Effects of ethanol administration and induction of anxiety-related affective states on the acoustic startle reflex in sons of alcohol-dependent fathers.

BACKGROUND

The high rate of comorbidity between alcoholism and anxiety disorders suggests some causal link. This study used the startle reflex to investigate whether increased reactivity to stimuli inducing fear or related affective states might be one mechanism by which a family genetic risk promotes the development of alcohol use disorders.

METHODS

Thirty-one sons of alcoholics (PH+) were recruited from the participants of a longitudinal epidemiologic survey representative of the Munich area population between 18 and 25 years. Thirty male low-risk participants without parental alcoholism (PH-) were matched for age and history of psychiatric disorders. The baseline acoustic startle reflex was elicited before and after subjects drank 0.6 g/kg ethanol or placebo in a randomized, double-blind, placebo-controlled crossover design. Thereafter, the startle response was investigated while the subjects' affective state was manipulated by announcement of aversive electric finger stimuli to induce fear potentiation and by presentation of photographic slides previously rated to be pleasant, unpleasant, or neutral in their emotional valence.

RESULTS

Plain startle response was lower in PH+ than PH- participants and was equally dampened by alcohol in PH+ and PH- subjects. Threat of finger shocks increased the startle response to the same extent in both groups. This fear potentiation effect was significantly attenuated by alcohol given on the second experimental day but not if alcohol was administered first and placebo on the second day. Pleasant and unpleasant slides decreased and increased startle response, respectively, and this effect was influenced by neither risk group nor alcohol.

CONCLUSIONS

The acoustic startle reflex seems to be reduced in sons of alcoholics. The nonsignificant results during startle modification do not support the concept of increased reactivity to anxiety-related environmental stimuli as a mechanism promoting alcohol use disorders in subjects at increased family genetic risk for alcoholism.