does not explore the consistent inverse relationships between most animal foods and cardiovascular disease. While it is possible that any or all of these figures require additional adjustments to account for confounding, Campbell offers no indication that he did so for patterns with vegetable consumption before embracing its inverse association with heart disease.

Likewise, while Campbell readily accepts favorable correlations with plant-food variables and disease, he does not account for the numerous correlations that run contrary to his hypothesis—particularly the association between all non-rice grains and heart disease, including: yearly ration of wheat (r = 0.51, p<0.001), yearly ration of corn (r = 0.31, p<0.05), yearly ration of sorghum (r = 0.31, p<0.05), yearly ration of millet (r = 0.37, p<0.05), wheat flour per day (r = 0.67, p<0.001), and “other cereal” intake per day, which includes corn, millet, sorghum, and barley (r = 0.39, p<0.01). Additional plant variables exhibit a positive association as well, including total fiber, per food composite (r = 0.30, p<0.05) and total plant protein, per food composite (r = 0.21), likely due to the influence of these grains.

Because these are unadjusted correlations, they are only preliminary and illustrative, not conclusive. However, if Campbell is seeking overarching patterns of nutrition and disease, it seems this is one worth inspecting.

Lastly, although Campbell also cites a correlation between apo-B and cardiovascular disease, the biomarker he typically uses to connect animal foods with health afflictions—total plasma cholesterol—is ineffective in the case of heart disease. In the paper “Erythrocyte fatty acids, plasma lipids, and cardiovascular disease in rural China,” Campbell et al conclude:

Within China neither plasma total cholesterol nor LDL cholesterol was associated with CVD [cardiovascular disease]. The results indicate that geographical differences in CVD mortality within China are caused primarily by factors other than dietary or plasma cholesterol.[34]

5. The use of unadjusted univariate correlations to link fiber with reduced colorectal cancer rates, green vegetables with reduced stomach cancer rates, and plant-food biomarkers with reduced stomach cancer rates.

Drawing from unadjusted China Study data, Campbell cites several perceived effects of plant foods and plant biomarkers on colorectal health and stomach cancer. While Campbell has stated his approach to nutrition is one of holism rather than reductionism, repeated use of unreliable correlations ultimately weakens the hypothesis they help construct.

In citing an inverse association between 14 fiber fractions and colorectal cancer,[35] Campbell provides no indication that he tested for confounding variables—a significant oversight, given that schistosomiasis infection appears to be both a major risk factor for colorectal cancer (r = 0.89, p<0.001) and less common in regions with high fiber consumption (r = -0.23 for total fiber intake). As demonstrated visually and verbally in my first response to Campbell, the protective effect of each fiber faction convincingly echoes its correlation with schistosomiasis, suggesting schistosomiasis may potentially create or accentuate the inverse relationship between fiber and colorectal cancers.[36]

Similarly, Campbell cites other unadjusted correlations related to plant foods. He notes an inverse association with stomach cancer and green vegetable intake, plasma beta-carotene, and plasma vitamin C[37]—patterns aligning with his hypothesis that plant foods are protective against disease.

The problem isn’t that the correlations are invalid; they may, after more analysis, persist. However, Campbell selects them above stronger associations that contradict his hypothesis and provides no indication of adjusting for appropriate factors. This approach allows him to build a repertoire of supportive evidence that may only be superficially congruous with his hypothesis. Scientific rigor mandates more even-handed analyses, which Campbell has not done.

6. The use of a three-variable chain to connect animal-based foods with cholesterol and cholesterol with “Western” diseases.

To form a comprehensive method for examining disease patterns, Campbell creates two dichotomous sets of diseases—one associated with affluent living conditions and one associated with poverty. While searching for underlying nutritional patterns characterizing the diseases of affluence, he observes that plasma cholesterol has a positive correlation with the collective group, and concludes that “one of the strongest predictors of Western diseases was blood cholesterol.”[38]

Given that a variety of factors—dietary and otherwise—can influence cholesterol and the cause-and-effect relationship between cholesterol and disease is not always clear, Campbell’s use of cholesterol as an intermediary between animal foods and disease is unsubstantiated. For instance, a shift from a highly active lifestyle in agriculture-dominated regions to a more sedentary one in industrialized areas may, in itself, be enough to explain higher cholesterol levels in certain areas[39]—a plausible theory, given that regions with greater industry employment in the China Study tended to have higher total cholesterol (r = 0.45, p<0.001) but exhibited no significant association with animal protein intake (r = 0.04).[40]

More importantly, a different plasma variable may be even more relevant than cholesterol in the occurrence of Western diseases: blood glucose.

Blood glucose: an overlooked clue

Although Campbell cites cholesterol as a consistent risk factor for Western diseases, blood glucose also exhibits associations with the chronic conditions most prevalent in affluent nations—including the ones less convincingly linked to cholesterol.

Notably, blood glucose tends to have a distinct nonlinear relationship with disease, and its association with cardiovascular diseases, cancer, and diabetes may therefore appear diminished when studying only linear correlations, as Campbell has generally done with cholesterol. The following graphs present the subtle “U-curve” pattern between blood glucose and diseases common to Western nations, juxtaposed with the same diseases and cholesterol.

On all left-side graphs, the horizontal axis represents blood glucose levels as mg/dL, while the vertical axis represents disease mortality per 1000 deaths. On all right-side graphs, the horizontal axis represents total cholesterol as mg/dL, while the vertical axis represents disease mortality per 1000 deaths.

Acronyms: MI/CHD = myocardial infarction/coronary heart disease; BC = breast cancer; LC = lung cancer; CC = colorectal cancer.

An examination of the Third National Health and Nutrition Examination Survey (NHANES) revealed that every 50 mg/dL increase in plasma glucose corresponded with a 22% increase in cancer mortality risk, possibly due to the proliferative and anti-apoptotic properties of glucose and insulin.[41] In another study, a cohort of more than 140,000 Austrian adults revealed that elevated blood glucose is associated with multiple cancers in both men and women, including liver cancer, breast cancer, bladder cancer, gallbladder cancer, non-Hodgkin’s lymphoma, and thyroid cancer.[42]

Although averaged blood glucose levels in China all fell within the normal range, if Campbell hypothesizes that increases in even very low cholesterol collide with greater disease risk, it would not be a stretch—by his logic—to suggest that small increases in even normal-range blood glucose could do the same.

On pages 78-79 of “The China Study,” Campbell writes:

As blood cholesterol decreased from 170 mg/dL to 90 mg/dL, cancers of the liver, rectum, colon, male lung, female lung, breast, childhood leukemia, adult leukemia, childhood brain, adult brain, stomach and esophagus (throat) decreased.

However, citing the same univariate correlations, he could have also written:

As plasma glucose decreased, cancers of the liver, rectum, colon, male lung, female lung, breast, childhood leukemia, adult leukemia, childhood brain, adult brain, stomach, bladder, and cervix, as well as childhood and adult lymphoma, decreased.

In addition to potentially spurring cancer growth, blood glucose and insulin may play a pivotal role in the development of atherosclerosis. A 2009 paper by Nunes and Silva[43] reveals that, “among several systemic parameters studied, plasma glucose was found to be correlated to coronary artery atherosclerosis lesions” and remained strongly correlated after accounting for other variables. The researchers note:

In the context of the present investigation, one may speculate that higher plasma glucose, probably in the presence of elevated plasma insulin, could be associated to a growth-stimulating effect on atherosclerotic lesions, perhaps involving magnesium as a cofactor for insulin-stimulated growth.

In addition, Nunes and Silva mention that “in the present study, we could find no evidence of an association between lipid fractions and CADB [coronary artery disease burden].”

A separate study by Brunner et al determined that glucose intolerance associates with increased mortality risk from all causes, stroke, and respiratory disease. The researchers state that the findings of their study “provide clear evidence that coronary mortality is raised among those with marginal postload hyperglycemia,”[44] and suggest several possible explanatory mechanisms:

A raised glucose level at baseline may indicate emerging insulin resistance and a downward trajectory in glycemic control, with increased risk of glucose intolerance, diabetes, and CHD in subsequent years. … Other pathways include oxidative stress and formation of advanced glycation end products that accelerate atherosclerosis when blood glucose is only slightly raised.

It is, of course, impossible to determine a cause-and-effect relationship in epidemiological data, but given that there is already corroborating research and biological plausibility for links between glucose, insulin, and disease, it seems the glucose-disease trend is one worth exploring. A combination of diet and lifestyle changes—especially ones associated with industry-dominated regions, where diseases of affluence tended to occur—could serve as precursors for metabolic abnormalities and insulin resistance, contributing to or occurring alongside heightened risk for cardiovascular disease and many cancers.[45],[46]

Dismissing other relevant variables

Campbell claims that “even small increases in the consumption of animal-based foods” were “associated with increased disease risk” in the China Study data,[47] but dismisses other relevant food variables because they are eaten in lower quantities in China than in most Western nations, and are thus “probably more indicative of general economic conditions and other local circumstances than of biological relationships to disease.”[48] The illogic in this statement becomes apparent when comparing the actual ranges of these variables. For instance, once the outlier Tuoli is omitted, animal protein consumption in China ranged from 0g to 23.92g per day, whereas processed sugar and starch consumption ranged from 0g to 27g and beer intake ranged from 0g to 357.1g per day. Yet even though Campbell finds the small intake animal protein intake to be relevant, he dismisses other variables with even wider ranges due to being “consumed in much lower quantities” than in the United States.[49]

How can Campbell be certain that increases of animal protein from 0g to 24g are relevant, but increases in processed starch and sugar from 0g to 27g are not—especially if those increases coincide with other shifts towards a more Western lifestyle, such as decreased physical activity?

The potential significance of other variables cannot be dismissed based on subjective assessments of their importance. As explored later in this paper, some ethnic groups who have subsisted on a constant traditional diet for centuries or millennia respond with disproportionate levels of disease to the introduction of new, Western-style foods and lifestyle habits.[50] In studies of immigrants, Asians eating Western diets appear to have excessively high rates of diabetes and insulin resistance compared to their non-Asian counterparts,[51] suggesting a “predisposition to insulin resistance and its metabolic abnormalities.”[52] In addition, studies of lean Chinese adults have demonstrated that insulin resistance often occurs independent of obesity, and even normal-weight Chinese are susceptible to impaired glucose tolerance.[53]

If there is widespread inability to handle high-glycemic foods like sugar and a predisposition to metabolic abnormalities, then what Campbell deems an insignificant intake by Western standards may, in actuality, be highly pertinent to the Chinese.

Projection of casein’s carcinogenic properties to all forms of animal protein

As I explored in my original critique and clarified again in my follow-up post, Campbell’s extrapolation of his casein research to all forms of animal protein—as well as the assumption that casein behaves the same way in whole-food form as when isolated—is supported by neither clinical evidence nor logic.

Campbell draws his animal protein/cancer hypothesis from a series of experiments conducted on aflatoxin-exposed rats, which revealed dramatic differences in the cancer growth depending on the level of protein consumed. As Campbell explains, rats fed a diet of 5% protein in the form of casein exhibited dramatically fewer lesions than rats fed a diet of 20% casein.[54] Additional experiments showed that wheat and soy protein did not promote cancer growth, even when fed at the 20% level.[55] From this, Campbell concludes that casein could be the “most relevant carcinogen ever identified.”[56]

Yet in a 1989 study, Campbell discovered that wheat protein exhibited similar carcinogenic properties as casein when lysine, its limiting amino acid, was restored.[57] This suggests that any complementary combination of amino acids will spur cancer growth under certain experimental conditions, and that carcinogenic qualities are not unique to casein nor to animal protein at large. The sole reason plant protein appeared protective in rat studies was due to a deficiency in one or more amino acids, a scenario that rarely occurs in real-world situations when a variety of foods—whether plant or animal in origin—are consumed. Campbell himself notes that eating a variety of plant foods provides a full spectrum of amino acids[58]—indicating that even a plant-only diet can yield the complete protein Campbell claims to be carcinogenic.

However, the notion that complete protein is inherently carcinogenic is contradicted by more recent literature. Although Campbell’s focus on casein is understandable, given the research is chiefly his own, he does not acknowledge the abundance of similar studies showing that whey—another milk protein—consistently boasts anti-cancer properties,[59],[60],[61] including when studied under the same experimental conditions that demonstrate the carcinogenic qualities of casein.[62],[63] This is significant, as even a single example of animal protein inhibiting rather than spurring cancer invalidates Campbell’s hypothesis that the effects of casein can be extrapolated to all animal protein.

Section 2:

Biological Models and Cited Papers

An evaluation of Campbell’s cited papers and relevance to biological models

In Campbell’s second response to my critique of “The China Study,” he notes:

The China project encouraged us not to rely on independent statistical correlations with little or no consideration of biological plausibility. In the book, I drew my conclusions from six prior models of investigation to illustrate this approach: breast cancer, liver cancer, colon cancer (minimally), energy utilization/body weight control, affluent disease-poverty disease and protein vs. body growth rates.[64]

Campbell then cites “a few representative publications” in which he applies supportive data to biological models, purportedly demonstrating their congruency.

Do these publications and the biological models they employ implicate animal products as causative of disease? To answer this question, I’ve examined several of Campbell’s cited papers, evaluating in each case whether the biological models Campbell draws from support his use of specific data to verify an animal food/disease hypothesis.

Breast cancer

Publication: Marshall JR, Qu Y, Chen J, Parpia B, and Campbell TC. “Additional ecological evidence: lipids and breast cancer mortality among women age 55 and over in China.” Eur J Cancer. 1992;28A(10):1720-7.

In the first paper he cites for breast cancer, Campbell et al use the China Study data to explore the relationship between breast cancer mortality and a variety of risk indicators— searching specifically for associations between fat consumption and higher cancer rates. They note that, although animal experiments consistently demonstrate greater breast cancer risk from increasing dietary fat, that “human data are less consistent,” and that “several well-designed and executed case-control studies apparently failing to show any association.”

Drawing from plasma samples, red blood cell samples, diet survey results, and questionnaire answers, Campbell et al study breast cancer mortality in relation to:

  • total cholesterol
  • high density lipoprotein (HDL) cholesterol
  • low density lipoprotein (LDL) cholesterol
  • triglyceride levels
  • apolipoprotein A-1
  • apolipoprotein B
  • total lipid saturates
  • total lipid polyunsaturates
  • ratio of total lipid polyunsaturates to saturates
  • total dietary lipid intake
  • total caloric intake
  • percentage of caloric intake from lipids
  • physical height
  • physical weight
  • Quetelet index
  • alcohol consumption
  • age at menarche
  • age at first pregnancy, and
  • total live births

For the diet variables, the researchers do not distinguish between animal and plant-derived fats—an important observation, given the equivalent contribution of plant versus animal fats to total fat intake after adjusting for the outlier county Tuoli, as explained in section 1.

From this study, Campbell et al conclude that, among cholesterol fractions, the “strongest and most consistent predictor of risk is apolipoprotein A-1,” and that “higher levels are consistently associated with greater breast cancer risk” even after adjusting for other variables. Incidentally, apolipoprotein A-1 appears to be significantly associated with rapeseed oil intake, but not with animal protein.[65]

The researchers also note that “increased red blood cell saturated fat is associated with an insignificantly lower risk of breast cancer” (r = -0.16), although the plasma lipid indicators may provide unreliable measures of county status.

Although researchers do cite a weak positive relationship between lipid intake and breast cancer rates, no examination of specific animal foods such as meat, fish, dairy, eggs, or total animal protein is included in this paper’s analyses. Similarly, researchers offer no rationale for using lipid intake or blood markers as a liaison specifically between animal products and disease.

Moreover, Campbell et al state that the China Study data offers only a weak indication of a relationship between diet and breast cancer. As mentioned in section 1, they conclude from their findings that the data “provides only modest support for the possibility of a diet-breast cancer link.”

Additionally, Campbell et al acknowledge that their results “may well be confounded,” particularly because their analysis unveiled several anomalous associations—such as a relationship between higher parity (number of live-born children) and increased cancer risk, as well as higher age at first birth and lower cancer risk. These associations, the researchers note, “contradict nearly all individual-based studies.” The accuracy of this particular data set and the trends extracted from it may thus be in doubt.

At best, the associated biological model involves a possible—but “modest”—role of lipid consumption in the development of breast cancer, with no distinction made between plant or animal sources of fat. While Campbell attempts to implicate animal foods due to a univariate correlation between animal protein and total lipid intake, the estimated correlation—as addressed earlier—is likely to be steeply overestimated due to the inclusion of Tuoli county in the calculation, an outlier whose survey data Campbell deemed “unreliable.”

