Arrested adaptation and "diseases of civilization"

While I was browsing papers for a research project, I happened to re-open the paper, “Stone Agers in the fast lane,” written by S. Boyd Eaton, Melvin Konner, and Marjorie Shostak in 1988. This paper reviewed the idea that many chronic disorders like diabetes and cardiovascular disease are actually “diseases of civilization” – brought on by a mismatch between the human genetic heritage and the current cultural milieu.

I’m citing this work as part of my continuing observations on biologists who predicted that human evolution must have stopped sometime in the Pleistocene. Eaton e-mailed me very soon after our acceleration paper was published, and it is only fair to say that the 2009 views of these authors may be very different from their 1988 publication. With that note, here’s a quick review:

The current genetic variation in any species is a product of evolutionary forces that affected that species’ ancestors in the past – that’s a basic precept of evolutionary theory. So it’s hardly more than a syllogism that if the human environment has undergone recent rapid changes, then our genes may do little to protect us from undesirable biological side effects of our new environment.

But Eaton and colleagues, like many human biologists, went rather further than this observation. They made a point of emphasizing that the pace of human adaptation has been incredibly slow. The hypothesis of very slow human evolution had an desired corollary: the “diseases of civilization” are not merely bad side effects of recent dietary Westernization, but may ultimately be traced to the transition to agriculture – an event that occurred 10,000 years ago in some societies. Let’s consider how they emphasized this idea that human evolution had been glacially slow:

The gene pool from which modern humans derive their individual genotypes was formed during an evolutionary experience lasting over a billion years. The almost inconceivably protracted pace of genetic evolution is indicated by paleontologic findings that reveal that an average species of late cenozoic [sic] mammals persisted for more than a million years, by biomolecular evidence indicating that humans and chimpanzees now differ genetically by just 1.6 percent even though the hominid-pongid divergence occurred seven millino years ago, and by dentochronologic data showing that current Europeans are genetically more like their Cro-Magnon ancestors than they are like 20th-century Africans or Asians. Accordingly, it appears that the gene pool has changed little since anatomically modern humans, Homo sapiens sapiens, became widespread about 35,000 years ago and that, from a genetic standpoint, current humans are still late Paleolithic preagricultural hunter-gatherers (Eaton et al. 1988:740).

Not only was the pace of evolution slow when it was happening, but we may have reason to think that recently our gene pool hadn’t been changing at all:

The Late Paleolithic era, from 35,000 to 20,000 B.P., may be considered the last time period during which the collective human gene pool interacted with bioenvironmental circumstances typical of those for which it had been originally selected (Eaton et al. 1988:740).

The word “originally” in this passage may admit of later changes in selection and thus in some genes. But the paper does not examine known cases of recent change, even on those genes where some kind of recent dietary adaptation was well-known in 1988 – such as lactase persistence or ALDH2.

Reading the paper from my current vantage point, where do I think it went wrong? The basic point in the paper is undoubtedly correct – many of today’s chronic diseases reflect the reaction of human biology to novel environments for which our genes are not well adapted. But we don’t need to exaggerate the slowness of human evolution to arrive at that conclusion. Recent rapid evolution of humans does not mean that humans are perfectly adapted to the present. Far from it – if human populations have undergone rapid genetic changes into the past thousand years, it is a strong sign that fitness has not yet maximized in the post-agricultural environment.

Besides that, dietary influences on health may implicate the rapid cultural and ecological changes of the past 200 years. Westernization of diet is a characteristic of post-industrial economies, not early agriculturalists. Given the reduction in variance of mortality in the last 100 years as well as the short time, it is pretty likely that the genes of human populations have changed little in response to dietary Westernization.

I think that the rapidity of recent adaptive evolution does imply a different perspective on the “diseases of civilization.” For one thing, some people may be resistant to these diseases because they have inherited new protective alleles. If humans had hardly evolved in the post-agricultural environment, we would expect all populations to be equally susceptible to type 2 diabetes, cardiovascular disease, and cancer. Instead, we find that different populations have different characteristic rates of these diseases after adoption of a Western diet.

Another insight is that some undesirable phenotypes may themselves be the consequences (or side effects) of recently selected alleles. Overdominant alleles like sickle cell naturally stand out in this regard. But the flushing reaction to alcohol, common in Asians with the selected ALDH2 allele, is a less fatal example.


Eaton SB, Konner M, Shostak M. 1988. Stone Agers in the fast lane: chronic degenerative diseases in evolutionary perspective. Am J Med 84:739-749.