Mental health articles

Several large-scale behavior genetic studies of anxiety disorders in adults have been conducted using DSMIII or DSM-III-R diagnostic criteria. Kendler, Neale, Kessler, Heath, & Eaves, using data from the same Virginia-based, adult female sample described before, conducted model-fitting analyses on liability to DSM-III generalized anxiety disorder and reported that the best fitting model included additive genetic and learned or nonshared environmental influences, and about 30% of the variance in liability was attributable to additive genetic influences. The same authors conducted univariate analyses of liability to DSM-III-R panic disorder in women from the same twin sample. Results were similar to those for generalized anxiety disorder, that is, a model including additive genetic and nonshared environmental influences provided the best fit to the data for most definitions of panic disorder, and genetic influences accounted for about 30% of the variance in liability. In the case of phobias, Kendler et al. reported that liability to any phobia (agoraphobia, social phobia, animal phobia, or situational phobia) in women drawn from the Virginia population-based sample was attributable solely to additive genetic and nonshared environmental influences, and the heritability was .32. The only phobia subtype for which shared environmental influences contributed significantly to liability was situational phobias (e.g., phobias of tunnels, bridges, and airplanes). No significant heritable influences were found for this phobia subtype. Shared environmental influences, it was estimated, accounted for 27% of the variance in liability to situational phobias, and the remaining variance was attributable solely to nonshared environmental influences. Heritabilities were moderate (and similar) for agoraphobia (h2 = .39), social phobia (h2 = .32), and animal phobias (h2 = .32). Univariate behavior genetic analyses have suggested that both depression and anxiety are moderately heritable in adults. Expressed differently, these findings suggest that nonshared environmental influences account for at least half of the variance in symptoms of anxiety and depression in adults.

Bear in mind, however, that part of the nonshared environmental portion of the variance represents measurement errors; therefore, when estimates are corrected for unreliability of measurement, heritability estimates may increase somewhat. Still, environmental influences almost always account for a significant portion (usually at least a third) of the population variance in symptoms of these disorders, even after correction for measurement error. There is little evidence, however, that shared environmental influences are an important source of variation in adults’ symptoms. Children and Adolescents.There have been several univariate twin studies of depressive symptoms in childhood. Eley and Stevenson obtained evidence for a small-tomoderate effect of shared environmental influences (accounting for about 20% of the variance) as well as additive genetic influences (accounting for about a third of the variance) in children’s selfreported depressive symptoms. Thapar and McGuffin found that the presence of shared environmental influences on depressive symptoms depended upon the age of the children. In younger children (age 8–11), variation in symptoms was attributable predominantly to shared environmental influences (c2 = .77), whereas in adolescents (ages 11–16), shared environmental influences could be dropped from the model, and additive genetic influences, it was found, accounted for the majority (70–80%) of the variance in symptoms. Eaves et al. also found modest shared environmental influences (as well as moderate genetic influences) on depressive symptoms, but only when children’s self-report was used (h2 = .15–.16; c2 = .14–.26). When parent report was used, depressive symptoms in children were highly heritable, and there was no evidence for shared environmental influences (h2 = .54–.66).

Tags: anxiety, hereditary, learned