Publication: Key TJA, Chen J, Wang DY, Pike MC, and Boreham J. “Sex hormones in women in rural China and in Britain.” British Journal of Cancer 1990(62):631-636.

In the second paper Campbell cites, researchers examine plasma concentrations of hormones implicated with breast cancer in Chinese versus British women—namely oestradiol, testosterone, sex hormone binding globulin, and prolactin. In comparing several physical and reproductive variables between Chinese and British women, researchers highlight significant differences in height, weight, age of menarche, age of first pregnancy, and age of menopause.

Results of the analysis reveal that British women generally had higher concentrations of oestradiol and testosterone than did the Chinese group, but that variations in testosterone “may be due to the difference in body weight.”

The researchers note several shortcomings in the comparisons between these two countries, stating:

  • The Chinese samples were collected at a different time of day than the British samples, and were only collected during a three-month period rather than year round—a significant observation, because hormone levels often fluctuate throughout the day as well as varying seasonally.
  • Blood sample collection and processing methods differed between the two countries, possibly confounding the results.

Potential data inaccuracies aside, the researchers hypothesize that the differences in oestradiol between Chinese and British women may be due not only to the Chinese’s low fat diet, but also to their greater levels of exercise, additional dietary practices, or other lifestyle factors that differ between the two populations. As with the previous paper Campbell cited, this publication does not discuss a potential role of animal foods as either direct or indirect causative agents of breast cancer. More specifically, it offers no rationale for assuming animal foods, as a collective group, cause elevated hormone levels more than other dietary or lifestyle constituents.

Liver cancer

Publication: Campbell TC, Chen J, Liu C, Li J, Parpia B. “Nonassociation of aflatoxin with primary liver cancer in a cross-sectional ecologic survey in the People’s Republic of China.” Cancer Res 1990(50):6882-6893.

In exploring risk factors for primary liver cancer in rural China, Campbell et al conclude that liver cancer mortality was unassociated with exposure to the carcinogen aflatoxin, but was positively and significantly associated with hepatitis B infection, total cholesterol, and intake of cadmium from plant foods. The paper notes a high correlation between cholesterol and liver cancer, and posits animal foods as the cause:

Plasma cholesterol was highly significantly associated with PLC mortality rates. … In this study, even though it was very low compared to the United States, it tended to be associated with the intakes of foods of animal origin.

The referenced table cites a list of univariate correlations between cholesterol and 12 variables, as follows:

Campbell et al used only univariate correlations to link animal food variables to cholesterol, without adjusting for other cholesterol-raising factors that may cluster alongside them. Moreover, had the researchers omitted Tuoli county from these calculations—a reasonable choice, given that the erroneous data of this region strongly influences any correlations involving meat, dairy, fat intake, and animal protein intake—several of the figures would be somewhat attenuated. The corrected data set yields a correlation of 0.18 instead of 0.24 with animal protein and cholesterol, 0.03 instead of 0.21 for dairy, and 0.18 instead of 0.26 for meat. These numbers are lower than other variables correlating with cholesterol, such as daily beer consumption (r = 0.32, p<0.01), daily liquor consumption (r = 0.20), total daily alcohol consumption (r = 0.21), intake of soybean, corn, cottonseed, sesame, or peanut oil (r = 0.20) and industry employment (r = 0.45, p<0.001)—with the latter accompanying other lifestyle factors that may lead to higher cholesterol, such as reduced physical activity.

Most importantly, cholesterol may not actually be a cause of liver cancer—but rather, an effect. In a study of 792 Chinese patients with liver cancer, Hwang et al discovered that 11.4% of subjects were hypercholesterolaemic, but they exhibited a return of normal cholesterol levels following surgery and chemoembolization for their conditions:

Serum cholesterol levels fell to the normal range after treatment and rose to abnormal levels again when tumours recurred after surgery. … Serum cholesterol levels may serve as another marker in identifying tumour recurrence and the presence of a viable tumour mass in hypercholesterolaemic HCC patients.[66]

Thus, liver cancer itself may cause cholesterol to rise, independent of diet or lifestyle factors. If this is the case, the influence of animal products on blood cholesterol would be irrelevant, and a direct link between animal foods and liver cancer would be necessary to prove their association. With the exception of fish—which Campbell et al have explained associates with liver cancer due to climatic and geographical factors[67]—such a relationship is not apparent.

In addition, it should be noted that this paper has received criticism from other cancer researchers who consider its conclusions unfounded. In 1991, Christopher P. Wild and Ruggero Montesano of the International Agency for Research on Cancer submitted a letter to Cancer Research stating:

We were concerned by the conclusions drawn by Campbell et al. in their recent paper in which they reported (a) a lack of association between urinary aflatoxin metabolites and primary hepatocellular carcinoma in 48 counties in the People’s Republic of China and (b) a positive association with plasma cholesterol. We consider the conclusions unsubstantiated and misleading …[68]

Wild and Montesano proceed to outline flaws in the experimental methods used by Campbell et al—including problems associated with the urinary assay of aflatoxin, the researchers’ lack of adjustment for urine concentration, and seasonal variations in aflatoxin exposure that could yield misrepresentative data. Therefore, the validity of the paper itself may be in question.

Energy utilization

Publication: Campbell TC and Chen J. “Energy balance: interpretation of data from rural China.” Toxicol Sci. 1999 Dec;52(2 Suppl):87-94.

In this paper, Campbell and Chen synthesize information from earlier lab rat studies, other animal research, and the China Study—particularly data recorded during a three-day diet survey, which revealed that rural Chinese citizens have a high average calorie intake compared with most Americans. Based on this apparent calorie paradox, they hypothesize that a low-protein diet increases thermogenesis, and that:

some unknown but significant, and probably difficult to measure, amount [of extra calorie intake] could be due to increased energy expenditure associated with non-post-prandial basal metabolism.

The implication is that low-protein diets may be effective for maintaining a healthy body weight because they divert a “biologically meaningful but difficult to measure” amount of energy away from weight gain and into body heat. Although the researchers do not specifically describe how this mechanism would occur in humans, they draw from animal involving brown adipose tissue metabolism.

However, the researchers concede that the increased calorie intake exhibited by the Chinese may simply be due to exercise:

Undoubtedly, much of the increased energy intake but lower body weight in rural China, as measured in this survey, was attributable to their greater physical activity (i.e., it is common to see most office workers riding bicycles to work) …

Moreover, given Campbell’s earlier disclosure that one county was “essentially eating as if it were a feast to impress the survey team”[69] during the three-day survey, the validity of the recorded energy intake is in question. How certain is Campbell that other counties were not altering their eating habits to give the impression of greater wealth or food abundance, thus leading to an overestimate of the average calorie intake for the Chinese?

Given the possible overestimation of calorie intake in the China Study, the reliance on animal rather than human studies, and the inability to calculate whether the increased calorie consumption was or was not fully offset by physical activity, this hypothesis rests on the accuracy of many unknowns. While its validity is still possible, the evidence at hand is insufficient to confirm it.

Affluent-poverty diseases

Publication: Campbell TC, Junshi C, Brun T, Parpia B, Yinsheng Q, Chumming C, and Geissler C. “China: From diseases of poverty to diseases of affluence. Policy implications of the epidemiological transition.” Ecology of Food and Nutrition 1992(27):133-144.

The publication Campbell cites to explain his “diseases of poverty” and “diseases of affluence” model has already been mentioned throughout this paper, but briefly, its premise is that two disease clusters naturally emerged from the China Study data. Diseases in one group are “generally associated with impoverished conditions,” while diseases in the second group are “characteristic of more affluent societies.” The second self-clustered group includes stomach cancer, liver cancer, colon cancer, lung cancer, breast cancer, leukemia, diabetes, and coronary heart disease. By viewing each assembly of diseases in the aggregate, Campbell seeks to identify underlying nutritional patterns in their collective emergences—potentially deciphering the source of rising disease rates in affluent nations.

While this method may be useful for examining general disease patterns, Campbell’s chief errors are as follows.

  1. Disregard for potentially critical variables in disease proliferation. Although Campbell acknowledges that numerous variables associate with the “diseases of affluence” cluster—including intake of processed starch and sugar, beer intake, fish consumption, egg consumption, and industry work—he dismisses all but cholesterol, citing the rest as “probably more indicative of general economic conditions and other local circumstances” than as causative of disease. In addition, other biomarkers such as plasma glucose may be of equal or greater relevance compared to cholesterol but receive no mention in his publication. Campbell’s disregard for these variables appears to be subjective, rather than a result of the thorough analysis necessary for deeming them insignificant.
  2. “Reductionist” use of cholesterol as a disease indicator. In examining health and nutritional trends, Campbell takes the same reductionist approach he censures elsewhere by targeting cholesterol as the chief predictor for disease. By linking cholesterol solely to animal food consumption and disregarding the numerous other variables that may cause it to rise, Campbell overlooks the larger context of disease mechanisms as they pertain to diet and lifestyle.
  3. Inaccurate representation of true diseases of affluence. Campbell’s dichotomization of diseases, while useful in some cases, does not accurately reflect disease rates in developed countries:
    • Stroke, the third leading cause of death in the United States,[70] does not fit cleanly into either the affluent or poverty disease group, so Campbell omits it entirely.
    •Heart disease correlates only weakly positively or, in three cases, inversely with the other diseases in the affluent cluster, suggesting it may not be strongly associated with the other conditions and is potentially a result of separate geographic, nutritional, or lifestyle variables.
    •Liver cancer is relatively uncommon in affluent nations, but exhibits strong correlations with the variables Campbell ascribes to diseases of affluence, most notably cholesterol. This provides further indication that cholesterol may not be an appropriate or dependable biomarker for examining true Western diseases in relation to diet.
  4. Oversight of a third, potentially significant disease cluster. Myocardial infarction, hypertensive heart disease, stroke, brain and neurological diseases, and diseases of the blood and blood-forming organs share strongly statistically significant correlations with each other and with shared nutritional variables, such as non-rice grain consumption, while correlating inversely with the variables associated with diseases of affluence. Despite this, Campbell forces myocardial infarction into a disease cluster it does not naturally align with, and ignores the remaining diseases rather than attempt to explain their anomalous nonassociation with other Western conditions.

Consequently, Campbell’s use of these disease clusters to identify relationships between diet and diseases of Western nations may be unsound, especially given a myopic focus on cholesterol to the point of excluding other pertinent factors.


While biological models, as Campbell notes, are essential for developing a comprehensive understanding of nutrition and disease mechanisms, the ones he employs do not validate the claim that animal foods are unhealthful—the hypothesis that inspired my original skepticism and critique. The biological models he cites fail to support the three-variable chains he creates to implicate animal products with cancer, heart disease, and other chronic conditions, and his use of univariate correlations to impose these links remains unfounded.

Moreover, the models Campbell cites center on individual biomarkers in disease mechanisms—examples of the same reductionism Campbell claims to oppose. If disease mechanisms work in a “symphony,” as Campbell has described, and if animal products are harmful in the aggregate rather than due to single nutrients, then a direct relationship between animal food consumption and disease should be identifiable.

Section 3:

Response to Points Raised by Campbell

Although the previous sections have covered—directly and indirectly—my rationale for citing certain errors in Campbell’s work, I will use the following pages to address more specific concerns Campbell raised regarding my critique.

Wheat: confounded variable or legitimate concern?

In his second response to my critique, Campbell cites a rhetorical remark I included in my analysis—an inquiry as to why he did not appear to have explored the strong (r = 0.67, p<0.001) correlation between wheat and heart disease,[71] despite citing far weaker correlations as a means to implicate animal products with various conditions. In offering possible explanations for the wheat-heart disease link, Campbell presents several relevant correlations that are “all highly statistically significant (p<0.01 to p<0.001),” including:

Higher wheat flour consumption, for example, is correlated, as univariate correlations, with lower green vegetable consumption (many of these people live in northern, arid regions where they often consume meat based diets with little no consumption of vegetables).[72]

Although Campbell is correct in noting a highly statistically significant (r = -0.63, p<0.001) inverse correlation between wheat flour and green vegetable consumption, he uses the same variable whose speciousness I discussed earlier: frequency, rather than quantity, of green vegetable intake. Citing this correlation only shows—somewhat redundantly—that wheat is consumed in northern regions where many crops grow seasonally rather than year-round. The correlation with quantity of green vegetable consumption, however, is an attenuated -0.16, and wheat happens to positively correlate with protective plant foods such as light-green vegetables (0.10) and carrots (0.27, p<0.05).

Additionally, Campbell’s claim that “many of these people … consume meat based diets” is fairly incongruous with the China Study data itself, which reveals that only one county—the now-discredited Tuoli—consumed any significant portion of meat, even though 22 counties consumed at least 100g of wheat flour per day. And in contrast to what Campbell asserts, wheat flour correlates at -0.22 with frequency of meat consumption and at -0.09 with amount of daily meat intake (reducing further to -0.23 and -0.22, respectively, when recalculated without Tuoli). Although animal protein correlates at 0.17 with wheat flour consumption when using all 65 counties, this figure, too, reduces when Tuoli is excluded from calculation, dropping to -0.06.

Campbell is likely aware of the lack of a wheat-meat link, as a paper he coauthored in 1998, entitled “Diet, lifestyle, and the etiology of coronary artery disease: the Cornell China Study,” presents the following conclusion:

Nonetheless, the wheat-flour effect appears to be independent of meat consumption, so enhancement of coronary artery disease risk by wheat consumption may be a possibility.[73]

Despite the “possibility” that one of the most widely-consumed grains may contribute to heart disease, Campbell does not pursue this issue further through research or in his book, continuing to focus instead on animal foods.

In his response, Campbell points to another pertinent correlation with wheat: “greater body weight (higher risk of heart disease),” which correlates at 0.59 (p<0.001) with wheat flour intake.[74] This, of course, raises an important issue: Why do people in wheat-eating regions tend to have significantly higher body weight than citizens of other areas? The answer does not appear to be calories, as wheat flour only correlates at 0.07 with total caloric intake.[75] Nor is the answer lower activity associated with industrial employment, as wheat flour correlates at -0.24 with percentage of the population employed in industry.[76] And given the lack of association with meat or other animal foods, animal protein is an equally unlikely solution. Does wheat encourage body mass gain or spur growth in a way that rice, for instance, does not?

Given that wheat flour does not have an obvious relationship with other energy-dense foods Campbell ascribes to increased growth, it does seem wheat itself may be a factor. This is not a topic that can be feasibly analyzed in the span of this paper, but it may be a relevant one to explore in the future.

Another correlation Campbell notes is higher serum levels of urea, which he mentions is a biomarker of protein consumption. Although Campbell’s implication may be that animal protein is the cause—thus lending credence to his animal protein-disease theory—an examination of the data reveals otherwise. A notable feature about grain consumption in China is its dichotomization: Rice dominates southern regions while strongly inversely correlating with wheat consumption (r = -0.76, p<0.001) and other cereal grains (r = -0.68, p<0.001)[77] in the north. Given that wheat flour, depending on whether whole-grain or refined, is nearly twice as high in protein compared to white rice on a per-calorie basis,[78] it logically follows that areas where wheat is a staple have higher protein intakes—and thus higher serum urea—than areas where rice is a staple.

Indeed, wheat flour correlates at 0.34 (p<0.01) with plant protein and at 0.35 (p<0.01)[79] with total protein intake, whereas rice intake correlates at -0.20 with plant protein and -0.23 with total protein intake.[80] Coupled with the fact that wheat flour inversely associates with all forms of animal food except for milk—which is generally only consumed in three counties—a logical interpretation is that a greater intake of plant protein results in these higher urea levels. A higher intake of plant protein, perhaps, may also contribute to the higher body weights exhibited in wheat-eating regions, particularly given Campbell’s supposition about protein-restricted diets limiting weight gain and higher-protein diets fueling it.[81]

The next point Campbell raises may be significant: the relationship between wheat flour and certain serum lipid fractions. Although Campbell states that wheat flour intake is associated with “lower serum levels of monounsaturated fats,” which he notes can increase risk of heart disease, wheat also correlates with lower total lipid docosahexaenoic acid (DHA) (r = -0.34, p<0.05)[82]—an essential fatty acid linked to cardiovascular health by abundant research,[83],[84] including a China Study-based publication Campbell coauthored.[85]

Campbell implies that unfavorable lipid profiles may be responsible for the high rates of heart disease independent of wheat, thus creating a false correlation between wheat consumption and cardiovascular conditions. However, another possibility is that the wheat itself contributes to unfavorable blood lipid profiles, especially in the absence of more heart-protective foods such as fish—which is rarely consumed in wheat-eating regions (r = -0.37, p<0.01) but more frequently in rice-eating regions (r = 0.32, p<0.05) where heart disease is far less common (r = -0.58, p<0.001).[86] If wheat as a dietary staple is nutritionally inadequate, this would suggest that wheat-based diets may require careful planning or supplementation to reduce heart disease risk, especially in supplying certain fatty acids difficult to obtain from plant foods.

