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Chapter 3: Short genes, alcohol use, and childhood experience
Summary: This story is dramatic, but shown only in monkey research so far. Be cautious in interpretation of this single study. We see here that getting two long serotonin transporter alleles seems to have some protective value against alcohol use. We also see that getting at least one short allele does not necessarily lead to increased alcohol use. Instead, that risk goes up only if there is also a rough childhood experience.
Acknowledgement: This study was reported by a team from the National Institute on Alcoholism and Alcohol Abuse, led by Dr. Christine Barr.
Link to Chapter 4
The effects of the serotonin transporter alleles on alcohol use have been studied so far primarily in monkeys. But the one result shown here fits very well with the studies in humans reported in Chapter 1, as you'll see. The result shown here is so similar, in fact, that even though it's a monkey study, it seems worth showing now, even before further studies are reported. The implications are very important, I think you'll agree. We'll just have to remember that this is an early report and that these kinds of results need to be repeated and expanded.
Remember from Chapter 1 that having two short versions of the serotonin transporter gene is associated with a greater risk of becoming depressed, especially in individuals who had a rough childhood. But, as you will also recall, only the "blue people", the ones with two short alleles, were more likely to become depressed if they had experienced "maltreatment" as children. The "yellow people" (two longs) had about the same rate of depression, whether they had maltreatment as children or not. Now we'll see that same relationship in terms of alcohol use.
In November 2004, Dr. Barr and her colleagues reported the effects of a "rough childhood", in monkey terms, and adult alcohol consumption.Barr These grown-up monkeys were given access to extra drinks: one with alcohol, and one without. The results of their drink choice, as a percentage of their total extra drinks, are shown below.
Here's what the graph shows. First of all, they had no monkeys with two short alleles. So the comparison is between individuals with two longs, and those with a long and a short.
As long as the monkeys had a normal monkey childhood, their alcohol consumption was the same, regardless of which alleles they had inherited. But the "rough childhood" group on the right grew up very differently: they were separated from their mothers at birth, and raised without her all the way to adulthood, which is very traumatic for monkeys. For that group, getting even just one short allele was associated with a dramatic increase in drinking alcohol. (Although this group's blue bar looks shorter than the blue bar on the left, it is not statistically different, as there were not many monkeys in each group. It's the red bar on the right that's clearly different from all the rest.)
Looking at this result the other way around, one can see getting two long alleles seems to protect monkeys against liking alcohol as adults, even if they have a rough time as infants. That's exactly the same result we saw in humans, for depression as adults (shown again below): the long/long inheritance seemed to protect against depression, even when there was childhood maltreatment. By comparison, getting a short allele leaves an individual vulnerable to childhood maltreatment.
On to Chapter 4