In the earlier discussion when we examined the myth that dairy causes cancer, we briefly ran into this myth: that animal protein, in general, causes cancer. This myth was probably initially stoked by Campbell’s The China Study.
Recently, however, the myth received a major shot in the arm when an article in Cell Metabolism (Levine, et al., 2014) reported a positive correlation between high animal protein intake and cancer risk in those between the ages of 50 and 65 (though high animal protein intake was shown to correlate inversely in those 65 and over, meaning it could be protective in that group). So what is going on here? What is the truth?
To begin with, let’s look at Campbell’s China Study claims. He boldly claims that high animal protein intake positively correlates to increased cancer rates. He bases this claim on two things.
First, he claims that a series of laboratory tests that he performed on rats demonstrated that high protein intake “switched on” cancer in the rats. Secondly, he claims that his massive epidemiological study shows a positive correlation between populations that eat high protein diets and cancer, whereas those who eat low protein diets have low rates of cancer. Specifically, he singles out animal protein as being problematic.
Unfortunately for Campbell, his own rat studies largely disprove his own theory. As Chris Masterjohn points out, in Campbell’s own studies in the 1970s, his low-protein (5 percent) rats failed to grow and developed fatty livers.
Campbell actually reported in those studies that the low-protein rats developed a massively increased susceptibility to aflatoxin, the carcinogen used to induce cancer. Not only were they more susceptible to aflatoxin, but the toxicity of some pesticides increased by 2100 fold in the low-protein rats! The low-protein rats were suffering from protein deficiency and malnourishment.
The high-protein rats, on the other hand, being fed 20 percent casein, showed a great deal more resilience when compared to the low-protein rats. Campbell exposed the high-protein rats to 5 ppm aflatoxin, but had to use only half the dose with the lowprotein rats, because the 5 ppm was lethal to the low-protein group.
Campbell’s later studies showed that rats exposed to aflatoxin developed pre-cancerous lesions. There were four groups of rats. Two groups were fed low protein (5 percent) for the first part of the experiment.
Two groups were fed high protein (20 percent) for the first part of the experiment. Then, in the second half of the experiment, one group from the low-protein group was switched to a high-protein diet and one group from the high-protein group was switched to a low-protein diet. In other words, there were lowlow, low-high, high-low, and high-high groups.
What is interesting is that the group that fared the worst by far was the low-high group. The low-low group and the high-high groups were fairly similar. And the high-low group fared the best by far.
Although it is possible to interpret the data as suggesting that the ideal diet is one that is high in protein in childhood and low in protein in adulthood, it turns out that would be misleading. The reason being that, as we saw in Campbell’s earlier studies, extremely low protein (5 percent qualifies as a significant protein deficiency) produces a whole bunch of undesirable effects.
If Campbell’s study has any applicability in humans (and that is yet to be seen), it seems extremely unlikely that eating a protein-deficient diet, even if it may offer protection against some types of cancer, is a good idea.
And the obvious question remains: if protein intake plays a role in cancer protection, might a moderate protein diet offer the same benefits without producing a protein deficiency? Also, since no one actually eats isolated casein as their sole protein source, might not the effects of a high-casein diet be due to the unnatural and unbalanced exclusive nature of the diet? And might a natural diet containing the balance of amino acids and complementary nutrients found in normal foods offer protection against cancer that a casein diet doesn’t?
Furthermore, Campbell makes a point to tell us that a high-casein diet failed to offer protection against aflatoxin, while vegetable proteins tested (namely, gluten) seemed to prevent pre-cancerous lesion formation.
But in his own report, he writes that “lysine supplementation of wheat gluten during the postinitiation period enhanced the gammaglutamyltransferase-positive response to a level comparable with that of the highquality protein.”
In other words, adding lysine as found in beans, for example (remember the vegetarian adage to combine beans and rice to get a “complete protein”), produced the same results. By Campbell’s own admission, by eating a diet of any sort, so long as the diet supplies sufficient complete protein, the outcomes can be expected to be the same. That is to say that beans and rice will produce the same “carcinogenic” effects as a hamburger.
Campbell’s second argument is that the epidemiological study data for The China Study showed a strong positive correlation between animal protein intake and diseases of all kinds, including cancers of every sort.
But unfortunately for Campbell, the data has now been analyzed by others to show that no such correlation exists. In fact, contrary to Campbell’s claim, the data shows a correlation between vegetable protein intake and various cancers!
Campbell wasn’t strictly fudging the data. Instead, he was using blood cholesterol levels as a proxy for animal protein consumption. And because blood cholesterol levels correlate positively to various diseases, he jumped to the (incorrect) conclusion that animal protein intake was responsible. But it turns out that he was wrong.
Blood cholesterol levels can be influenced by a great many factors, and animal protein intake isn’t a strong factor. And, in any case, for all we know, high blood cholesterol levels are a consequence of various diseases, or there may be absolutely no connection at all.
Finally, a study published more recently in Cell Metabolism gave rise to a bunch of sensationalistic headlines such as: “Diets high in meat, eggs and dairy could be as harmful to health as smoking.” The study looked at data for over 6,000 people over age 50, and attempted to find the relationship between protein intake and disease.
The study began with a hypothesis: researchers found that among people with a particular condition known as growth hormone receptor deficiency, and among those who practice caloric restriction (without malnutrition), there were no cancer mortalities or cases of diabetes.
So they speculated that this may be due to reductions in growth factors or the effects of growth factors. They wanted to see if protein restriction might produce the same sorts of effects.
Despite the sensationalistic way in which the study has been handled by media, the authors of the study are reasonably even-handed. The paper even states that “protein restriction or restriction of particular amino acids, such as methionine and tryptophan, may explain part of the effects of calorie restriction and GHRD mutations on longevity and disease risk.” In other words, the effects of protein restriction may be obtainable simply by reducing (or offsetting) particular amino acids.
What is of note is that several studies have now shown that restriction of methionine alone can produce many of the same benefits of caloric restriction in terms of longevity and protection from disease.
But perhaps even more importantly, a 2011 study shows that (at least in rats) simply supplementing a diet with the amino acid glycine offers all the same benefits, even without having to restrict methionine (Brind, et al., 2011).
Methionine is found in large amounts in muscle meats in particular, but approximately 50 percent of the protein in an animal is collagen (gelatin), which is very high in glycine. The implication here is that eating the whole animal or simply supplementing with gelatin may offer major health benefits and protect against cancer.
Finally, the study only looked at adults age 50 and older. The results suggested that eating large amounts of methionine-rich protein correlates to increased cancer risk for those between 50 and 65, but it correlates to decreased cancer risk in those over 65.
So a large segment of the population studied may potentially benefit from eating lots of methionine-rich protein, and we have no idea what correlations may exist in younger populations.
In conclusion, the idea that animal protein causes cancer is extremely weak. It seems likely in many cases that moderate or high protein may be protective against cancer. And in any cases where it is not, protective effects may be had by either reducing methionine-rich protein sources or supplementing with glycine-rich proteins.