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Gene Linked to Anxiety Disorders

A Common Gene Variation May Make Some More Prone to Anxiety


Updated January 26, 2009

There is scientific evidence to support a genetic link in the development of anxiety disorders, including panic disorder. But, identifying the specific genes that contribute to the risk of developing an anxiety-related illness, continues to be challenging. In a study published in the August 2008 issue of Behavioral Neuroscience, researchers looked at common variations of the gene COMT (catechol-O-methyltransferase) as a possible suspect in the occurrence of anxiety disorders.

The gene COMT is responsible for triggering an enzyme that breaks down the neurotransmitter, dopamine, thus weakening its signal. COMT has two variations, Val158 and Met158. Roughly one-half of the population carries one copy of each COMT variation. The other half carries either two copies of Val158 or two copies of Met158.

Who Was Studied?

The researchers recruited 96 Caucasian female participants of German origin. The participants were recruited from the Giessen Gene Brain Behavior Project’s (GGBBP) genetic data bank of 800 healthy participants. Participants of this study were psychology students, previously recruited for the GGBBP. The participants ranged in age from 17 to 38 years, with a mean age of about 22 years.

The Procedure

To measure the participant’s startle response, electrodes were attached to their eye muscles. If they were emotionally aroused, the muscles would contract, and the electrodes would cause the eye to blink. While attached with these electrodes, the participants were seated in front of a computer and were shown random pictures of emotionally pleasant, neutral and unpleasant pictures. The pleasant pictures consisted of, for example, family photos, animals or a baby. Neutral pictures included a hair dryer or a power outlet. The unpleasant pictures consisted of portrayals of fear, a threat or violence.

The Results

This study found that people with two copies of COMT variation Met158 had significantly greater startle reflex when shown unpleasant pictures than did those with either two copies of Val158 or one copy of each gene type. The researchers theorize that the Met158 variation causes an increase in dopamine in certain areas of the brain, essentially resulting in poor emotional regulation. This process may also result in what the researchers term, “inflexible attentional focus on aversive stimuli.” In other words, those with two copies of MET158 may find it difficult to turn away from something that’s emotionally arousing, be it good or bad.

Implications of the Study

The researchers acknowledge that a single gene variation may only explain a small portion of anxious behavior. According to one of the study’s authors, Christian Montag, the COMT is likely “only one of many factors influencing such a complex trait as anxiety. Still, to identify the first candidates for genes associated with an anxiety-prone personality is a step in the right direction.”

It seems that identifying which specific genes play a role in the development of anxiety disorders is complex and at this time, not very clear. But studies such as this one will, undoubtedly, incite future scientific inquiry that may give us a better picture of the role genes play in the genetic risk for anxiety disorders. This greater understanding will allow for the development of improved treatment strategies.


Montag, C., Buckholtz, J.W., Hartmann, P., Merz, M., Burk, C., Hennig, J. and Reuter, M. (2008). “COMT Genetic Variation Affects Fear Processing: Psycholphysiological Evidence.” Behavioral Neuroscience, Vol 122, No 4, 901-909.

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