Some Problems with the Casein Cancer Claim
by Dr. Melissa Davis |
Feb 19, 2019
Casein causes cancer––it’s a common fear so there must be something behind it, right?
Well yes and no. There is a reason this idea came into being, but there was also something that inspired fears of chupacabra––doesn’t make either misunderstanding true.
Let’s talk about the poorly done and misinterpreted studies that pushed this correlation and pick apart how and why the conclusions drawn were wrong. Once we have the facts clear we can make everyone comfortable with their RP nighttime casein shake.
Animal research and the false casein cancer correlation:
The rodent research done that supposedly supports the casein cancer connection was in a nutshell this: rats were given an incredibly (toxically) high dose of the tumor causing agent, aflatoxin. One group was fed 5% casein along with grains and fats and the other group 20% casein protein along with grains and fats. The 20% casein group’s tumors grew much faster. Seems terrible, right? We don’t want to feed tumors. Before drawing any strong conclusion however, we need to look at what happened to the other, low protein group. Well, they died prematurely. It turns out that the extremely high exposure to aflatoxin coupled with low protein meant that the liver could not keep up its detox duties and rather than causing tumor growth, aflatoxin just killed the rats. The same results were observed in earlier studies that ignited Campbell’s interest in casein and cancer correlations––the low protein group died at a much higher frequency than the high protein group. It is difficult to grow large tumors when you are dead.
A decade or so later the casein and aflatoxin experiment was repeated in monkeys, only this time using a less toxic dose of aflatoxin. This dose would cause tumor growth, but was not likely to kill the animals via toxicity. This study designed allowed a better comparison of tumor growth levels because both groups of animals would survive the duration of the experiments. Casein percentages were the same as Campbell’s rat groups: 5% or 20%. In this study the low protein-fed monkeys grew tumors while the high protein group remained tumor free. This highlights the importance of good scientific study design. The rat studies overdosed the tumor-causing agent so that all animals would develop tumors and tissue damage. In that case, in the absence of enough protein to grow tumors or regenerate damaged tissue, sure, tumors were smaller, but animals were also dying. The animals with more protein were still alive, but their tumors also grew because amino acids support cell growth and there was enough tumor-causing agent around to ensure that both healthy and cancerous cells multiplied––meaning they both stayed alive and grew larger tumors. Under more realistic toxin exposure doses, high protein was cancer preventative and as a bonus these animals also stayed alive.
Interestingly, Campbell did his rodent study additionally with wheat protein supplemented with lysine (to create a complete amino acid profile) and saw the same instance of larger tumors in the higher protein group and more death in the lower protein group. He does not site or include this research, but it does support the idea that complete protein supports cell growth and high doses of aflatoxin kill––the more correct conclusions to draw from these studies.
Human Research and the false dangers of animal protein:
There are a few issues with the giant China study that forms the backbone of Campbell’s more general claims regarding animal protein and health. The first and likely most important problem is that although his conclusion is with regard to animal protein and cancer, across sixty-five counties and nearly 7,000 human subjects, a direct correlation between these two was not actually found. The only significant correlation seen between an animal product and cancer was between fish consumption and a few specific types of cancer, but as we know correlation does not equal causation. There are other much more likely variables that account for the cancer aside from fish consumption. Areas where more fish was consumed tended to be coastal and industrialized, and the actual cancer-causing agent might be toxin exposure via industry for example.
Further, there were nearly three times as many positive correlations between plant proteins and cancer observed in these data. This can likely also be taken with a grain of salt since an extensive assessment of other relevant variables was not performed. These plant protein correlations were not highlighted by the author. Correlations seem to have been cherry picked and data assessment seems to have been adjusted to bias the results. Since the animal protein-cancer association did not play out, it appears that Campbell looked for another way to assess. What he actually correlated with cancer were biomarkers he claimed were associated with the consumption of animal protein. The problem with this is that those biomarkers and their association to particular foods will vary with general food consumption habits across regions, vary between the sexes and even within the sexes at different ages and hormone levels. In short, it is faulty to assume food consumption based on biomarkers and makes no sense to do so when actual food consumption was also assessed and available.
To be clear, food consumption was assessed, but animal protein consumption and cancer were not reliably associated in any way. So the authors looked at blood biomarkers that were correlated to cancer and then claimed these biomarkers were evidence of animal product consumption and that animal consumption was therefor correlated to cancer. This is like finding that people who eat raspberries are just as healthy as people who eat peaches, but then finding that those with red stains on their mouths are more likely to get colds and concluding that raspberries cause colds.
Animal fat does tend to be the most saturated and therefor one of the least healthy of your fat options. Fats from plants in contrast are almost always mainly monounsaturated (the healthiest fat option available). Thus fattier meats should be eaten in moderation and there is nothing wrong with avoiding them entirely. Animal and dairy protein however are among the highest quality and best-absorbed protein sources, so barring a moral opposition to meat consumption, avoiding these is throwing the baby out with the bath water. The moral argument for avoiding animal products is another one entirely and is not without significant merit. If you are morally opposed to the consumption of animal products there are absolutely alternatives to animal protein and a careful diet with some supplementation can give you all the same benefits as any omnivore diet these days. It may be tempting to want the health repercussions of an omnivore diet to align with the morals of a vegan diet––in other words to wish that both morality and health supported avoiding meat, but this is just not the case. Likewise many meat eaters may wish that they could justify their choice as superior for health and performance, but this is not the case either. We each must make the choice to eat healthfully without violating our own morals. The moral question is individual, but science can guide nutrition based health decisions. Animal protein does not cause cancer, but that does not mean you have to eat it.
For a much more in depth (9000 word!) blog eloquently and playfully picking apart the data from the China studies see: https://deniseminger.com/2010/07/07/the-china-study-fact-or-fallac/
Campbell, TC. et al. The China Study. United States. BenBella Books. 1995
Junshi C., et al. Life-style and Mortality in China: A Study of the Characteristics of 65 Chinese Counties. Oxford: Oxford University Press, 1990.
Madhavan, T.V. and C. Gopalan. “The effect of dietary protein on carcinogenesis of aflatoxin.” Arch Pathol. 1968 Feb;85(2):133-7.
Masterjohn, Chris. “The Curious Case of Campbell’s Rats—Does Protein Deficiency Prevent Cancer?” September 22, 2010.
Mathur, M. and N.C. Nayak. “Effect of low protein diet on low dose chronic aflatoxin B1 induced hepatic injury in rhesus monkeys.” Toxin Reviews. 1989;8(1-2):265-273.
Minger, Denise. “A Closer Look at the China Study: Fish and Disease.” June 9, 2010.
Schulsinger, D.A., et al. 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.