Continuing in this vein, Campbell writes:

[The] correlation of wheat flour and heart disease is interesting but I am not aware of any prior and biologically plausible and convincing evidence to support an hypothesis that wheat causes these diseases.[87]

Because my initial mention of wheat’s correlation with heart disease was intended to be speculative rather than assertive, I did not offer corroborating theories or evidence to substantiate a wheat-heart disease link. However, Joel Fuhrman—a plant-based diet advocate whom Campbell cites as one of his “physician colleagues”—has stated:

Many scientific studies show a strong association between the consumption of white flour products, such as pasta and bread, with diabetes, obesity, and heart disease. … Whole grains are the least nutrient-dense food of the seed family, and they do not show the powerful protection against disease that is apparent in the scientific studies of fresh fruit, vegetables, beans, raw nuts, or seeds.[88]

Since the China Study data provides no indication as to whether the wheat flour consumed was whole-grain or refined, the following can only be guesswork. However, one noteworthy feature of refined grains such as white flour is their connection with elevated triglyceride levels, a condition widely associated with heart disease.[89],[90]Another of Campbell’s colleagues, John McDougall, asserts that refined grains cause blood triglycerides to increase, and states in his October 2006 newsletter:

My experience has been that people who are having problems getting their … triglycerides under control need to stop using refined flour products and simple sugars.[91]

Indeed, wheat flour in the China Study is strongly associated with high triglyceride levels (r = 0.51, p<0.001).[92] Given that omega-3 fats have a mitigating effect on triglycerides,[93] it could be posited that rice-eating regions in China, with their frequent consumption of omega-3 rich seafood, could be more protected from heart disease than wheat-eating regions—even though white rice alone may exhibit the same effects as other refined grains.

Of course, epidemiological data cannot prove causative relationships, only highlight correlations that may or may not be meaningful. And also importantly, the above web of univariate correlations is in no way conclusive, as many of these values may change when accounting for nonlinearity and confounding. When searching for overarching themes and material for future research, however, such univariate correlations are a useful place to start, as they are often the first indication of patterns that gain magnitude once fully excavated and analyzed. Given that connections between processed grains and heart disease are already corroborated by research as well as by biological plausibility, an authentic connection between wheat and heart disease is not unfeasible.

Selection of univariate correlations and confirmation bias

My largest concern with Campbell’s conclusions, as stated in this paper and elsewhere, is that his approach to both China Study data and related research has been angled by the pursuit of a specific hypothesis—rather than an evenhanded evaluation of information and subsequent formation of a theory. In Campbell’s explanation of his approach, he writes:

I first inquired whether a collection of variables in the China survey (ranging from univariate correlations to more sophisticated analyses) could consistently and internally support each of these biologically plausible models and, second, I determined whether the findings for each of these models were consistent with the overarching hypothesis that a whole food, plant-based diet promotes health.[94]

Had Campbell approached the data from a different angle—or, better, from diverse and opposing perspectives in search of the most accurate one—he may have found multiple biologically plausible ways of incorporating China Study data trends with  known physical mechanisms. By not testing alternative hypotheses alongside his own, Campbell runs the risk of investigative tunnel vision, and cannot truly determine whether his hypothesis is more valid than another.

In his second response to my critique, Campbell also writes:

As I’ve said many times, not all the evidence in the China database supported this conclusion, although the large majority did.[95]

Considering the complexity and abundance of trends in the raw data, I would like to know what methods Campbell used to analyze and adjust the majority of the 8,000 statistically significant correlations in a way that yielded supportive results for his hypothesis. I propose that the China Study has generated enough material to bolster nearly any theory, regardless of actual validity—and for this reason, mandates an impartial and multi-perspective approach rather than a search for a predetermined outcome.

While the limitations of using univariate correlations are clear, Campbell has expressed willingness to employ them when they “consistently and internally support … biologically plausible models.”[96] Yet it appears Campbell’s chief criterion for deeming correlations valid is not just whether they’re objectively plausible, but whether they support his hypothesis. In the instances they do, as explained earlier in this paper, he cites them without performing deeper analyses; in the instances they do not, he gives them no mention nor delineates a methodology for explaining their inconsistency with his theory. Rather than evaluating discrepancies within the data, he dismisses them—a choice ultimately leading to confirmation bias, potential misrepresentation of true trends, and a missed opportunity to rework his hypothesis to account for apparent anomalies.

Tuoli county and erroneous data

In discussing my observation of the apparent good health of a Chinese county whose diet, per China Study data, was high in animal protein, Campbell clarifies:

[Tuoli county was] intentionally … excluded from virtually all our analyses on meat consumption because this county ranked very high when meat consumption was documented at survey time, but much lower when responding to the questionnaire on frequency of meat consumption. That is, these nomadic people migrate for part of the year to valleys, where they consume more vegetables and fruits.[97]

Although the information Campbell provides is useful, meat was not the dietary feature noted in my discussion of Tuoli: dairy was. Both the three-day diet survey and the frequency questionnaire reveal high intakes of dairy for Tuoli citizens, with the questionnaire indicating milk products are consumed an average of 330.3 days per year, and closer to 350 in one township.[98] In addition, despite Campbell’s comment that the Tuoli migrate seasonally and consume more vegetables and fruit for part of the year, the China Study frequency questionnaire indicates Tuoli’s vegetable intake is only twice per year and fruit intake is less than once per year on average.[99]

If Campbell believes both the three-day diet survey and frequency questionnaire were in error, I must question why Tuoli county was not excluded entirely from the data set—especially given its pronounced influence on virtually all associations involving meat, dairy, and animal protein, many of which Campbell cited as verification for his animal foods-disease hypothesis.

Efficacy of whole-food, plant-based diets versus whole-food diets with animal products

In his second response to my critique, Campbell states:

[The] results of people using a diet of whole, plant-based foods, as shown by physician colleagues (previously mentioned, McDougall, Esselstyn, Ornish, Barnard, Fuhrman, et al) as well as by many of the readers of our book are nothing less than incredible.[100]

Campbell cites several examples of physician colleagues who have successfully employed plant-based diets—often in conjunction with other lifestyle modifications—to improve patients’ health and reverse chronic conditions such as heart disease. Although these doctors unanimously advise limiting animal food consumption, their diet programs are characterized by more than just plant-based nutrition: They also drastically reduce or eliminate refined carbohydrates, processed sugar, and hydrogenated oils—foods that tend to feature prominently in Western-style cuisines alongside animal-based products.

  1. John McDougall. While McDougall’s program embraces whole plant foods, he also advises against consuming refined flour, refined and sugar-coated cereals, soft drinks, vegetable oils, white rice, and other processed carbohydrates.[101]
  2. Caldwell Esselstyn, Jr. The diet promoted by Esselstyn involves not only the elimination of animal products, but also the avoidance of vegetable oils and refined grains—including white rice, white flour, and products made from enriched flour such as pastas, breads, bagels, and baked goods.[102]
  3. Dean Ornish. Along with eschewing meat, Ornish’s program—as outlined in the book Eat More, Weigh Less—also involves reducing “sugar and simple sugar derivatives” such corn syrup, white flour, and white rice, avoiding margarines and vegetable oils, limiting alcohol, and avoiding commercial products with more than two grams of fat per serving, which is likely to disqualify most ready-made processed foods from dieters’ menus.[103] Ornish also notes that his program involves more than just a plant-based diet: He emphasizes increased exercise[104] and other lifestyle changes to achieve better health.
  4. Neal Barnard. In his book Dr. Neal Barnard’s Program for Reversing Diabetes, Barnard advises his readers to “keep vegetable oils to a minimum” and “favor foods with a low glycemic index,”[105] which ultimately eliminates refined carbohydrates, most processed foods, high fructose corn syrup, and other common sweeteners. Barnard also recommends avoiding fried foods, including fried starches such as potato chips and French fries.[106]
  5. Joel Fuhrman. Along with reducing or eliminating animal products, the diet Joel Fuhrman espouses shuns refined grains, refined oils, and refined sweets; Furhman lists these foods as less healthful than all forms of animal food in terms of nutrient density,[107] and notes that “eating a diet that contains a significant quantity of sugar and refined flour … leads to an earlier death.”[108] Fuhrman also notes that “a low-fat diet can be worse than a higher-fat diet” if it centers on refined carbohydrates and contains trans fat,[109] stating specifically:

A vegetarian whose diet is mainly refined grains, cold breakfast cereals, processed health food store products, vegetarian fast foods, white rice, and pasta will be worse off than a person who eats a little turkey, chicken, fish, or eggs but consumes large volumes of fruits, vegetables, and beans.[110]

Although plant-based diets eschewing white sugar, refined grain products, trans-fatty acids, high fructose corn syrup, and other highly processed ingredients are likely to improve health compared to a standard Western diet, research comparing unprocessed plant-food diets with unprocessed omnivorous diets is sparse. The success of whole foods, plant-based diets is not itself an indication that animal foods are deleterious; to determine this would require juxtaposing the results of whole-food vegan diets with equally “clean” omnivorous eating plans and demonstrating consistent superiority of the former.

Non-Westernized omnivorous diets

As current research indicates, other dietary paradigms may offer similar benefits to the plans promoted by McDougall, Esselstyn, Ornish, et al, without the reduction of animal products. Recent studies have shown “Paleolithic” style diets—which eschew grains, dairy, legumes, processed carbohydrates, and refined fats while embracing minimally processed meat, fish, vegetables, eggs, fruit, and nuts—may reduce fasting glucose levels, improve diastolic blood pressure, promote weight loss, improve glycemic control, lower triglycerides, raise HDL or “good” cholesterol, and generally reduce risk factors for cardiovascular disease, all while allowing for liberal consumption of non-dairy animal products.[111] In a study of diabetic patients, these effects were more pronounced in a Paleolithic diet group than in a group fed a standard low-fat diet including abundant plant-based foods such as whole-grain bread, other whole-grain cereal products, vegetables, and fruit, along with low-fat dairy.[112]

Similarly, a 1999 study by Frassetto et al discovered that non-obese subjects consuming a diet “comprising lean meat, fruits, vegetables and nuts” while excluding cereal grains, legumes, and dairy led to consistent and nearly immediate improvements in blood pressure, reduction in plasma insulin, lowered total cholesterol, reduced low-density lipoproteins, and decreased triglycerides.[113] In their publication, Frassetto et al conclude:

Even short-term consumption of a paleolithic type diet improves BP [blood pressure] and glucose tolerance, decreases insulin secretion, increases insulin sensitivity and improves lipid profiles without weight loss in healthy sedentary humans.[114]

Additionally, a study conducted by Lindeberg et al showed that a grain-free diet with animal products improved glucose tolerance and reduced waist circumference more effectively than an unprocessed “Mediterranean” diet featuring whole grains, abundant plant foods, low-fat dairy, and minimal red meat.[115]

Additional clues herald from Australia. Research from O’Dea on the health and dietary patterns of Australian aborigines reveals that those eating a traditional cuisine—typically high in animal foods such as organ meats, fat deposits, and bone marrow along with tubers, vegetables, seeds, and fibrous fruits—exhibited “no evidence of the chronic diseases” common to Westerners,[116] including heart disease, diabetes, and obesity.[117]

Yet despite the apparent lack of adverse effects from their native high-meat diet, aborigines exhibit disproportionately high rates of diabetes and obesity after adopting a Western diet and lifestyle,[118] indicating genetics alone is not what protects them. If this surge in disease rates occurs with other groups shifting from a traditional omnivorous diet to a Western one, it suggests that factors other than animal food consumption may be responsible for the diseases plaguing developed countries.

In addition to the health of non-Westernized aborigines, virtually nonexistent rates of Western diseases have been reported of the Kitava, a traditional Melanesian society consuming no grains or processed carbohydrates but subsisting on a native diet of tubers, fish, coconut, and fruit.[119],[120] A compilation of research collectively known as the Kitava Study revealed that “stroke and ischaemic heart disease appear to be absent in this population,”[121] despite their consumption of animal products and lack of purportedly “heart-healthy” grains.

The Masai of East Africa—who consume copious amounts of meat and milk—also patently defy Campbell’s hypothesis, particularly as it relates to animal foods and heart disease. After conducting a field survey of 400 Masai in the 1960s, researchers Mann et al observed that “Despite a long continued diet of exclusively meat and milk the men have low levels of serum cholesterol and no evidence for arteriosclerotic heart disease.”[122]

In a guest editorial published in the American Journal of Clinical Nutrition, these researchers expand on their findings, describing the high animal-fat diet of the Masai and their paradoxically low serum cholesterol—a mean of 135.4 mg/dL on average, a level on par with the rural Chinese consuming plant-based cuisines:

The average daily caloric intake was estimated to be about 3,000 kcal, with 66% of the calories derived from fat. The estimated average daily cholesterol intake was from 600 to 2,000 mg per person. The serum cholesterol levels of 254 Masai of various ages were determined; a low average value of 135.4 +/- 33.5 mg/100 ml … was observed.[123]

To provide further evidence of the Masai’s noteworthy lack of heart disease, the authors note that “gross, histochemical, and chemical studies of the aortas and coronary arteries of 10 consecutive autopsies gave direct proof of the paucity of atherosclerosis in the Masai.”[124]

In Alaska, researchers have observed rising rates of cardiovascular disease coinciding with a shift away from traditional dietary patterns and towards Western-style eating and lifestyle habits—a testimony to the health risks conferred by processed foods rather than animal foods in the aggregate. In 2009, cardiovascular disease risk factors were examined in relation to differing diet patterns among Alaska Eskimos, including a native diet featuring abundant animal products, wild foods, and no sugar or other refined carbohydrates:

Participants following … the “traditional” diet consumed fish, native sea and land mammals and their fats and oils, wild greens, stew with mostly meat, stew with mostly rice or noodles, native birds, wild berries, and native berry agutuk.[125]

Compared to Eskimos following other eating patterns, including a Western-style diet and “healthy” store-bought diet, individuals consuming traditional foods had the most “desirable cardiovascular risk factor profile,” including lower blood pressure and lower homocysteine.[126]

In a separate study, Alaskan Natives who replaced processed store-bought foods with traditional Eskimo foods—including meat from sea and land creatures—resulted in reduced diastolic blood pressure, lower total and low-density lipoprotein cholesterol, lower fasting glucose, and improved glucose tolerance.[127] Additional research shows that native diets emphasizing marine mammals, fish, game animals, berries, and wild greens results in lower triglycerides, increased high-density lipoprotein cholesterol, and better cardiovascular health—even while providing levels of animal fat exceeding those of most governmental recommendations.[128]


If both whole-food vegan diets and non-Westernized omnivorous diets yield similar health benefits, this is a strong indication that the results achieved by McDougall, Esselstyn, Ornish, et al are not due to the avoidance of animal products but to the elimination of other health-harming items. Western diets involve far more than increased consumption of animal products, and for some groups—such as Alaskan Natives—a switch from a traditional diet to a Westernized one entails reduced animal food consumption, with the caloric void replaced by refined carbohydrates, hydrogenated oils, grains, sugar, and convenience foods. The fact that a dietary shift towards Western fare inevitably leads to proliferation of “diseases of affluence”—regardless of changes in animal food consumption—suggests that another factor, or lattice of factors, instigates this decline in health.

The success of the Chinese on plant-based diets does not invalidate the experiences of other populations who evade disease while consuming animal products. Nor does individual success on a vegan program nullify the disease reversal seen by those adhering to specific omnivorous diets. Rather than studying the dissimilarities between healthy populations, perhaps we should examine their areas of convergence—the shared lack of refined carbohydrates, the absence of refined sweeteners and hydrogenated oils, the emphasis on whole, unprocessed foods close to their natural state, and the consumption of nutritionally dense fare rather than empty calories or ingredients concocted in a lab setting. Modern foods, and the diseases they herald, have usurped the dietary seats once occupied by more wholesome fare. It is this commonality—the thread bonding healthy populations—that may offer the most meaningful insight into human health.

