And if you can\u2019t wait till then, head on over to Gene Expression<\/a>, where Razib has covered it and made pretty much all the points I was going to make, although more solidly and in much more detail! Damn you gotta move fast in the internet age! In my defence, I\u2019ve been like, buying a new car and stuff. Priorities, priorities\u2026<\/p>\n But first I want to tell you about something that\u2019s critically important to understanding evolutionary psychology, and that\u2019s the tortuous link between genes and behaviour.<\/p>\n Most people are familiar with the fundamentals of genetics. You have a gene, and that generates a trait. The classic example of this is the pea experiment by Gregor Johann Mendel. The gene for height occurs in two versions, and the pea plant will either be short or tall depending on which version it gets.<\/p>\n You won\u2019t be surprised to hear that it\u2019s rarely as simple as this (in fact, the father of statistics, RA Fisher, accused Mendel, the father of genetics, of fudging his data \u2013 because they were too clean!).<\/p>\n One complicating factor is that gene expression is responds to your environment. Take a Himalyan bunny and raise it in a cool environment, and it will have black ears, nose and feet. Raise its identical twin in a warm environment, and it will be all white. Same genotype, different phenotype. OK that\u2019s a simple example, but there are plenty<\/a> more<\/a>.<\/p>\n However, these environment effects just scratch the surface of the true complexity, and I\u2019m going to take you just a short way on this extraordinary journey. If you want to go further, take a look at the fabulous article<\/a> in the New Scientist, written by Ed Yong (of Not Exactly Rocket Science<\/a>). But be prepared to have everything you thought you know about genes and psychology overturned!<\/p>\n Ed\u2019s article deals with a gene which is a codes for an enzyme: mono-amine oxidase (MAO). When it works, MAO breaks down a certain neurotransmitters, like serotonin, dopamine and noradrenaline. When it doesn\u2019t, these neurotransmitters build up. That\u2019s it.<\/p>\n Like all genes, it doesn\u2019t have any grand designs, or plans. But variants of MAO do affect personality.<\/p>\n For example, one common, low activity version (MAOL), was found to be linked to aggression and gang membership in some boys. Yet the same gene was also linked to depression in pregnant women \u2013 a very different psychological \u2018effect\u2019. Another study found that MAOL was only linked to antisocial behaviour in boys who had an abusive childhood. The high activity version, MAOH, was linked to fraud, but only in people who associated with other delinquents.<\/p>\n In other words, this gene did not cause aggression. The effect it had on behaviour depended on the environment.<\/p>\n So the environment affects the link between genes and personality. But in fact it\u2019s even more complicated than that.<\/p>\n Take that study on pregnant women, which found they were more likely to become depressed if they had the MAOL gene. Well, that\u2019s not the whole story. It turns out that they were only more likely to become depressered if they were also carriers of another gene (COMT).<\/p>\n \u00a0It\u2019s not, then, just the external environment that messes around with the psychological trait produced by a particular gene. The genetic environment also effects an individual gene.<\/p>\n So the effect of a gene will vary depending on what other genes it has pitched up with in the particular individual\u2019s genome. The trait a gene is linked to will change depending on what other genes you have.<\/p>\n What all this means is that it\u2019s fearsomely difficult to link genes to personality. So difficult, in fact, that no-one\u2019s done it yet. Neurocritic reviews the lates<\/a>t in a series of failures in the attempt to find a link.<\/p>\n It should be said that it\u2019s not just psychology that has this problem. Over the summer I went to a lecture where the the leading lights in the genetic study of adult-onset (type 2) diabetes summed up the state of play. Their findings: well, they haven\u2019t really found anything yet.<\/p>\n The problem is that diabetes is a very complicated disease, with a huge number of genes involved, all of which interact in complicated ways with each other and with the wider environment. There is no \u2018gene for adult-onset diabetes\u2019. What there are are genes that, in the presence of certain other genes, and in the right environmental context, seem to increase your risk for type-2 diabetes. <\/p>\n So what does this mean for all those twin studies that regularly show a genetic link to religion?<\/p>\n Well, you have to remember that they are looking at closely-related individuals. These individuals share a lot of genes. So, what these studies show is that, in a particular cultural setting (say, Minnesota), a particular combination of genes can affect your religious tendencies.<\/p>\n Take any one of their individual genes, and put it in a different genetic or cultural environment, and it could have a different effect. <\/p>\n And the cultural environment is particularly important for religion, because religion is a culture and not not a personality trait. In fact, the types of personalities attracted to religion are different<\/a> even in the USA and Europe \u2013 which are about as similar as any two cultures you could find!<\/p>\n So if you can\u2019t even link individual genes to personalities, how can you possibly link them to religion?<\/p>\n OK, in conclusion. I\u2019m not saying that there is no link between genetics and religion. Clearly there is.<\/p>\n But what I am saying is that there is no single gene (or genes) that codes for religion: there are too many intervening steps (other genes, environmental effects on gene expression, and cultural differences in what it means to be religious) to make that simplistic link.<\/p>\n It seems like a trivial distinction, but it\u2019s critically important to understanding the relationship between evolution and religion. Because evolution acts on individual genes, and there is no such thing as a gene for religion.<\/p>\n A new paper by Robert Rowthorn, an economics professor at Cambridge University, has been in the news recently. I\u2019m a bit behind the curve on this one, and in fact today\u2019s post is more by way of a preamble. I\u2019ll give you the low-down on the paper itself in the next post (probably on Thursday). […]<\/p>\n","protected":false},"author":2091,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[1],"tags":[],"class_list":["post-214","post","type-post","status-publish","format-standard","hentry","category-uncategorized"],"yoast_head":"\n
\n![\"Creative](\"https:\/\/i.creativecommons.org\/l\/by-sa\/2.0\/uk\/88x31.png\")
<\/a><\/span> This article by Tom Rees<\/b> was first published on Epiphenom<\/a>. It is licensed under Creative Commons<\/a>.<\/p>\n<\/body><\/html>\n","protected":false},"excerpt":{"rendered":"