Ancestral Genetic Basis for Diet

With the domestication of mammals, another new food source became available, animal milk and milk products.  

Through the millennia, mammals were weaned from mother’s milk and then lost the ability to manufacture lactase, an enzyme that helps change lactose from milk into glucose in their digestive systems.  Without lactose, consumption of milk can lead to digestive difficulties such as nausea, cramping, bloating, diarrhea, and flatulence, so-called lactose intolerance. 

Some human populations, however, have developed lactase persistence in which lactase production continues into adulthood. Research reveals intolerance is still more common globally than lactase persistence (about 75% intolerant), and that the variation is genetic. Lactase persistence is now thought to have been caused by recent natural selection favoring lactase-persistent individuals in cultures in which dairy products are available as a food source. Based on living populations, estimates for the time of appearance of this lactase persistence mutation are within the last 10,000 to 5,000 years and has accelerated in the past 1,000 to 3,000 years, a very recent incomplete genetic modification.

In this transition to lactase persistence there is likely a spectrum of toleration that can lead to partial or periodic intolerance with attendant symptoms of indigestion. So this is one example of a genetic mutation allowing for the consumption of an “unnatural” food source taking place over a short evolutionary interval illustrating the remarkable adaptive capability of the evolved human.

Apolipoprotein E (ApoE) is a protein that is essential for the normal catabolism of triglyceride-rich lipoprotein constituents found in meat. ApoE has a number of alternative forms that can result in different traits; the three forms are called ApoE2, ApoE3 and ApoE4. The ApoE4 variant, apparently predominant in pre-modern hominids, is a known genetic risk factor for impaired lipid regulation leading to elevated cholesterol, triglycerides and poor modulation of inflammation and oxidative stress predisposing an individual to a range of abnormal conditions from vascular disease to Alzheimer’s disease.

However, this is less true of the ApoE3 (and ApoE2) variant that is dominant today (80%); the emergence of this increased frequency of the protective form of ApoE can be traced to within the past 200,000 years, possibly much more recently than that. Is this a result of the increase in the addition of meat to the diet that adds exogenous cholesterol, triglycerides, and inflammatory  to the diet? Likely.  If so, this is another example of a genetic adaptation that has taken place over a relatively short time interval. 

Another genetic transition has to do with cooking.  Apparently the ease with which foods are processed in cooking has led to a genetic transition in which the size of the jaw is decreasing, resulting in a crowding of the teeth. This may be a factor in the vestigial wisdom teeth.

In Chapter 2, we mentioned the genetic mutation of more than 50 MYA that led to the loss of the ability to produce the essential nutrient thiamine, vitamin B1.  In 1897, Christiaan Eijkman observed that when chickens were fed the native diet of white rice, they developed the symptoms of thiamine deficiency, or beriberi. When he fed the chickens unprocessed brown rice, they did not develop the disease. The reason is that the outer rice bran contains thiamine.  Processing in this case brown to white rice removes this vital component.  This is an example based on genetic reasons how “processing” plants can lead to an unfavorable outcome and why whole-food plants is to be preferred.  

The genetic mutations that occurred many millions of years ago that led to our inability to make thiamine as well as riboflavin, niacin, vitamin A, and vitamin C appears to be unaffected by the addition of animal products to the diet, indicating either an  irreversible mutation or that the inclusion of animal products was to a predominantly plant-based diet even in the hunter-gatherer time interval.

Why didn’t hominids over the past 250,000 years develop protective mechanisms for diseases arising from the inclusion of meat in their diet?  Two reasons are apparent.  First, the amount of meat in the diet was small and, second, such diseases only become significant if the hominid lives at least into what we consider early middle age, certainly past the estimated life expectancy of that era of 25 years .  Natural selection is based on reproductive age.

In short, there is no genetic evidence that we have evolved to favor the consumption of animal products .  We can tolerate it but at the expense of longevity.