A year ago I attended an event with other science writers at the Brookhaven National Laboratory. Since then I have been getting emails about new discoveries and developments. A few days ago I received one about how genetics affects reaction to alcohol. Specifically,
dopamine receptor deficiency leads to significant brain changes in response to drinking. Two genetic variants of mice were used to compare the brain's response to long-term alcohol drinking in two genetic variants of mice. One strain was genetically normal, and another lacked the gene for dopamine D2 receptor, the brain's "feel good" chemical, that produces feelings of pleasure and reward. In the dopamine-receptor-deficient mice (but not the genetically normal strain), long-term alcohol drinking resulted in significant biochemical changes in areas of the brain well know to be involved in alcoholism and addiction. The scientists were interested in the dopamine system research, which suggests that deficiency in dopamine D2 receptors may make people (and animals) less able to experience ordinary pleasures and therefore more vulnerable to alcoholism, drug abuse, and gluttony. The scientists were able to breed mice deficient in the D2 gene. Each of the groups were divided in half: One-half had water, while the other half had a solution of 20% ethanol to simulate heavy drinking.
The scientists observed the levels of brain receptor cannabinoid type1 (CB1) after six months in the four groups of mice. These receptors are located near dopamine receptors and are known to influence dopamine receptors and alcohol consumption and addiction. The water-drinking mice without D2 receptors had increased levels of CB1 receptors in brain regions associated with addiction, compared with water-drinking normal control animals. Thanos explained that this may indicate that D2 receptors inhibit the growth of CB1 receptor gene. However, in the mice with D2 receptors which ingested ethanol, this possible effect was negated: These mice had about half the CB1 levels compared to the D2-deficient water drinkers.
In 2005, Houchi et al. had found that CB1 knockout mice had an overexpression of D2 receptor. This increase in humans may decrease their desire for alcohol. The study was published in Neuropsychopharmacology. Thanos said: "This down-regulation of CB1 after alcohol intake in the D2-deficient animals could underlie the lower reinforcing effects of ethanol in these mice," he added. In other words, fewer CB1 receptors may eventually increase D2 receptors, which may steer humans away from desiring a lot of alcohol.
This was an example of an epigenetics sutdy. The alcohol is the environmental factor influencing existing genetics. The main researcher, Panayiotis Thanos Ph.D., will conduct future studies with female mice to see if gender changes results.