A theory as purportedly universal as Campbell’s should, by definition, unite the various health and disease patterns of global cultures without generating frequent anomalies. By  naming animal products as the source of Western afflictions, Campbell has created a hypothesis valid only under hand-picked circumstances—one that cannot account for other epidemiological trends or even recent case-controlled  studies. This is a symptom of a deficient theory, embodying only partial truths about broader diet-disease mechanisms.

I propose that the China Study remains a largely untapped resource for revealing potential diet-health patterns, expanded awareness of the source of disease, and inlets for future nutritional research—possibilities Campbell has not fully explored in his quest to validate a predetermined hypothesis. I invite Campbell, if he has the time and the interest, to present a more detailed account of his methodology, such as the unpublished book chapter he cited in his first response to my critique.[129] It is only through ongoing discussion and clarification that the field of nutrition can continue to evolve, progressing towards an increasingly unified understanding of health.

Lastly, I suggest that the “symphony” Campbell has heard thus far is only a partial opus. To cease listening now would be—at best—a missed opportunity for heightened health awareness, and at worst a perpetuation of the misinformation already degrading public and scientific understanding of diet and disease. I thank Dr. Campbell for both the harmonies and the dissonance his work has supplied to the field of nutrition, but implore him to continue listening. The final note has not yet sounded.

[1] Segelken R. “China Study II: Switch to Western diet may bring Western-type diseases.” Cornell Chronicle. Retrieved from

[2] Junshi C, Campbell TC, Junyao L, Peto R. Diet, Life-style and Mortality in China: A Study of the Characteristics of 65 Chinese Counties. Oxford: Oxford University Press, 1990, p. 264.

[3] Campbell TC, Junshi C, Brun T, Parpia B, Yinsheng Q, Chumming C, and Geissler C. “China: From diseases of poverty to diseases of affluence. Policy implications of the epidemiological transition.” Ecol. Food Nutr. 1992(27):133-144.

[4] Junshi C et al. Diet, Life-style and Mortality in China, p.264.

[5] Yin SN, Li GL, Tain FD, Fu ZI, Jin C, Chen YJ, Luo SJ, Ye PZ, Zhang JZ, Wang GC, Zhang XC, Wu HN, Zhong QC. “A retrospective cohort study of leukemia and other cancers in benzene workers.” Environ Health Perspect. 1989 July; 82: 207–213.

[6] Hayes RB, Yin SN, Dosemeci M, Li GL, Wacholder S, Chow WH, Rothman N, Wang YZ, Dai TR, Chao XJ, Jiang ZL, Ye PZ, Zhao HB, Kou QR, Zhang WY, Meng JF, Zho JS, Lin XF, Ding CY, Li CY, Zhang ZN, Li DG, Travis LB, Blot WJ, Linet MS. “Mortality among benzene-exposed workers in China.” Environ Health Perspect. 1996 Dec;104 Suppl 6:1349-52.

[7] Junshi C et al. Diet, Life-style and Mortality in China, p. 572.

[8] Campbell TC. “A Challenge and Response to the China Study.” Retrieved from

[9] Ibid.

[10] Junshi C et al. Diet, Life-style and Mortality in China, p. 640.

[11] Ibid, p. 638.

[12] O’Connor TP, Roebuck BD, Peterson F, and Campbell TC. “Effect of dietary intake of fish oil and fish protein on the development of L-azaserine-induced preneoplastic lesions in the rat pancreas.” Journal of the National Cancer Institute 1985 Nov;75(5):959-62.

[13] Marshall JR, Qu Y, Chen J, Parpia B, and Campbell TC. “Additional ecological evidence: lipids and breast cancer mortality among women age 55 and over in China.” European Journal of Cancer 1999(28A):1720-1727.

[14] Campbell. The China Study, p. 87.

[15] Ibid.

[16] Muti P. et al. “Fasting glucose is a risk factor for breast cancer: a prospective study.” Cancer Epidemiology, Biomarkers and Prevention 2002 Nov;11(11):1361-8.

[17] Stoll BA. “Western diet, early puberty, and breast cancer risk.” Breast Cancer Res Treat. 1998 Jun;49(3):187-93.

[18] Gunter MJ, Hoover DR, Yu H, Wassertheil-Smoller S, Rohan TE, Manson JE, Li J, Ho GY, Xue X, Anderson GL, Kaplan RC, Harris TG, Howard BV, Wylie-Rosett J, Burk RD, Strickler HD.. “Insulin, insulin-like growth factor-I, and risk of breast cancer in postmenopausal women.” Journal of the National Cancer Institute 2009 Jan;101(1):48-60.

[19] Minger D. “The China Study: Fact or Fallacy?” Raw Food SOS. Retrieved from

[20] Junshi C et al. Diet, Life-style and Mortality in China, p. 118.

[21] Wang Y, Crawford MA, Chen J, Li J, Ghebremeskel K, Campbell TC, Fan W, Parker R, Leyton J. “Fish consumption, blood docosahexaenoic acid and chronic diseases in Chinese rural populations.” Comparative Biochemistry and Physiology Part A: Molecular and Integrative Physiology 2003 Sep;136(1):127-40.

[22] “Hepatocellular Carcinoma (Liver Cancer): FAQs.” Johns Hopkins Gastroenterology and Hepatology.

[23] Chu CW, Hwang SJ, Luo JC, Tsay SH, Li CP, Chang FY, Lee SD, Lui WY, Chiang JH. “Manifestations of hypercholesterolaemia, hypoglycaemia, erythrocytosis and hypercalcaemia in patients with hepatocellular carcinoma: report of two cases.” J Gastroenterol Hepatol. 1999 Aug;14(8):807-10.

[24] Campbell TC, Parpia B, and Chen J. “Diet, lifestyle, and the etiology of coronary artery disease: the Cornell China Study.” Am J Cardiol. 1998 Nov 26;82(10B):18T-21T.

[25] Segelken R. “China Study II: Switch to Western diet may bring Western-type diseases.” Retrieved from

[26] Junshi C et al. Diet, Life-style and Mortality in China, p. 618.

[27] Ibid, p. 716

[28] Segelken R. “China Study II: Switch to Western diet may bring Western-type diseases.” Cornell Chronicle. Retrieved from

[29] Junshi C et al. Diet, Life-style and Mortality in China, p. 188.

[30] Ibid.

[31] Ibid, p. 798 – 806.

[32] Ibid, p. 612 – 618 and 716 – 724.

[33] Ibid, p. 280 – 288.

[34] Fan WX, et al. “Erythrocyte fatty acids, plasma lipids, and cardiovascular disease in rural China.”

[35] Segelken R. “China Study II: Switch to Western diet may bring Western-type diseases.” Cornell Chronicle. Retrieved from

[36] Minger D. “The China Study: My Response to Campbell.” Raw Food SOS. Retrieved from

[37] Segelken R. “China Study II: Switch to Western diet may bring Western-type diseases.” Cornell Chronicle. Retrieved from

[38] Campbell TC. The China Study, p. 77.

[39] O’Donovan G, Owen A, Kearney EM, Jones DW, Nevill AM, Woolf-May K, Bird SR. “Cardiovascular disease risk factors in habitual exercisers, lean sedentary men and abdominally obese sedentary men.” Int J Obes (Lond). 2005 Sep;29(9):1063-9.

[40] Junshi C, et al. Diet, Life-style and Mortality in China, p. 830.

[41] Parekh N, Lin Y, Hayes RB, Albu JB, Lu-Yao GL. “Longitudinal associations of blood markers of insulin and glucose metabolism and cancer mortality in the third National Health and Nutrition Examination Survey.” Cancer Causes Control. 2010 Apr;21(4):631-42.

[42] Rapp K, Schroeder J, Klenk J, Ulmer H, Concin H, Diem G, Oberaigner W, Weiland SK. “Fasting blood glucose and cancer risk in a cohort of more than 140,000 adults in Austria.” Diabetologia. 2006 May;49(5):945-52.

[43] Nunes JPL and Silva JC. “Systemic correlates of angiographic coronary artery disease.” PLoS ONE. 2009; 4(1): e4322.

[44] Brunner EJ, Shipley MJ, Witte DR, Fuller JH, Marmot MG. “Relation between blood glucose and coronary mortality over 33 years in the Whitehall Study.” Diabetes Care. 2006 Jan;29(1):26-31.

[45] Bruning PF, Bonfrèr JM, van Noord PA, Hart AA, de Jong-Bakker M, Nooijen WJ. “Insulin resistance and breast-cancer risk.” Int J Cancer. 1992 Oct 21;52(4):511-6.

[46] Bruce WR, Wolever TM, Giacca A. “Mechanisms linking diet and colorectal cancer: the possible role of insulin resistance.” Nutr Cancer. 2000;37(1):19-26.

[47] Segelken R. “China Study II: Switch to Western diet may bring Western-type diseases.” Cornell Chronicle. Retrieved from

[48] Campbell TC et al. “China: From diseases of poverty to diseases of affluence. Policy implications of the epidemiological transition.”

[49] Segelken R. “China Study II: Switch to Western diet may bring Western-type diseases.” Cornell Chronicle. Retrieved from

[50] O’Dea K. “Diabetes in Australian aborigines: impact of the western diet and life style.” J Intern Med. 1992 Aug;232(2):103-17.

[51] Knight TM, Smith Z, Whittles A, Sahota P, Lockton JA, Hogg G, Bedford A, Toop M, Kernohan EE, Baker MR. “Insulin resistance, diabetes, and risk markers for ischaemic heart disease in Asian men and non-Asian in Bradford.” Br Heart J. 1992 May;67(5):343-50.

[52] Dhawan J, Bray CL, Warburton R, Ghambhir DS, Morris J. “Insulin resistance, high prevalence of diabetes, and cardiovascular risk in immigrant Asians. Genetic or environmental effect?” Br Heart J. 1994 November; 72(5): 413–421.

[53] Wang G, Liu X, Christoffel KK, Zhang S, Wang B, Liu R, Li Z, Liu X, Brickman WJ, Zimmerman D, Xu X, Wang X. “Prediabetes is not all about obesity: association between plasma leptin and prediabetes in lean rural Chinese adults.” Eur J Endocrinol. 2010 Aug;163(2):243-249. Epub 2010 May 28.

[54] Appleton BS, Campbell TC. “Inhibition of aflatoxin-initiated preneoplastic liver lesions by low dietary protein.” Nutr Cancer. 1982;3(4):200-6.

[55] Campbell TC. The China Study, p. 60.

[56] Campbell TC. “Denise Minger Reply.” Campbell Coalition for Health Change. Retrieved from

[57] Schulsinger DA, Root MM, and Campbell TC. “Effect of dietary protein quality on development of aflatoxin B1-induced hepatic preneoplastic lesions.” J Natl Cancer Inst. 1989 Aug 16;81(16):1241-5.

[58] Campbell TC. The China Study, p. 30-31.

[59] Parodi PW. “A role for milk proteins and their peptides in cancer prevention.” Curr Pharm Des. 2007;13(8):813-28.

[60] Bounous G, Batist G, Gold P. “Whey proteins in cancer prevention.” Cancer Lett. 1991 May 1;57(2):91-4.

[61] Bounous G. “Whey protein concentrate (WPC) and glutathione modulation in cancer treatment.” Anticancer Res. 2000 Nov-Dec;20(6C):4785-92.

[62] Hakkak R, Korourian S, Shelnutt SR, Lensing S, Ronis MJ, Badger TM. “Diets containing whey proteins or soy protein isolate protect against 7,12-dimethylbenz(a)anthracene-induced mammary tumors in female rats.” Cancer Epidemiol Biomarkers Prev. 2000 Jan;9(1):113-7.

[63] Badger TM, Ronis MJ, Hakkak R. “Developmental effects and health aspects of soy protein isolate, casein, and whey in male and female rats.” Int J Toxicol. 2001 May-Jun;20(3):165-74.

[64] Campbell TC. “Denise Minger Reply.” Campbell Coalition for Health Change. Retrieved from

[65] Junshi C et al. Diet, Life-style and Mortality in China, p. 572.

[66] Hwang SJ, Lee SD, Chang CF, Wu JC, Tsay SH, Lui WY, Chiang JH, Lo KJ. “Hypercholesterolaemia in patients with hepatocellular carcinoma.” J Gastroenterol Hepatol. 1992 Sep-Oct;7(5):491-6.

[67] Wang Y et al. “Fish consumption, blood docosahexaenoic acid and chronic diseases in Chinese rural populations.”

[68] Wild CP and Montesano R. “Correspondence re: T. Colin Campbell et al. Nonassociation of aflatoxin with primary liver cancer in a cross-sectional ecological survey in the People’s Republic of China.” Cancer Res. 1991(51):3825.

[69] Campbell TC. “A Challenge and Response to the China Study.” Retrieved from

[70] “Leading Causes of Death.” Centers for Disease Control and Prevention. Retrieved from

[71] Junshi C et al. Diet, Life-style and Mortality in China, p. 608.

[72]Campbell TC. “Denise Minger Reply.” Campbell Coalition for Health Change. Retrieved from

[73] Campbell TC, Parpia B, and Chen J. “Diet, lifestyle, and the etiology of coronary artery disease: the Cornell China Study.” American Journal of Cardiology 1998 Nov 26;82(10B):18T-21T.

[74] Junshi C et al. Diet, Life-style and Mortality in China, p. 608.

[75] Ibid.

[76] Ibid.

[77] Ibid.

[78] “Nutrient Data Laboratory.” United States Department of Agriculture. Retrieved from

[79] Junshi C et al. Diet, Life-style and Mortality in China, p. 608.

[80] Ibid, p. 606.

[81] Campbell TC, Chen J. “Energy balance: interpretation of data from rural China.” Toxicol Sci. 1999 Dec;52(2 Suppl):87-94.

[82] Junshi C et al. Diet, Life-style and Mortality in China, p. 608.

[83] Pottala JV, Garg S, Cohen BE, Whooley MA, Harris WS. “Blood eicosapentaenoic and docosahexaenoic acids predict all-cause mortality in patients with stable coronary heart disease: the Heart and Soul study.” Circ Cardiovasc Qual Outcomes. 2010 Jul;3(4):406-12.

[84] Manerba A, Vizzardi E, Metra M, Dei Cas L. “n-3 PUFAs and cardiovascular disease prevention.” Future Cardiol. 2010 May;6(3):343-50.

[85] Wang Y, Crawford MA, Chen J, Li J, Ghebremeskel K, Campbell TC, Fan W, Parker R, Leyton J. “Fish consumption, blood docosahexaenoic acid and chronic diseases in Chinese rural populations.” Comparative Biochemistry and Physiology Part A: Molecular and Integrative Physiology 2003 Sep;136(1):127-40.

[86] Junshi C et al. Diet, Life-style and Mortality in China, p. 606.

[87] Campbell TC. “Denise Minger Reply.” Campbell Coalition for Health Change. Retrieved from

[88] Fuhrman J. “Eat for Health: Cut Back on Grains.” Disease Proof. Retrieved from

[89] Hokanson JE, Austin MA. “Plasma triglyceride level is a risk factor for cardiovascular disease independent of high-density lipoprotein cholesterol level: a meta-analysis of population-based prospective studies.” J Cardiovasc Risk. 1996 Apr;3(2):213-9.

[90] Iso H, Naito Y, Sato S, Kitamura A, Okamura T, Sankai T, Shimamoto T, Iida M, Komachi Y. “Serum triglycerides and risk of coronary heart disease among Japanese men and women.” Am J Epidemiol. 2001 Mar 1;153(5):490-9.

[91] McDougall J. “Refined Carbohydrates for Food Addicts.” McDougall Newsletter 2006:5(10). Retrieved from

[92] Junshi C et al. Diet, Life-style and Mortality in China, p. 608.

[93] Harris WS, Bulchandani D. “Why do omega-3 fatty acids lower serum triglycerides?” Curr Opin Lipidol. 2006 Aug;17(4):387-93.

[94] Campbell TC. “Denise Minger Reply.” Campbell Coalition for Health Change. Retrieved from

[95] Ibid.

[96] Ibid.

[97] Campbell TC. “A Challenge and Response to the China Study.” Retrieved from

[98] Junshi C et al. Diet, Life-style and Mortality in China, p. 732.

[99] Ibid, p. 716.

