I brought up this question a little bit in class yesterday, and wanted to do a little bit more research on it. While reading the articles for class, it was not clear to me exactly what people who are genetically predisposed to certain addictions are at a higher risk for. Are they more vulnerable to addictions of any type, due to dysfunction of the reward system, or to very specific drugs such as alcohol or nicotine? Originally, I was thinking that if the predisposition is to addictions in general, it may be possible to (after painful withdrawal stages of course), lower the rate of relapse by encouraging or allowing the person to develop a new, far less dangerous addiction, such as an addiction to … well, now I can’t think of one that’s not going to negatively impact one’s life- how about reading??! In short, can you replace one addiction with another? There would definitely be issues with this considering the fact that alcohol addiction likely makes long-lasting if not permanent changes to someone’s neurology, but these may be changes that ANY addiction would create (?).

I found an article that explored some of the different theories on neural markers for of genetic vulnerability to drug addiction. I was particularly interested in the hypothesis of serotonergic dysfunction. A study was done with primates that correlated early separation from mothers to lower serotonin turnover. Primates with this dysfunction of the serotonin system showed depressed mood, anxiety, aggression, and increased alcohol consumption. The depressed mood state mirrors the negative affect experienced by many drug addicts, and though greatly debated in recent years, serotonin has long been linked to depressive symptoms. Additionally, malfunctioning serotonin systems impairs alcohol-induced GABA-ergic sedation, meaning that the low serotonin levels resulted in decreased sedative effects of alcohol, consequently increasing the tolerance levels. The article really emphasizes the role of stress in causing serotonin dysfunction, citing several studies that subjected infant or young animals to stress, which then correlated with decreased serotonin levels. So, it does seem that the gene would certainly be no more than a predisposition- if required levels of stress are never encountered, then addiction may never develop. In regards to my original question, it seems that some precursors to addiction interact with other neural mechanisms particular to certain addictions. In this case, the serotonin system interacts with the inhibitory (GABA) effects that are so typical of alcohol, but for other drugs there may be different interactions. Also, I don’t really think there is only one system that is serving to predispose people to addictions- I think there are probably several of them, and each one may interact with certain drugs more than others. Possibly, a combination of a predisposition on a particular neural/neurotransmitter system and an encounter (or several) with a drug that interacts with that particular system, builds the foundation for addiction. But this still raises the question about addiction to things that are not ingested- though an addiction to shopping, for example, still has a chemical effects on our brain, wouldn’t that work differently than a drug that we directly ingest?

The article is called Neural Markers of Genetic Vulnerability to Drug Addiction (2009)
Authors: Daniel J. Mu¨ ller, Olga Likhodi, and Andreas Heinz