Teenager drinking


The serotonin transporter gene and binge drinking

18/8/03. By the National Institute on Alcohol Abuse and Alcoholism

Researchers have identified a genetic factor that may predispose young people to harmful drinking habits.

A team of scientists interviewed college students about their alcohol consumption and then analysed their genetic profiles, or genotypes. They found that students who shared a particular variant of the serotonin transporter gene (5HTT) consumed more alcohol per occasion, more often drank expressly to become inebriated, and were more likely to engage in binge drinking than students without the variant.

The study was published in the September issue journal Alcohol and Alcoholism.

"This research provides important new evidence that the risk of developing a maladaptive pattern of alcohol consumption is influenced by genetically determined neurobiological differences that exert their effects during young adulthood," says Ting-Kai Li, Director of the US National Institute on Alcohol Abuse and Alcoholism (NIAAA).

The researchers studied 262 male and female college students and analysed data from the largest homogenous group: 204 male and female Caucasian college students aged 17 to 23 years. To assess the frequency and patterns of alcohol consumption, the scientists asked all the students a set of questions, for example, how many times in the past two weeks they had engaged in binge drinking (five or more drinks for men and four or more drinks for women on one occasion).

The research team also analysed each student's genotype with a focus on the 5-HTT gene, which is involved in recycling the chemical serotonin after it is secreted into the synapse of a cell. The researchers determined which students had long or short versions of this so-called serotonin transporter gene.

Everyone inherits two copies of each gene, one from each parent. There are two normal variations, or polymorphisms, of the serotonin transporter gene, labelled the long and the short variants. Most people are heterozygous, that is, they have one copy of each variant, but about 30 per cent of the Caucasian population are homozygous (carry duplicate copies) of either the long or the short version. This percentage varies depending on the ethnic background of the individual.

The researchers found that the students who carried two copies of the short version of 5-HTT were more likely to report troublesome drinking patterns. NIAAA investigator Paolo DePetrillo says, "Our findings reveal a significant association of the serotonin transporter promoter polymorphism with increased alcohol consumption behaviour in the students that we studied. Taken together with other research, this finding suggests that genetically mediated differences in serotonergic response play an important role in mediating patterns of alcohol intake."

The students with two copies of the short form of the gene engaged more frequently in binge drinking, drank more often to get drunk, and consumed more alcoholic drinks per occasion than did students with the other genotypes.

Another difference the researchers observed was that students with at least one copy of the long variant of the 5-HTT gene tended to consume a smaller number of drinks at a sitting, even though they went out to drink as often as the other students.

Why should the presence of the shorter gene variant make such a difference? The authors speculate that, because individuals who are homozygous for the short version are known to be at risk for higher levels of anxiety, they may use alcohol to reduce tension. Further studies are needed to understand the influence of the serotonin transporter gene on drinking behaviour, with special attention given to replication in other ethnic groups.

Adapted from a press release by the US National Institute on Alcohol Abuse and Alcoholism.

Photo credit: Anthea Sieveking

Further reading

Herman AI et al. Serotonin transporter promoter polymorphism and differences in alcohol consumption behaviour in a college student population. Alcohol Alcohol 2003 Sep-Oct;38(5):446-9. Abstract ; Full text

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