[100] Campbell TC. “Denise Minger Reply.” Campbell Coalition for Health Change. Retrieved from

[101] McDougall J. Dr. McDougall’s Digestive Tune-Up. Summertown, TN: Healthy Living Publications, 2006: p.146.

[102] Esselstyn CB. Prevent and Reverse Heart Disease. New York: Penguin Group, 2007: p. 70.

[103] Ornish D. Eat More, Weigh Less. New York: HarperCollins Publishers, 1993: p. 43.

[104] Ibid, p. 61.

[105] Barnard N and Grogan BC. Dr. Neal Barnard’s Program for Reversing Diabetes. New York: Random House, 2007: p. 65.

[106] Ibid, p. 84.

[107] Fuhrman J. Eat to Live: The Revolutionary Formula for Fast and Sustained Weight Loss. New York: Little, Brown and Company, 2003: p. 121.

[108] Ibid, p. 33.

[109] Ibid, p. 135.

[110] Fuhrman J. “What You Need to Know About Vegetarian or Vegan Diets.” Dr. Fuhrman.

[111] Jönsson T, Granfeldt Y, Ahrén B, Branell UC, Pålsson G, Hansson A, Söderström M, and Lindeberg S. “Beneficial effects of a Paleolithic diet on cardiovascular risk factors in type 2 diabetes: a randomized cross-over pilot study.” Cardiovascular Diabetology July 16 2009 8:35.

[112] Ibid.

[113] Frassetto LA, Schloetter M, Mietus-Synder M, Morris RC Jr, Sebastian A. “Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet.” Eur J Clin Nutr. 2009 Aug;63(8):947-55.

[114] Ibid.

[115] Lindeberg S, Jönsson T, Granfeldt Y, Borgstrand E, Soffman J, Sjöström K, Ahrén B. “A Palaeolithic diet improves glucose tolerance more than a Mediterranean-like diet in individuals with ischaemic heart disease.” Diabetologia. 2007 Sep;50(9):1795-807.

[116] O’Dea K. “Traditional diet and food preferences of Australian aboriginal hunter-gatherers.” Philos Trans R Soc Lond B Biol Sci. 1991 Nov 29;334(1270):233-40; discussion 240-1.

[117] O’Dea K. “Cardiovascular disease risk factors in Australian aborigines.” Clin Exp Pharmacol Physiol. 1991 Feb;18(2):85-8.

[118] O’Dea K. “Diabetes in Australian aborigines: impact of the western diet and life style.” J Intern Med. 1992 Aug;232(2):103-17.

[119]Lindeberg S, Berntorp E, Nilsson-Ehle P, Terént A, Vessby B. “Age relations of cardiovascular risk factors in a traditional Melanesian society: the Kitava Study.” Am J Clin Nutr. 1997 Oct;66(4):845-52.

[120] Lindeberg S, Berntorp E, Carlsson R, Eliasson M, Marckmann P. “Haemostatic variables in Pacific Islanders apparently free from stroke and ischaemic heart disease–the Kitava Study.” Thromb Haemost. 1997 Jan;77(1):94-8.

[121] Lindeberg S, Lundh B. “Apparent absence of stroke and ischaemic heart disease in a traditional Melanesian island: a clinical study in Kitava.” J Intern Med. 1993 Mar;233(3):269-75.

[122]Mann GV, Shaffer RD, Anderson RS, Sandstead HH et al. “Cardiovascular disease in the Masai.” J Atheroscler Res. 1964 Jul-Aug;4:289-312.

[123]Taylor CB, Ho KJ. “Studies on the Masai.” Am J Clin Nutr. 1971 Nov;24(11):1291-3.

[124] Ibid.

[125] Eilat-Adar S, Mete M, Nobmann ED, Xu J, Fabsitz RR, Ebbesson SO, Howard BV. “Dietary patterns are linked to cardiovascular risk factors but not to inflammatory markers in Alaska Eskimos.” J Nutr. 2009 Dec;139(12):2322-8.

[126] Ibid.

[127] Ebbesson SO, Ebbeson LO, Swenson M et al. “A successful diabetes prevention study in Eskimos: the Alaska Siberia project.” Int J Circumpolar Health 64 (2005):409–424

[128] Bersamin A, Luick BR, King IB, Stern JS, Zidenberg-Cherr S. “Westernizing diets influence fat intake, red blood cell fatty acid composition, and health in remote Alaskan Native communities in the center for Alaska Native health study.”J Am Diet Assoc. 2008 Feb;108(2):266-73.

[129] Campbell TC. “A Challenge and Response to the China Study.” Retrieved from



  1. it’s great to have it all in on place but did you mean to put it all on the main page rather than the normal format of introduction with link to the full article…

    the previous articles might get lost behind the comments

  2. scrub that..i can see the comments don’t make their way to the main page

    an enjoyable read…i wonder if campbell will break his silence 🙂

  3. From

    “You also really should read Minger’s latest paper. She doesn’t take the time to harp on and explain every issue as much, but she hits a broard array and really dismantles the “animal products are unhealthy” hypothesis as argued by Campbell.

    A final issue to remember is that while Campbell does have many scholarly papers, the China Study is just some book where he is arguing his hypothesis. He has also indicated that in many ways he is approaching science from a newer, holistic viewpoint (one where he can cherry-pick simple univariate correlations as evidence…) that he himself recognizes that might not be well accepted or appreciated by other scientists. I think you need to be skeptical of attaching too much weight to his scientific credentials in cases such as then when he himself acknowledges that he is stepping out of the mainstream.”

    And here is the reaction of a supporter of Campbell (well not so much anymore 🙂 )

    “Thanks very much for your detailed comments. You’ve made a lot of good points. I’ve done some more checking and, I must admit, I’m growing more skeptical about Dr. Campbell’s recent work in light of what Harriet and others (including yourself) have written. He really “indicated that in many ways he is approaching science from a newer, holistic viewpoint”? If that’s the case, then yikes, that is a bit of a death march to camp Pseudoscience.

    “If in contrast, we start with explanatory models that represent the inherent complexity of nutrition and is accompanied by biological plausibility, then it is fair to look for supportive evidence among a collection of correlations, especially when we examine these correlations from multiple biological perspectives” – yes, I agree for sure, this is a credibility-disintegrating admission. Ouch.”

    So there you have it. You really are making inroads here Denise. 🙂


    1. This is an awesome paper. I came to my military class today with 1 cup of milk and someone quoted Campbell’s research. They stated I should quit drinking milk and eat vegetables high in calcium as an alternative.

      Campbell seemed to choose what correlations to use in order to support his theories or research. I lived on a farm in Montana where my family and I drank at least a cup of milk a day–sometimes raw milk. All live well into their 80’s and 90’s and had healthy bone density. No one developed osteoporosis from my knowledge. My Great Grandmother lived to 109. I just do not see the connection. There are too many variables involved here that could support or fully discredit his research. I’ll continue drinking my glass of milk per day. 😉

  4. Excellent and, as far as I can see, unassailable work, as usual.

    What might be your most important insight, and the least mathematical, is that humans beings apparently thrive on a variety of diets, and that instead of analyzing them based on their differences, we should examine what they have in common.

    Also, while advertising is clearly out of the question, I am firmly in the camp of those who think you should add a “Donate” button to your blog. The work you’ve done has real value, and there’s no reason you shouldn’t be rewarded for it.

    1. Thanks Anthony.

      I consider this blog my “volunteer work” and I’d feel pretty weird about asking for money, so I think I’ll pass on the donate button. If people want to help replenish my resources, they can come to Portland and buy me lunch. 🙂

  5. @Anthony Knox:

    “instead of analyzing them based on their differences, we should examine what they have in common.”

    That was already done by nutrition researcher Weston Price in “Nutrition and Physical Degeneration.” The healthiest native peoples, no matter where in the world they lived, all consumed animal foods, and lots of animal fats.

  6. Well, T. Colin Campbell asked for it. I don’t think you’ve left him much wiggle room for obfuscating the discussion with nonsense about your writing style, etc. Now he’ll have to stick to science and statistics. It will be interesting to see if he can come up with a response of similar quality and depth.

    Apropo quote from Albert Einstein: The important thing is not to stop questioning.

    By which I suppose Professor Einstein meant never stop questioning your own beliefs, as opposed to questioning those who disagree with you.

    1. Yes.

      “The first principle is that you must not fool yourself – and you are the easiest person to fool.”
      — Richard P. Feynman

    2. I think he’s probably done with me, to be honest. His “new and holistic approach” to science is fairly immune to hard facts and statistics, so I doubt anything I’ve written here will have much impact — its main purpose is just to collect all the criticisms in one document, stripped clean of cutesy and those terrible adjectives.

      I’ll be pretty excited if he does reply again, though! This is so much fun! 🙂

      1. I think by now he’s realized that every time he opens his mouth he winds up deeper in the briar patch.

        In the past, his ad-hominems worked. He would loudly denounce and condescend, the vegans would bleat along, and that would be the end of it.

        But with you, every time he pulls out his knife, he winds up in a gunfight.

        You’re simply…
        – smarter than him
        – can work harder
        – don’t need tenure; your livelihood is not dependent on finding the “right” answer
        – and, most of all, you are in it for FUN and scientific curiosity, not ego

        I almost felt bad for the guy when he resorted to claiming to hear a “symphony.” It was like hearing Norma Desmond say, “All right, Mr. DeMille, I’m ready for my close-up!”

        But think of how many lives he might have saved had he had the integrity to acknowledge that the data made his initial hypothesis very unlikely…and had the courage to have followed the data where it led.

        Instead, he hid the strong, direct correlations and highlighted weak, indirect ones. That’s so cynical and dastardly. Too bad he wasn’t in it for fun as well — he might have done some real science!

        But then, he would have risked his renown, his pocketbook, his Foundation, and his son’s upcoming “health food” brand.

      2. Like I said, I believe Campbell should be stripped of his academic titles for abusing his position and tarred and feathered for foisting pseudoscience on a public that trusts experts to provide them with the hard facts and not his personal fantasies about nutrition.

  7. Best quote:

    Campbell’s chief criterion for deeming correlations valid is not just whether they’re objectively plausible, but whether they support his hypothesis. In the instances they do, as explained earlier in this paper, he cites them without performing deeper analyses; in the instances they do not, he gives them no mention nor delineates a methodology for explaining their inconsistency with his theory. Rather than evaluating discrepancies within the data, he dismisses them—a choice ultimately leading to confirmation bias, potential misrepresentation of true trends, and a missed opportunity to rework his hypothesis to account for apparent anomalies.

    1. He keeps really trying to sell the idea that in doing all this that he is really doing some form of superior, holistic science. For me one of the most annoying things is that this supposed scientist is trying to teach people that this is how science works – you don’t really need to test hypotheses if you really like them.

      It is the same thing that the Creationists do. They start with a hypothesis they really like, and then they use this hypothesis to judge or disregard the science.

      In Campbell’s own words (from “A Primer on Statistics”
      “I agree that using univariate correlations of population databases should not be used to infer causality, when one adheres to the reductionist philosophy of nutritional biology and/or when one ignores or does not have prior evidence of biological plausibility beforehand. In this case, these correlations can only be used to generate hypotheses for further investigation, that is, to establish biological plausibility. If in contrast, we start with explanatory models that represent the inherent complexity of nutrition and is accompanied by biological plausibility, then it is fair to look for supportive evidence among a collection of correlations…”

  8. Very nice Denise! You are doing a very good job.

    I found something I think is a typo:

    “As with the previous paper Campbell cited, this publication does not discuss a potential role of animal foods as either direct or indirect causative agents of breast cancer. More specifically, it offers rationale for assuming animal foods, as a collective group, cause elevated hormone levels more than other dietary or lifestyle constituents.”

    Doesn’t make sense that the paper does not discuss the role of animal foods even as an indirect causative agent, but specifically offers rationale that they collectively cause elevated hormone levels more than those other things. It doesn’t even discuss it, but specifically offers rationale? Or is the case such that you don’t believe elevated hormones have something to do with breast cancer, and your point is that they talk specifically about animal foods increasing hormones, but not directly or indirectly causing breast cancer?

    But anyway I’m foreign and maybe what you said is correct, just confusing to me.

    Regarding the Masai, you can probably expect someone to bring up that paper that shows Masai do have atherosclerosis. You can read more about it here:

    I am an avid follower of Stephan’s blog myself and he is almost as brilliant as you! But you are way more prettier.

    1. Yikes! That sentences should read, “offers NO rationale.” Little word, big effect. Should be fixed now.

      I’ll probably be updating the Masai section pretty soon — thanks for the link!

  9. Here is an even better Einstein quote: “Everything should be made as simple as possible, but not simpler”.

    Numbers can make art just as well as noise. Instead of adhering to or fighting religious dogma why doesn’t each individual follow his/her senses to see whats right at any given moment? I suggest everyone google “instinctive nutrition”. First two links. 🙂

  10. Yes. The two terms are used interchangeably. Being a raw foodist I’m sure you’ve experienced this first hand but I was initially shocked at how strong the “taste change relationship” really is for raw foods and how devoid processed food is of this effect. So what do you think about anopsology?

    Earlier you mentioned that we should study the commonalities instead of the differences and you are very right. I would add that the most binding factor to us all is that we are each made up of the elements of the periodic table (indirectly or directly of course) and when one of those elements gets blocked or goes missing bad things are bound to happen. Further an individuals nutrient needs are going to change day by day so a one size fits all dogma (Dr. Campbell’s or anyone elses) isn’t likely to work for one or everyone for very long.

    An instinctive way of eating was the best way I found to always stay on top of things. If my body told me to be a vegan one week I was. If it said eat 640z of steak the next, I did. 65 pounds lighter and 6 months later I can say that I am a true believer. It just takes paying attention to the millions of years of evolution and the very senses that allowed us to survive in the first place while avoiding the modern “land mines”. (processed junk, drugs, etc etc)

    Being a nutrition nerd it was hard to stop asking questions and start listening for once but it paid off. Go figure, no wait, don’t go figure – you’ve done enough already and I’m sure your burned out ATM. Thanks for sparking good debate and stoking the fire. 🙂

  11. “Notably, blood glucose tends to have a distinct nonlinear relationship with disease, and its association with cardiovascular diseases, cancer, and diabetes may therefore appear diminished when studying only linear correlations, as Campbell has generally done with cholesterol. ”

    Bravo on the point about nonlinear relationships, one that is frequently overlooked.

  12. For anyone reading this — the long-ago-promised post on wheat will be up either today or tomorrow. It’s taken a lot longer than I expected because, quite frankly, I haven’t been able to find a darn thing to explain the relationship between wheat and heart disease apart from the wheat itself. I’m trying everything! Put away the bread, people!

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  16. Perhaps you can do a piece on organic food. Study after study trying to prove that organic foods are much better than you instead show that there is actually little to no benefit – the added expense in food could be better spent purchasing healthier foods. The organic food movement very much seems to be a pseudo-science based on wishful thinking, much the same way the veganism of “The China Study” was.

    1. Even if it could be scientifically proven that there is no harm in ingesting the synthetic pesticide residues found in conventionally grown foods, I would still opt to buy organically grown versions of the most pesticide intensive crops (the “dirty dozen”). I don’t worry about buying non-organically grown foods that are minimally sprayed, but IMO, it’s just common sense to avoid ingesting the larger doses of toxic chemicals whenever possible.

    2. You assume people don’t care about pollution and other ag-related environmental issues. While individuals may buy organics for health reasons, most involved in the organic food movement are concerned with the relationship between people and the land.

  17. If we didn’t spray vegetables with pesticides there would be less of them to go around and that means there would be more diseases. Remember, pesticides and the like aren’t being sprayed because companies like Monsanto are trying to kill us, they are trying to maximize output and lower price because that is what we are demanding that they do.

    Bananas are a prime example. If we all had organic bananas (grown at higher altitudes) then there would be MUCH less bananas to go around and that would mean exponentially higher prices. Start doing this to more and more food crops and health would turn into an “elitist” term more quickly than it already is. The health disparity between the poor and the affluent is already well documented.

    That said, the case against pesticides is great. Even if they don’t make you sick now a life time of accumulation is a different story, not to mention the concentrated chemical runoff “soup” from these farms contaminating ground water and damaging ecosystems or how about the Mexican slaves who are getting cancer from working in and around this stuff all day…

    What to do, what to do?

