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I recently posted about the genetic component of savings behavior. The paper I reviewed there said that one could account for about 1/3 of variation in savings behavior by appealing to genetic differences. Whatever the authors of this study found (rightly or wrongly), they did not identify the gene(s) for savings. They identified the proportion of savings behavior that is correlated with some as-yet-unknown set of genes.
This is not atypical for a paper on economic or social outcomes and genetics. The findings support the idea that “genetics” explain some proportion of behavior, but this does not mean that we know the specific genes involved.
An entirely different kind of study is one where the researcher looks at a specific gene(s), with a known biological function, and examines whether this has a social or economic influence. I’m going to highlight two papers by Justin Cook, who has undertaken exactly this kind of research on genes and economic development.
Justin’s first paper is on disease resistance and development. There is a human leukocyte antigen (HLA) system, which is determined by a set of 239 genes. The HLA system identifies foreign pathogens so that your immune system can kill them. Within populations, there is a lot diversity in this system. That is, people vary in their alleles in the HLA system. At the population level, this is good, because this means that even if I cannot identify the pathogen (and hence die a horrific death), *your* body can identify it and survive to live another day. Populations that are very uniform in the HLA system are thus more susceptible to disease, as one bad bug (or mutation of that bug) can kill them off more effectively. So a lot of heterogeneity in the HLA system in your population is good for surviving diseases, as a population.
You can measure the HLA variation at ethnic-group levels, and then roll this up into HLA variation at country-group levels based on their underlying ethnic composition. This is what Justin does, and then looks at how life expectancy or mortality are related to it. Sure enough, Justin finds that in 1960 there is a significant relationship of HLA heterozygosity (i.e. variation in HLA alleles) and life expectancy across countries. But as you go forward in time, the relationship weakens. By 1990 the relationship has half the estimated strength, and by 2010 only one-fifth. Further, by 2010 the relationship is no longer statistically significant.
There are a couple of interesting implications of this result for thinking about genetics and development. First, it shows that genetics are not fate. Yes, having low HLA variation in a country was bad for life expectancy in 1960, but with the advent of the epidemiological transition after WWII, the effect starts to fall. With antibiotics, vaccinations, public health measures, etc.., the underlying HLA variation matters less and less for life expectancy.
Second, prior to the epidemiological transition, genetics could have played a (statistically) significant role in variation in living standards. Justin shows that HLA variation (which is good) is positively related to the years since the Neolithic revolution in your underlying population, and also positively related to the number of potential domesticable animals in your underlying population. Longer exposure to agriculture and animals generated benefits in dealing with disease, presumably because the populations were exposed longer and to more pathogens. (By “underlying population” I mean the ancestry-adjusted composition of your population today – so the US HLA variation depends mainly on European exposure to diseases). Thus places that had longer histories of civilization, by building up variation in HLA, would have enjoyed higher life expectancies and (assuming that living longer is good), higher living standards. You could spin this out further to speculate that places with higher life expectancies had greater incentives to invest in human capital and achieve even more gains in living standards historically.
The second paper is on lactose tolerance and development. Simply put, if you can digest milk, then you have an additional source of nutrition that lactose-intolerant people do not have. It changes the productivity of dairy-producing animals, making them a better investment. But no other mammal, and the vast majority of humans, do not produce lactase (the enzyme to break down lactose) beyond weaning from breast milk. At some point in time a sub-population of humans acquired a mutation that allowed them to keep producing lactase beyond weaning, meaning they could continue to consume dairy and use the nutrition available.
Justin backs out the ethnic composition of countries in 1500 (you can do this by using data on migration flows and known ethnic groups). He can then look at lactose tolerance in countries in 1500 by using the existing lactose tolerance of ethnic groups (which is presumed to not have changed much in 500 years). He finds that population density in 1500 is highly related to lactose tolerance in the population. This holds up even after you throw a lot of other controls into the specifications, including continent dummies – which is important in establishing that this is not just a proxy for some broader Asia/Europe difference.
Lactose tolerance acted like a Malthusian productivity boost, raising population density in 1500. Did this have long-run consequences for living standards? Maybe. Places that were densely population in 1500 tend to be relatively rich today, even if you control for their contemporary lactose tolerance levels. So through that channel, lactose tolerance may have helped push up living standards today. The story here would be something about dense populations having greater capacity for innovation, or density indicating broader potential for productivity increases.
I think what Justin’s papers show is that a useful way of thinking about genetics and development is in the sense of budget constraints. Gene(s) change the relative price of different activities or goods, which can alter social and/or economic outcomes, without implying that they make one person or population superior. People who can drink milk without getting sick are not making better decisions than people who cannot, they simply are less constrained in their budget set. Genes, in this sense, are just like geography, which creates different relative prices for populations in different areas. This is different than saying that genes “determine” behavior (e.g. a “patience” or “savings” gene) and that this creates variation in how people respond to an identical set of constraints.