    1. I just came across this today unfortunately–and I must say I love this blog!!–however, I did want to comment on bananas. I wholeheartedly agree that if pesticides were suddenly eliminated, the global food crisis we are currently experiencing would become much, much worse. However, it is not well known that bananas in the West (i.e., the Cavendish, or the regular old banana we have in our cereal) have little to no resistance against certain diseases that attack bananas, mainly fungi, which if to go unchecked, could wipe out banana crops. It’s also interesting to note that the starchier, less-popular varieties tend to have less of these issues. Thus I think that people in the West really ought to pay attention to what it is that they are eating, not just because we want to avoid pesticides because pesticides are “bad” but because pesticides, herbicides, and fungicides might be the only thing allowing us to eat those items in the first place! We can’t always always have our bananas and eat them too 😦

  18. Someone posted this at the McDougall Message Board, which is here:

    Pretty effing hilarious if you ask me.

    “Regarding this Denise Minger person: While i’m certainly no expert on the topic, i have read a few telling things about her. She apparently removes comments from her blog by scientific researchers who point out flaws in her reasoning. According to, where Dr. Campbell’s eloquent and intelligent reply appeared, she tried to impugn his character. She tried to question his motives! What?? Yes, she deserves a bit of anger. My heart doesn’t go out to her at all. SHE is the one with questionable motives, and surely isn’t even remotely armed to engage in this kind of dialogue with someone as esteemed and prepared as Dr. Campbell. It’s not even a fair match. I’m amazed that he even bothered to answer her “critique”.”

    1. Wow! Translation:

      “Miss Minger is an heretic trying to befoul our revered and adulated leader Dr. Campbell. I’m amazed that our holistic leader even bothered to answer an actual scientific critique, she does not even view the world holistically, so there is no arguments to have with her, she is completely out matched.

      Dr. Campbell should not waste its time with this science non sense and instead should concentrate on engaging with other kind and esteemed holistic practitioners who can actually see the light and be swayed by its glory.”



      1. I’ve casually followed the McDougall site for a while as a friend tried the plan to lose weight, was successful, and it made me curious. Most of the people over there come to that place because they’re disturbingly unhealthy and wish to get well. They’re a pretty nice bunch except for a few that get very strident and angry when anything other than the McDougall philosophy is discussed or even mentioned. (Questioning the basic premises of the program isn’t allowed. This is, it is explained, because the site is essentially a support group for those on the program.)

        The level of scientific knowledge at that site isn’t that great, so it’s not surprising that the “tabloid mentality” predominates and that few if any there are educated enough to read these replies and responses and come to any understanding. What is kind of disturbing, as the excerpted comment above shows, is the level of hubris and outright pride in their lack of knowledge, worship of authority figures and drowning-man-clinging to a set of fixed ideas.

  19. You can tell they are getting very nervous about their faith in Campbell’s gospel if they can’t argue about Denise’s critique of his data analysis and instead resort to ad hominem attacks on Denise as a way of distracting those believers beginning to have doubts about Campbell’s assertions.

    1. What I find funny about this “nervous” posture some China Study believers have regarding Denise’s papers is that her latest paper clearly says such near-vegetarian diets are probably very healthy for many people. What the nervous Campbellites can’t seem to stomach is that there isn’t one, single way for everyone to eat that produces optimal health. Traditional diets, low-fat diets, raw diets, paleo diets, etc., all seem to produce great outcomes in different people.

      Why can’t people accept the fact that “one size does not fit all” when it comes to eating? Why are Campbell’s people so intent on fitting the whole world into a narrow mould?

  20. I just looked at Campbell’s PDF response on his site again. Part of his conclusion:

    “I suggest that those people who are so hostile to this message take another look at their reasoning. There is far more to this story than the interpretation of the scientific data alone. There are major issues of health care and health care costs, there are serious environmental issues that have not been adequately communicated to the public, and there are political, social and ethical issues that must be considered. Of most importance, there are people who deserve to hear this message—namely, the taxpayers who funded this work. For me to do anything less than to report on these findings is both immoral and unethical. In the current discussions about this issue, I would urge that it is vitally important that all of us keep these ideas in mind, while being very careful not to promote ideas simply for the sake of defending one’s own personal preferences. I strongly believe that discussion of these issues focus outwardly for the sake of all of us, not just inwardly for the satisfaction of personal ego.”

    Um, wow. Ignore the data because of environmental concerns? Has he shown conclusively that a not-exclusively-plant diet is inherently harmful to the environment? And the rest is just a mess of distractions…so many instances of implying that his point of view is the correct one and that to disagree is to risk the environment or let your biases, agenda and ego cloud your judgment…and that taking issue with his findings is to want him to not report to the taxpayers (never mind that all this discussion was about his commercially-released book), which would be immoral and unethical. Because, of course, his work is infallible, so the only choices are to “report” or to waste the taxpayers’ money. To take issue with some of his conclusions is to be “hostile to this message,” to not care about health care costs, to deny people the right to hear his message (has anyone suggested Campbell not be allowed to write/publish?), to want only to satisfy your ego and not be concerned with the outer world and humanity. And this is all in just one paragraph! I could almost pick any paragraph at random from his introductions and conclusions and find this kind of stuff. I know I keep posting on this aspect of the debate, but it just frustrates me to no end that a man of science would either disingenuously slander his questioners or be so lacking in self-reflection that he doesn’t realize there’s a problem with this kind of tactic…and that so many of his followers are okay with this kind of logic and his constant implications of imaginary motivations and associations. Why is the guy who cloaks himself in science encouraging his followers to treat diet as a religious/faith/moral issue?

    Interesting that Denise’s name has all but disappeared from the Campbell sites, and that there’s no reference to her recent formal response. I suspect that there won’t be, sadly.

    1. Heh…I thought Rick was addressing Karn as “Denise” for some reason and had some kind of insider name info. I got confused. 🙂

  21. Ah, Greg, now you’re pushing the discussion into the realm of psychology and human behavior. Be careful, my man, or you’ll have us all quoting Shakespeare.

    “Reputation, reputation, reputation! O, I have lost my reputation! I have lost the immortal part of myself, and what remains is bestial.”

    See what I mean? Don’t go there!


  22. As far as Campbell goes…power, has the ability to make people believe anything, even their own B.S. When you inflate your ego with hot air and float “high” above it all, firm grounding (science) is distant memory. Unfortunately these positions of power have the ability to compel people with less of it to believe the same B.S. as well. People are very malleable. Think of the Stockholm Syndrome where individuals fall in love with and defend their captors. Slavery worked on much the same premise.

    And that sir is why we have the Internet. Knowledge is power and by giving those of us that power who would not otherwise have it, the net has become the great equalizer of our times. People in positions of power like to control the flow of information (news media anyone?) and the net makes that near impossible.

    There are some who have aligned their “worth” with the group they “belong” to and therefor will defend it to the bitter end even when faced with the supposedly undeniable truth. So it goes and we are seeing it played out that this was long ago not a Science Vs Science play but a Science Vs Dogma, Ego, Vanity, Religion, People, Community and the infinite complexity of humankind. The more things change the more they stay the same.

    I believe its all okay though. There will always be beacons of intelligence (Denise) who gather those of us with open eyes to learn. Since we don’t blow with the wind, our foundation slowly but surely becomes more and more substantial. “Just the facts ma’m”, indeed.

    1. Well put. People will defend there group no matter what. It is scary. I did it, but I caught myself. The whole S Syndrome is very interesting.

  23. Denise, thanks for the great work you’ve done here – again !

    Regarding wheat and heart disease, Loren Cordain has written interesting pieces called “Whole Wheat Heart Attack” part 1 and 2. I found the second one on google:

    “Common dietary lectins are potent stimulators of
    inflammatory cytokines in white blood cell cultures20,21.
    In Figure 3 you can see that lectins
    from lentils, kidney beans, peas and WHEAT
    potently increase the production of inflammatory
    cytokines (IL-12, IL-2, and INFγ). WHEAT lectin
    (WGA) also stimulates production of two other
    inflammatory cytokines (TNFα and IL-1β)21 that
    promote the atherosclerotic process.”
    – –
    called matrix metalloproteinases (MMPs),
    secreted by white blood cells and other cells
    within the plaque, are known to cause collagen
    and elastic tissue within the fibrous cap to disintegrate.
    Consequently, any dietary or environmental
    factor which facilitates synthesis of MMPs
    is not a good thing for cardiovascular disease
    patients. Well guess what? Lectins from wheat,
    WGA22, and lectins from kidney beans, PHA23,
    cause tissue cultures of white blood cells to increase
    their production of MMPs.”
    – –
    “WHEAT lectin also influences
    the final and fatal step in
    atherosclerosis, the formation
    of a blood clot in an artery.
    Integral to the formation of
    clots are platelet cells, which
    circulate in the bloodstream..
    Platelets are normally activated when they contact
    collagen from a damaged blood vessel.
    WGA directly causes the activation of platelets
    and potently increases their aggregation
    (clumping) 24. Hence, the consumption of WHOLE WHEAT
    may be integral in the thinning and destruction
    of the fibrous cap as well
    as the formation of the fatal clot.”

    Click to access Wheat%20lectins,%20heart%20disease,%202008.pdf

    Caps added by me – I didn’t want you to miss the best parts. ^^
    Have fun !

  24. AMAZING, this is a work of Taubesian proportions. Have you considered science/health journalism? Keep up the awesome work, it’s very important.

  25. Also here:

    This commentary concerns the The China Study and the critique thereof started by Denise Minger. I read the China Study book with a point of view derived from having followed nutrition for over 3 decades, having generated over 20 ref’s in Medline re nutrients and heart disease and having published a not-for-profit 11 year old website [] about the topic. With this take of the science, I have the following issues with the “animal foods are bad, vegetable foods are good and don’t use a multivitamin supplement” conclusions:

    1. Campbell avoids the topic of total mortality. I have never seen data that these people in China in those years lived longer healthier lives than Westerners.

    2. Animal foods raise cholesterol which is bad. The reality is different. For example, central Europeans in the lowest group (quartile) for cholesterol die first. This was the result of a massive study on 150,000 people and ~ 1 million blood analysis/examinations: i.e. the Vorarlberg study. MANY studies support that finding but even 1 discordant data point must be considered; it was not. One ugly fact can destroy a pretty hypothesis.

    3. If animal foods are so bad, why did original Inuit not have substantial heart disease, have little high blood pressure and no diabetes? This is another discordant data point not considered: almost no plant food and none of these age-related diseases:

    4. Campbell et al missed THE most important confounder: homocysteine. This is an amino acid that is extremely corrosive to our structural and functional proteins, and it is high when B vitamin intakes are low. The China Study DID HAVE community pooled blood samples but did not measure that toxin. Moreover, it is our and China’s best indicator for low B vitamin intakes [B2, B6, folate i.e. B9, and B12]. The China study found very low levels of B2 and stopped there.

    I know, mainstream medicine discards homocysteine since its reduction does not quickly cure the diseases it is related to: heart, bone fractures,
    Alzheimer’s and cancer, but it is a [or the main] cause or premature
    decline, and statistically a confounder that HAS TO BE included
    otherwise nonsensical results are found.

    A similar problem is that they apparently did not adjust for selenium and that we know varies tremendously across China and is a major cause of cardiomyopathy. A different issue not discussed and that affects diabetes is that rice eaten in China as a kernel does NOT have the same glycemic response as a grain milled into a powder and then cooked or baked. Same chemicals, different response.

    5. Campbell had his start preventing or slowing cancer or
    in rats given a carcinogen using plant [soy, wheat]
    based protein versus casein, the main protein in milk. Was this
    defatted [skim] milk powder [??], was this purified casein [??] or did
    it contain traces of oxidized cholesterol/steroids, known to affect cancer?? I
    was unable to find anything about that “casein” used. Is it possible that this casein was not chemically pure casein?

    The book also does not give the amino acid differences [normally given per 1000 amino residues] between the proteins used, leaving that aspect unexplained and entirely puzzling. Protein is decomposed into amino acids during digestion and after which about the only difference between plant and animal protein is the lower content [about 1/3rd] in plants of the essential amino acid methionine, not known to cause ill health [if the B-vitamin intakes are optimal]. The book does not deal with the methionine = homocysteine = methylation pathways, known to affect cell health and expression at a fundamental level [epigenetics]. Homocysteine is related to well over 100 diseases and conditions; to Campbell’s credit, he mentions its discoverer, McCully, but he then does not follow the implications of above minimal homocysteine.

    6. Campbell misrepresents study results, for example those of our common hero, Lester M. Morrison’s, and his brilliant early heart disease research. Campbell suggests the benefit was from reduced fat and cholesterol while in reality it probably was by supplementing with massive vitamin-nutritional supplements that included methionine [!], betaine and lecithin. Morrison’s 1958 book recommends “.. each day B complex vitamins in the most potent form“. Morrison promotes [non processed] meats: “Meat is the greatest source of animal protein for human consumption and he promotes the consumption of liver. Rather than fearing milk, he allows “3 cups of cow’s milk whole”. [Library of congress book # 58-9308]

    Campbell, on the other hand, fervently advises AGAINST the use of vitamin supplements with the only but conditional exceptions of B12 and D. But do vegetarians really store “enough” B12 for 3 years? [no reference given and obviously not enough to minimize homocysteine.] In some rare circumstances he recommends to take a “small” B12 supplement (there is no toxic dose) or to get your “B vitamins and homocysteine checked annually”, something that would cost hundreds of dollars more than this superb high-dose no child proof cap multivitamin but without solving deficiency problems that are everywhere. Also, why use the “smallest dose of vitamin D you can find” when not getting sufficient [sic] sunshine. In fact, when the sun is below 45 degrees above the horizon, nobody can make any D3 and what’s sufficient? [tip: your shadow has to be shorter than your height when not wearing sunscreen or coverings.] At one point Campbell even mocks vitamin B6, an undisputed deficiency shown to cause rapid atherosclerosis in primates …

    From the landmark books by Morrison, McCully, Williams, Willett, Atkins and Pauling, there is agreement that a good multivitamin is essential to health and it is here that I believe Campbell’s outlier advise does the greatest harm. The science of the micro-nutrients has evolved. Any modern [cooked and/or refined] diet requires a multivitamin and probably the use of plant and fish based omega-3 [the latter in a pill] to allow optimal long-term health. Campbell does not deal with the omega-3 prostaglandins, an unfortunate omission yet he promotes doubt about omega-3’s benefit [contrary to the AHA and ISSFAL].

    These comments are in addition to the various statistical and methodological comments made by others: when confounders and study results are not all considered, the results cannot be relied upon.

    To end on a positive note: “The China Study” has nice sections about the corrupting influence of big industry and big medicine and it has some telling inside and personal stories. My suggestion: this book has to be part of a larger picture and without proper supplementation [that has NEVER shown to degrade people’s diets or food choices] it is not sufficiently healthy. To its credit, there is no mention of cholesterol-lowering statin drugs or of other medications that do not extend lives.

    Try instead McCully’s simplest book about nutrition and heart disease: Here is the simplified homocysteine science that was ignored in Campbell’s book:

    1. David, don’t let Denise’s freedom get in the way! feel free to enrich us all with the gift of your time, provide us with your own analysis. Because yeah, who does Ms. Minger think she is!? burning the midnight oil and relinquishing her own life in order to make us all smarter about what we choose to eat. What gall!

    2. It’s coming, I promise! I had some unforeseen, non-blog-related delays — but it’s still in the queue. Maybe if I refrain from giving time estimates, I’ll stop jinxing myself and get it done sooner. 🙂

      -Denise/AKA “Girl Who Cried Wheat”

  26. Campbell just shut down the site.

    I think Colin realized it was a mistake to respond to you.

    You really scare the fiber out of him. 🙂

    1. Are you sure it is really closed and not just down for remodeling?

      At first I thought he might be trying to hide the evidence, but is “Primer on Statistics” article from the CampbellCoaliton website where he espouses pseudoscience is presented prominently on his main foundation website under the title Correlation vs Causation. The last half or so of the paper is his defense of his “wholistic” approach to science, where he says:

      “In summary, I agree that using univariate correlations of population databases should not be used to infer causality, when one adheres to the reductionist philosophy of nutritional biology and/or when one ignores or does not have prior evidence of biological plausibility beforehand. In this case these correlations can only be used to generate hypotheses for further investigation, that is, to establish biological plausibility. If in contrast, we start with explanatory models that represent the inherent complexity of nutrition and is accompanied by biological plausibility, then it is fair to look for supportive evidence among a collection of correlations…”

      He uses this logic to cherry pick simple correlations as “evidence”, to ignore contradictory correlations, to ignore confounding variables, to ignore his own multivariate analyses, and to justify the fact that given thousands of simple correlations he still had to use questionable intermediate variables to indirectly indict animal protein.

      1. For an update on this (I noticed the site was down when following other links on other posts):

        The site isn’t just down, the DNS name is for sale by a hosting company.

        He literally closed up shop, at least there. I imagine he’s got some serious egg on his face among the scientific community for this. Worse than that his “holistic’ (ie non-scientific) approach to science would probably get him into the most trouble. Possibly career-ending trouble. If he can’t understand why starting with a hypothesis and finding observations to confirm it is bad, he does not deserve the title of “scientist”.

        Frankly, that’s as it should be.

        On the other hand I think it would be awesome to see studies with a Dr. Minger, PhD attribution. 😉

        What I find most hilarious about the whole thing is, by most people’s definition, Denise is a vegetarian. Really, only hair-splitters would say otherwise.

        1. This is from the 30 Bananas a Day site regarding the Campbell Coalition Website.

          they’ve taken the site down because they are in the process of regrouping their strategy.

          from what nelson said, i do not think that the site will return – it only showed up in of june, 2010 as a trial initiative to get plant-based diets promoted along the lines of campbell’s discoveries. (some of the ‘cheerleaders’ on minger’s blog like to think that it was developed as a response to her efforts, but i think that fantasy should be left to those who have enough time on their hands to reshape the universe in their own minds 😀 ).

          having acquired some preliminary ‘data’, my guess is that they have a better idea now as to the possible directions they feel are efficient ways in which to proceed. several weeks ago colin told us that there are some very interesting opportunities that they are exploring. i do not know any details, but he was quite enthused by these. so it is quite likely that they have shifted their energies to prepare for these rather than spend it on developing the site (which was after all little more than a collection of blog entries).

      1. I think a more plausible and holistic explanation for the disappearance of the website is that Denise hacked it while under control of the microchip that the WAPF implanted in her brain.

      2. The suggestion of a WAPF microchip is an uncorrected correlation though. It is unsupported in my plausible model of WAPF mind control that utilizes psychic energy rather than microchips. The symphonies in my head tell me this is the most holistic model, so there is no need to test it. It is supported indirectly through intermediate variables though – Campbell has convinced many people that he is still a scientist when he has obviously turned to pseudoscience; therefore psychic mind control must be at work. And as I said, psychic mind control is what I like best…I mean that is what the symphonies say…So this must be the case with the WAPF. Campbellian pseudoscience is praised -> psychic mind control -> WAPF psychically-controlled website hackers. So QED.

  27. “Veganism is a matter of faith, not science”

    Well, so was the Inquisition, and we know how that turned-out…

  28. Not to be a nag, but how’s the wheat post coming? I’m really looking forward to that.

    I think it’ll be important. (My guess is that’s why it’s taking a while.)

    1. Should be up within 24 hours! Sorry this has taken soooooo long. I had to redo all of the calculations because I realized (after the fact) that the data didn’t copy and paste cleanly from Excel into the stats software I was using — so most of the results were at least a little bit off. Big facepalm moment. All fixed now, though. 🙂

  29. Same with me. I am realy looking forward to it. But take all the time you need. And thanks in advance!

  30. this was almost too much – to read such a **magnificent** dissection – no, i mean evisceration – done with such panache and intelligence –

    aahhh – please forgive me for allowing my pre-disposed nutritional bias to wallow in the glow of such and remarkably bright and lovely young woman!

    interesting things will come of this Denise – will be very curious to watch them develop –

    and thank you!

  31. Hi Denise and everyone,
    I just started going thru all this amazing material, from both sides of this debate, and am a bit saddened actually by all this. You are all missing the point. Virtually all studies are flawed if you take a close look. There is a lot of junk science going around masquerading as science – and a lot of good solid evidence for a plant-based diet being denigrated as anecdotal. I just cannot believe the amount of energy and time that has been spent here debating a bunch of data points, when the real point is how are we going to empower people to live a more balanced, healthy and compassionate lifestyle. It ain’t by endless debates over how many data points it takes to screw in a light bulb!

    Denise, I am not sure what kept you up that first night when you started analyzing the China Study, or what motivates you now. You appear to be a sincere raw food vegan, yet are allowing yourself to get caught up in a debate which seems to be only clouding the issue – from the point of view of people who are trying to make life-changing decisions about their health and diet. It’s all a bit nit-picky to me. We can use science to add credibility to a point of view but inevitably someone will find flaws in this study or that, or come up with a study that proves the opposite.

    I think it is more important to find ways for the larger community of people interested in healthier ways to live more compassionately on the planet to work together in harmony! Dr. Campbell is clearly reaching out to the world with a message intended to help people, despite anything else about his work. You are also doing that here, for the most part. The debate over statistical data points is actually a huge distraction, it distorts the search for the truth rather than adding to it. It is like getting into an argument about the interpretation of a particular verse in the Bible – it never ends…and worse, it doesn’t inspire.

    I invite us all to try to get past the data points if we can and get back to helping everyone we can touch discover a more balanced, compassionate way of living on the planet with each other.

    – Robert

    1. “We can use science to add credibility to a point of view …”

      Only if it’s not bad science, and that’s really the whole point. It’s hardly nit-picky if people are making diet decisions based on twisted statistics and fantasy disguised as truth.

      Is that how you want people to come to your lifestyle? By fooling them? If it’s about compassion, then let it be about that.

    2. Hi Robert,

      It is more than just debating statistical data points. What Campbell is doing is abusing science and invoking pseudoscience to justify it. One of the really unfortunate things that Campbell has done is made people more stupid about science. He has used his past scientific credentials to convince some people that what he is doing really is still science, and as his defense of his pseudoscience becomes more and more farce, his supporters merrily embrace the farce as how science is supposed to work.

      Science isn’t just something as you say “to add credibility to a point of view;” it is a tool to find a better point of view.

      Many people don’t trust nutrition science because as you say, “someone will find flaws in this study or that, or come up with a study that proves the opposite.” I think the solution to this is to require better science (and to call people out when they do bad science) instead of just writing off science. Again, the problem with Campbell is just more than bad science; he has embraced a pseudoscientific “holistic” approach where hypotheses do not require testing and where he can cherry-pick epidemiology to prove his hypotheses.

    3. Robert:

      “We can use science to add credibility to a point of view but inevitably someone will find flaws in this study or that, or come up with a study that proves the opposite.”

      Yikes! We don’t “use science to add credibility to a point of view”. What a complete misunderstanding of the process of scientific inquiry.

      Seeking and finding the flaws in the studies IS the science. If smart people did not dig in, find the flaws and challenge the conclusions, our knowledge would never advance and we would be at the mercy of our faith-based beliefs. That’s why peer review is an integral part of the process. Ideas have to hold up under rigorous scrutiny and repeated studies or else get discarded. And they do get discarded, all the time.

      You are free to come to conclusions about what we should eat based on faith or philosophy, but if that is what you choose, I think you are in the wrong place. This discussion is about the evidence and what conclusions can be drawn from it. Whether the study is flawed or not is exactly the point of what Denise has written.

  32. @Robert:

    Wow. Talking about missing the point.

    On the other hand, I have to give credit where credit is due. You make a very eloquent case for ignorance.

    “It doesn’t matter whether or not the information people use to make decisions about their lives is correct, only that they become more balanced and compassionate.”

    1. jeeze – thank you sam!

      the whole argument that information need not be correct but invoke the “balanced and compassionate” response sounds more than vaguely like “fair and balanced” used by -ummm – now who is that saying by anyway?? 😦

      its that ever-so-slippery slope that “the end justifies the means” argument used to such sad and miserable results throughout our human history- whose end and what means??

      i, for one, have spent my life trying – often in vain – to find and discern what information is better/more truthful/more useful for my needs than other information. to make a compassionate and balanced decision i personally NEED to see the arguments both for and against issues in order to even consider a decision affecting my/my families well-being and survival – and i applaud campbell at least for his efforts in the massive data collection … but i equally will deny him carte blanch to shove his conformational bias down my throat (oh – sorry – had to go there… 🙂 )

      i am ELATED that Denise, Ned and others give us a good look at other possible sides of this data–

  33. the last bit really hits home for me..’ Rather than studying the dissimilarities between healthy populations, perhaps we should examine their areas of convergence—the shared lack of refined carbohydrates, the absence of refined sweeteners and hydrogenated oils, the emphasis on whole, unprocessed foods close to their natural state, and the consumption of nutritionally dense fare rather than empty calories or ingredients concocted in a lab setting. Modern foods, and the diseases they herald, have usurped the dietary seats once occupied by more wholesome fare. It is this commonality—the thread bonding healthy populations—that may offer the most meaningful insight into human health.’

    I now suspect that my raw vegan diet was not what helped me get healthier and improve my leukemia.. but the omission of factory farm animal products, non organic produce, factory dairy etc….would have been a whole lot easier to just eat better foods and omit the nasties.
    but I did learn a lot from those 2 1/2 years, so it’s all good

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  35. Wow this was not very digestible for us lay people. I had to skip to the conclusion and was still scratching my head.

    Is anyone out there offering a good diet book that I can buy and follow that will help me, a middle aged obese female, now while everyone is arguing about this or that?

    My youngest daughter who is 22yrs old is a Celiac and yesterday an Italian researcher just announced that you can acquire Celiac as an adult not just at birth. Once again he has turned the tables upside down on this topic. First it was considered rare then he comes over here and actually studies it and it turns out 1 in 133 Americans have it. This condition has been around for a very long time and it took someone fairly recently from Italy to come over and conduct some samplings. Now docs are being trained to look for it so folks are just now finding out it runs in their family and they have it. It would take an average of 11 yrs to get a correct diagnose for this condition at best.

    Shall we bring up the whole issue of folks with certain types of stomach ulcers and it turned out it was a bacteria that needed two weeks of antibiotic treatment rather than telling them to stop eating spicy foods and it’s all in their head. That was not that long ago.

    Now this Italian researcher announces you can get Celiac as an adult. This is a big thing. The whole story on gluten including wheat is still playing out. Our immune systems are or can be so easily impacted by what we think of as harmless and by other agents. Is wheat/gluten our friend or foe? I did find in some obscure research I think in England or Europe that milk in some cases causes the immune system to react in the same way gluten does by destroying the villi in the small intestines. Many Celiacs have to avoid milk because they say the protein is just to hard to digest for Celiacs. Some can drink milk while others can’t?

    Another NW link to this is the first scope to look at the villi to confirm the havoc gluten was causing was jerry rigged in Seattle in the 1950s. The first Celiac group was started in Seattle. The only reason they thought to check this out was based on observations in Holland during WWII where sickly children who were not able to get bread during the worst of the war showed vast improvement.

    There is so much that hasn’t been researched regarding food and our immune system and so many assumptions that have yet to be challenged. What I am getting at is even your great analysis may likely be flawed but I am glad you are doing it. I do not think you are a bad person or do not have good intentions. Even if you did which is hard to prove really, I do not think you shouldn’t continue to break down for us where you see the short comings in things. I do not know Mr. Campbell or all of his assumptions but I think I am much more convinced of an argument when I do not feel like there is a meanness to the challenge or comments but rather an openness of facts and almost a kindness in the challenge to discourage the readers of any negative bias. Just as with law I don’t know why the writing has to be so convoluted. The best teachers make the most complicated easy to understand. User friendly to all.

    I think researchers must love mysteries. I also think that anyone willing to take the time to move the discussions along whether half baked or not is worthy. They play their part in the whole process. Where one leaves off or provides holes another is able to see the holes. There was a PBS series years ago called Connections and they showed how ideas and progress moved along through the centuries. Highly recommend it.

    Dr. Campbell clearly doesn’t have all the ideas, who does, but he has certainly got you all a thinking and challenging it and we need more of that. Even if you find him annoying or whatever at least he is getting you to think about it and has clearly put himself out there with a bulls eye on his back and willing to take the inevitable shots. For the sake of argument I think whether his work is well intended or not he is helping folks get clearer on what is wrong and right with his findings. I would be thanking him for his contribution. Even your analysis may well be disproved in the years ahead for overlooking or for dismissing too quickly another piece of the puzzle which will seem so obvious looking back.

    It is nice to see a gal from Portland taking this on and I for one would be glad to buy you lunch to find out how I can apply all of this to real life. We live across the river from Portland. It shocks me that we can go to the moon but we have yet to figure out what is healthy and yet to mandated this in indirect ways through school lunch programs and such.

    Please do not attack me I bruise easily, and am just a housewife with no credentials who just wants to know what is the best information as we know it today from your perspective.

    Whose book does the best job of explaining and helping folks, with affordable meal ideas, who are trying to lose a lot of weight while avoiding foods that are linked with or seem to be linked with cancer and such? If you have a book recommendation, I would love to know your impressions of why you like the book.

  36. Deanne,
    As a nutritionist, and personally, I’ve come to the conclusion over the last 10 years, that eating in line with pre-agricultural diets gives by far the best results both in health and fat loss. Whether this is raw, as Denise practices or using both cooked and raw food (more conventional) it always seems to work for my clients. Here are a few people before and after when some clients took on a 6 week trial:
    A good book just released would be Robb Wolf’s Paleo solution
    All the best, I am also gluten sensitive – only discovered it last year as a 50 year old! But this way of eating has changed my life and my health.


  37. The Masai, because of their diet, get atheroma (plaque) accumulations in their arteries. The only reason it doesn’t kill them is because they get an incredible amount of exercise.

    “A final historical report relating to the impact of exercise on coronary artery size relates to autopsy studies performed on 50 tribal Masai from Tanzania and Kenya (Mann et al. 1972). The coronary intimal thickness of the older Masai exceeded that of a cohort of US subjects aged 60–69 years and there was widespread presence of atheroma, similar to that expected in American men of similar age. However, symptomatic cardiovascular disease was rare in these subjects (Mann et al. 1964) and the autopsies revealed that the coronary lumen displayed marked enlargement, such that the intimal thickening was not compromising. The Masai were remarkable fit (Mann et al. 1965) and the authors speculated that they were protected from the clinical manifestations of atherosclerosis by physical fitness, which caused their coronary arteries to enlarge.”

  38. I just had to say… wow. I can’t imagine how much time you put into analyzing, compiling, writing, and editing this … I seldom write responses to anything but I HAD to tell you that you ROCK.

  39. I’ve been hearing from muliple sources (vegan- dr. Scott of scott’s fasting by design on his website) and others (Hal Huggins even, of mercury free dentistry)- people far and wide, that say cholesterol, even the bad kind, is not the cause of heart disease and coronary disease. Rather, it may be a marker. I’m sure it’s a body defense mechanism- as most (all?) diseases inevitably turn out to be. I’ve heard (dr. Batmanghelidj) that cholesterol is a guard for the arteries to defend against dehydration, water loss from the artery cells. He says cholesterol is never found in the veins. I’m not sure if I quote him right, but his book well worth reading is “your body’s many cries for water”. I’m no nutrition expert but since these voices are so diverse, they are probably right. It’s also easy to get confused.

    I’ve heard that the heart disease and heart attacks, MIs are caused by inflammation breaking out. So who knows. but cholesterol may not be so much the enemy.

    That itself doesn’t make animal foods better or worse than before. They could still be bad. I myself still shun them and I see to do well on plant foods- avoiding nightshades, fat, getting my carbs, sometimes cooked but I do do well physically on raw no downside there if sufficient sweet fruit exists, except time and energy and money sometimes… I do well when i drink enough water and get enough sun. Those are the major things, I think water is so underrated. Anyway cholesterol itself might not be the cause of anything that we think it is. Inflammation is usually the first or second stage of disease after irritation and toxemia, according to natural hygiene health philosophy. It makes sense, the body sends it’s blood in there to heal and nourish and defend. Food for though

  40. Thank you for your “formal” paper. The other version was terribly distracting and annoying. Now, I am better able to assess your differences with Dr. Campbell but it seems that you have more in common with him than not.

    1. it seems that you have more in common with him than not.

      limuel, you have a reading comprehension problem if you think that.

  41. Heard about this (re: milk & whey):

    Laron syndrome (those with poor growth): “causes short stature and a *resistance* to diabetes and cancer.”​ki/Laron_syndrome are protected.

    Saw this study today:!/DrEa​des/status/100600941677514752
    “Individuals with Laron syndrome who carry mutations in the growth hormone receptor (GHR) gene that lead to severe congenital IGF-1 deficiency with decreased insulin/IGF-1 signaling (IIS) exhibit reduced prevalence rates of acne, diabetes and cancer. Western diet with high intake of hyperglycemic carbohydrates and insulinotropic dairy over-stimulates IIS. The reduction of IIS in Laron subjects unmasks the potential role of persistent hyperactive IIS mediated by Western diet in the development of diseases of civilization and offers a rational perspective for dietary adjustments with less insulinotropic diets like the Paleolithic diet.”

    Part of conclusion: “Future efforts should be undertaken to lower the high insulinemic index of milk (I.I. 140) and other whey-based milk products to reach values of beef (I.I. 51) or cheese (I.I. 45) [16,29]. Furthermore, combinations of hyperglycemic carbohydrates and insulinotropic dairy with potentiating effects on IIS should be restricted. ”

    What about this?

  42. OK, you’ve made some salient points, Denise, but the fact is that there is a VERY strong positive correlation between a vegan diet and lower rates of both cancer and fertility problems.

    Note, if you would, the p-factor, in the graphs on MY research page, mirrors on 3 servers -in case the Internet highway has …uh,,… a ‘traffic jam!’:
    or even:

    The p-value on the top cancer graph (relating vegan vs animal food with cancer) is SCARY! — it is 0.0000001.

    Do you remember your basic statistics, Denise? That p-value answers the question: What are the chances the dots just randomly fell into this pattern like raindrops or whatever… The chances that the pattern is mere “correlation” but not causation is 1-in-10,000,000 –yes!! One in TEN Million!!

    NOT die by chance… now… moving right along… look at the tight pattern and the ‘R’ (relatedness) values of each of the graphs, OK?

    The translation of the various R-values means that while other factors in lifestyle may affect health, diet is a VERY strong influence.

    Case closed, discussion over: The scientific evidence is OVERWHELMING that a vegan diet is a chief factor in health -and the graphs put into “picture language” what the peer-reviewed scientific papers say in plain-English.

    Mind you, the key word is “peer-review” scientific studies –not tripe and urban legend force-fed by the US Government –with such nonsense is ‘Milk Does the body Good.’ — .. LOL… NOT.

    The science is in, and the food pyramid is out.


    Gordon Wayne Watts, editor-in-chief, The Register, scientific research blog /

    BS, The Florida State University,Biological & Chemical Sciences
    double major with honours
    AS, United Electronics Institute, valedictorian, class of 1988

  43. “OK, you’ve made some salient points, Denise, but the fact is that there is a VERY strong positive correlation between a vegan diet and lower rates of both cancer and fertility problems.”

    You’re in over your head, Gordon.

    Get out while you can.

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  45. Denise, you’re an English major and not a scientist.

    You have an impressive lexicon, but other than that this is the most diluted piece of (read:) literature I have ever read.

    Most of your “claims” in no way debunk this double-decade study, and I sincerely hope you further your research.

    I appreciate your efforts, but I ask you to stop relying on such intricate sentencing structures and start to study more actual data involving many people’s correlations in regards to consuming high amounts of meat products and general sickness. I for one never had energy until I dropped ALL meat and dairy and went vegan, that is all the proof I need.. Btw, cavemen didn’t eat meat as the muti-million dollar meat packing facilities want you to believe, but vegetables, seeds, nuts, herbs and fruits.

    If this makes your primal mouth water, and/or you feel this is healthy for your body and doesn’t cause cancer or heart disease than you’ve got issues:


    Wheatgrass alone contains ALL essential amino acids.

    Here is Ty, a bodybuilder who is and has been 100% vegan:

    I, unlike you, don’t have circle-jerk debates with fellow intellectual junkies, but base my life decisions on significant self-testing, and real world results. If you can truly tell me you look and feel better after consuming a nice big cooked-to-death steak, than go for it!!!! I don’t.. I feel like I’m in a walking state of bliss and euphoria everytime I eat fruits and veggies. When I eat meat, I feel like utter shit from acidosis, and look like ass.

    Have you read the Essene Gospel Of Peace?? I suggest you do. I know a guy who met Edmond in Canada when he was running from Vatican city. It’s the real deal.

    Also, I never truly saw massive gains inside the gym until I switched to a 100% raw, plant-based organic diet. I know this evidence may seem anecdotal to you, but I’m asking you to open your eyes. Most of the paleo community are pencil-neck dweebs who have no more meat on their bones than Michael Jackson did. Or they’re bulky, like most bodybuilders are, but f*cking tired all the time and sick and toxic inside, like I was.

    My personal belief is Mark Sisson is just using the age-old marketing principle of specialization. The only good thing that man says is stay away from grains and refined sugar.

    You’re hot, btw.


    1. You missed one:

      is the link to “Mimi Kirk (World’s Sexiest Vegan) 71-year old talking about her RAW FOOD DIET”

      That video is old, and a related vid shows her at 72.

      Gordon Wayne Watts
      LAKELAND (between Tampa & Orlando), Fla.

  46. Cancer cells slurp up fructose, US study finds

    BINGO: Moreover, another variable may be more relevant than lipids when exploring the mechanisms behind breast cancer occurrence. Although Campbell emphasizes the importance of biological models and clinical research to corroborate epidemiological data, particularly univariate correlations, he does not examine the positive correlations between breast cancer and blood glucose or processed starch and sugar consumption in the China Study data,[15] even in light of research showing these associations may be highly relevant. Research spanning the previous decade has revealed a potential role of blood glucose levels in the development of breast cancer,[16] has linked hyperinsulinaemia with both early menarche and breast cancer,[17] and has shown that high insulin levels are a risk factor for breast cancer independent of estrogen.[18] Additional discussion of the relationship between blood glucose, insulin, and cancer is included under item 6.

  47. Excellent blog you have got here.. It’s hard to find high-quality writing like yours nowadays. I honestly appreciate individuals like you! Take care!!

  48. @neisi

    Why do I feel so good on a plant based diet ? Why have most of my health problems disappeared? Why does everyone I have met on a plant based diet look better, seem happier and live with so much more energy ? My food bill has decreased significantly in value and I have so much more energy.

    Wikipedia these would you please;

    “World meat consumption map”
    “World dairy consumption map”
    “World cancer map”

    Drop them on top of each other.


    1. Easy. Anecdotal evidence. And your eyes see what they want to see. I personally know vegetarians and they vary in health, two of whom I strongly think they should rethink their ideology. One is sickly, eyes sunken in, can’t think straight, etc. The other one eats meat when she starts feeling sick and then feels better. Go figure.

  49. With regards to ones health or lack there of, we should be able to find the “lowest common denominator” in the disease process and not justify our assumptions by “the greatest common denominator” By this I mean, when are we going to look at the micro-nutrient content of those good vs bad foods as well as any possible contaminants that may be from generalized practices(eg., pesticide use) and local variations in nutrients.

  50. “Lastly, I suggest that the “symphony” Campbell has heard thus far is only a partial opus. To cease listening now would be—at best—a missed opportunity for heightened health awareness, and at worst a perpetuation of the misinformation already degrading public and scientific understanding of diet and disease. I thank Dr. Campbell for both the harmonies and the dissonance his work has supplied to the field of nutrition, but implore him to continue listening. The final note has not yet sounded.”

    too pretentious of an ending, which doesn’t correspond to your lighter, witty, smart tone of the prior 30,000+ words. Stay true to yourself.

    Congrats by the way. Very important points made on refined sugars, flours, empty calories, etc. Campbell does briefly mention these in TCS, but just like you (from personal experience) I think they are more detrimental than what modern veg(*)an beliefs assess.


  51. Interesting analysis. I didn’t have time to read all of it. This certainly shows what a complicated field of study nutrition is. Your thought about the increase in refined carbohydrates being possibly more relevant than the increase in animal foods is one that I have had. However, if you do follow the recommended whole foods plant-based diet it is a moot point since you wouldn’t be eating refined carbs with added sugar. Which is probably why it was not focused on in Dr. Campbell’s findings.
    I wondered about your conclusion regarding casein protein not being the same as other animal proteins due to the study you cited with whey protein. I think the main point of Dr. Campbell’s protein research is not so much the kind of protein as much as the amount. Hence the fact that too much wheat protein will also cause cancer formation if the missing amino acid is added. When protein is limited so is cancer formation in lab animals. The AIN 93 diet fed the rats in the study you cited is 13% protein which is likely in excess of their dietary requirements. While whey protein appeared to be less carcinogenic than casein there is no evidence that it is not carcinogenic when in excess (as is soy as demonstrated in Dr. Campbell’s experiments). This is why even 24g of animal protein may tip the scales since just a plant-based diet provides the 8-10% of calories RDA for protein. Adding a concentrated source of protein like animal foods to this diet will almost certainly put people into excess.
    From these 2 points it can be seen that taking a reductionist view can get one into trouble – even Dr. Campbell. It can get you lost in a particular stand of trees and you lose sight of what’s going on in the whole forest. Perhaps he has a bias (I expect he would be the first to agree) but he came to it through years of having his original biases challenged through his work and research. You have biases too. Have yours been challenged through years of research? Or through personal experience and then you started to research? I think I am going to trust the former.

  52. I was shocked when I did find these critics of you and how much people believe you. I just found out about this book now, even it was published years ago. I guess this is because of your work to ruin a great book of a brave scientist. I was reading your homepage and you know, you are right a college degree is not everything, but at least it prooves knowledge. Everyone can tell he read a lot and but where is your proof? You know I’m a studied civil engineer and at least 50 % fail their degree in my country because its hard and they are just not capable of it. Would you let build your house by someone who just read about technical mechanics instead of someone who can proove that he managed passing a lot of hard exames? Otherwise you risk your life when your house breakes down. It’s the same thing here, people believe you for your work that might be bullshit. You are not a biologist nor do you have the same experience as the author of the book. And the way you look at statistics is how a kindergarden child would do it, seriously. So people here, what is wrong with you? You believe a socket puppeter more than a scientist? Something is clearly wrong with you. Start questioning yourself and not believe a person who is just questioning maybe wrong. Tell me why does no other scientist critisize this book? Because it was done correct. I hope you are brave enough to keep this comment and show it to your fans since they seem to like questioning eveything, they should questioning you.

  53. I, like Minger am not a medical doctor but do know a thing or two about science. (apologies about spelling and grammar btw)
    Now it’s clear that she has agenda- defending meat eating by any means necessary. Now theres nothing wrong with that. Biases are all present in science. Some labs push WFPB, some paleo. It’s natural-even in science.If you’ve spent your whole life dedicated to a movement than its hard to see it crumbling day by day.

    But also from reading her comments, some of her them aren’t actually counterarguments, but actually just comments, but the way in which she delivers her message makes out she has made a criticism when she actually hasn’t. She uses her degree in English to advantage- that’s fair enough- shes worked hard for it and uses it. But they may work well with her small flock but it won’t get passed anyone with a decent level of medical training to someone well versed in the field. Two examples-

    In her critic of Garth Davis’ book she claim

    ‘In nutrition, citing a 15-year-old review paper as evidence that low-carbing is bad would be like citing a 165-year-old map as evidence that North Dakota doesn’t exist. Sometimes the passage of time changes a thing or two!’

    This is simply incorrect. In fact there are so many cases of medical interventions, that if a metaanalysis had been performed earlier, many medical procedures would have been deemed dangerours/beneficial years before their time. (PLoS One. 2014 Jul 28;9(7):e102670.)
    Minger would do well to read the following if she hasn’t already.
    How to Read a Paper: The Basics of Evidence-Based Medicine by Trisha Greenleigh

    ;as I really think she is not seeing the bigger picture and is getting to bogged down in the data and trying to defend her team. She is all too happy to wuote
    Good science is good science- as long as its controlled for and presented clearly- regarless of when it was performed.

    Another example-In her criticism of ‘How not to Die’ by Dr Gregor she mentions the blurring of what plant based is in the Kempner Study from 1958, but saying this diet doesn’t fit in with Greger’s WFPB diet. “In other cases, Greger seems to redefine what “plant-based” means in order to collect more points for his dietary home team…
    …no caveat that the highly processed, vegetable-free diet in question is a far cry from the one Greger recommends”.

    That comment misses the point. Dr Gregor is very clear about his dietary recommendations. The study set out to answer a specific question. The point was that a high carb diet (>90% in this case), with low fat and protien (yes admittedly too low probably if we want to be 80:10:10, and probably nutrient deficient) and (this is what probably stings her the most) no meat whatsoever can and does *reverse* diabetes.
    The exact amount of sugar is unknown in the study but we should consider that in the 50’s refined sugar was a far smaller proportion of the American diet.

    These are just two examples. There are many more comments in her crtiques and reviews- which are fair comments- but don’t actually change the message being delivered by the respective authors.

    To her credit she does cite Kempner and Ornish in her talks on Youtube- but really downplays the benefits in her video what the paleo movement can learn from vegan (as though this is some popularity contest?), with her and the audience left scratching their heads.

    Secondly I think she cherry picks her criticism. Again, looking at her criticism of Garth Davis’s book, ‘Proteinaholic’. She chooses to gloss over the IGF-1 data
    Now Minger knows the IGF-1 data. – she’s extremely well read. Yet she chooses to ignore the IGF-1 story (intentionally) claiming that mechanim is still shrouded. Again an incorrect claim- the biology of IGF-1 has led several pharmaceutical companies to develop anti-IGF1 monoclonal. Yet there is no mention of IGF-1 studies where it was reconstituted in to cell cultures and led to tumour growth. A wonderful set of experiments which really nails why vegans have lower cancer risk- but casually glossed over.

    There also seems to be misuse of the paleo/low carb studies. For example I was looking over her criticism of Colin Cambells work and she cites a paleo study from 2009 where patients were put on lean meat, fish, fruits, vegetables, root vegetables, eggs and nuts.
    (Cardiovascular Diabetology July 16 2009 8:35). When I read the work, they used 13 patient and there was no change in glucose tolerance or insulin. So even though some of the numbers changed slightly- there was no clinical benefit. Note- that was even after they cut out refined fats, sugar, beer and candy! So the study is hardly one in her favour- but she picks the -right- numbers in her response (which aren’t even that impressive)

    On a side note they are both right in saying that no one study provides rock solid evidence….but what about some meta-analysis… There was the annals of internal medicine one from 2010 (animal based low carb was associated with higher all cause mortality. veg based low carb was not) and then the 2012 one from Plos One (>270,000 patients. significantly higher risk of all-cause mortality ). The question we should be asking is not, how people do well in-spite of being on a vegan diet, but how people can do well inspite of not being on one!

    These are just a handful of examples and I could go on, but there really seems to be ‘twisting’ of the data and narrative to push her point that meat is ok. That sounds familiar…I really think she needs to think about the advice from Colin Cambell and Garth Davis. From reading her work and the comments it seems that Denises weapon of choice to defend the high fat diet is what the tobacco industry’s was- doubt.

    It’s odd- excerpts from her videos on youtube actually show her commending WFPB and she rightly cites Ornish, Pritikan etc as the data is exceptional. But on her website she maintains hard nosed as ever.

    Any challenge to the orthodoxy is welcome, but it seems that if Ms Minger wants to tussle in the nutritional arena than she must be willing to hold herself to, and be open to the same academic standards and rigour she wishes to hold others to.

    Now, Minger could be forgiven for some of these things but not for supporting the cause of the Weston A. Price Foundation. Go on to the website and whats the first thing you see…meat, cheese and dairy. But there is a whole section on HOMEOPATHY. HOMEO-FKIN-POTHY. As a scientist this really annoyed me! This organisation supports raw milk (dangerous) and Science based medicine reported that this organisation has an appalling legacy and cite it as one of the worst on the internet! It’s shrouded in controversy and is part of the mainstream medical establishment. They have an agenda to uphold the status quo of diet.

    It’s a shame that she had to turn this into an us and them thing. Not very successfully I may add. The WFPB movement has taken off and has left paleo/low car/atkins in the dust. Dr Gregor has an open invite for anybody to debate with him, but none of the low carb Dr’s have taken him up on it. I wonder why….

  54. More than a decade later, I still come across a significant number of people who keep referencing the China Study as if it were valid and meaningful scientific evidence. Even when I point out your work, the kind of person who looks to the China Study in the first place tends to be those who would refuse to read your work.

    One can make some sweeping claims without basis in mentioning the China Study. But to actually understand why it’s wrong takes more careful thought. An analysis like this is awesome, if few who should read ever will. Once an ideology has been established in official institutions and mainstream thought, it’s extremely hard to dislodge. I’m not sure how to get past that obstacle of human nature.

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