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Depression Hereditary or Environmental

Rende, Plomin, Reiss, & Hetherington found shared environmental influences for extreme depression scores in adolescents (c2 = .44) and no significant genetic influence on extreme scores. In contrast, these authors found genetic influences, but not shared environmental inf luences, for individual differences in the normal range of depressive symptoms (h2 = .34). With regard to anxiety symptoms, Thapar and McGuffin  reported that variation in parent ratings of children’s anxiety symptoms (using the Revised Children’s Manifest Anxiety Scale) could be accounted for by additive genetic and nonshared environmental influences, and that the heritability was .59. In contrast, when child report was used, additive genetic influences could be dropped from the model, and shared environmental influences accounted for 55% of the variance. Topolski et al. reported that shared environmental influences, but not additive genetic influences, substantially influenced liability to DSM-III-R separation anxiety disorder (SAD) in children ages 8–16 using children’s self-report (c2 = .40). For overanxious disorder (OAD, a DSM-III-R diagnosis that corresponds to DSM-IV GAD), on the other hand, they found that shared environmental influences could be dropped from the model without a significant reduction in fit, whereas additive genetic influences, it was estimated, contributed moderately to the variance in liability (h2 = .37).

The finding of shared environmental influences on children’s anxiety symptoms is not limited to self-report data, however. Slutske et al. reported that genetic and shared environmental influences each accounted for roughly half of the variance (h2 = .52; c2 = .38) in lifetime DSM-IV SAD symptoms in adolescent girls using mother report. Similarly, Feigon et al. found moderate genetic and shared environmental influences on parent-rated DSM-III-R SAD symptoms among nonreferred Australian twin children ages 4–18 (h2 = .46; c2 = .22). The same authors  also found moderate shared environmental, as well as genetic, influences on DSM-IIIR avoidant disorder symptoms (h2 = .41; c2 = .52) and somatic complaints (h2 = .45; c2 = .37) in children. Eley and Stevenson found that shared environmental influences accounted for about a third of the variance in children’s anxiety symptoms using several self-report scales, and about 10% of the variance was due to genetic influences. Feigon and Waldman  obtained similar estimates of genetic and environmental influences on mother reports of SAD symptoms (h2 = .58; c2 = .27) and GAD symptoms (h2 = .36; c2 = .35) but did not find any shared environmental influences on social phobia symptoms (h2 = .67) in twins aged 5–18 recruited from the Georgia Twin Registry. The authors also found significant etiological heterogeneity due to sex in the case of SAD and evidence for shared environmental influences on girls’ but not boys’ symptoms. Genetic influences on SAD symptoms were greater in boys than girls (h2 = .83 and .49, respectively).

In contrast to other findings that support a substantial shared environmental contribution to children’s anxiety symptoms, Eaves et al. did not find evidence for shared environmental influences on symptoms of either DSM-III-R SAD or OAD in children ages 8–16. In their sample, additive genetic influences, it was estimated, accounted for about 75% of the variance in SAD symptoms for girls ages 8–16 when parent report was used, but there was no substantial familial correlation among boys. When child report was used, the heritability estimates were modest in boys (h2 = .19) and girls (h2 = .31), but there was still no evidence for shared environmental influences in either sex. For OAD, they found moderate additive genetic influences in both boys and girls (h2 = .30–.66). Surprisingly, in contrast to the results for SAD and OAD, shared environmental influences were moderate on a self-report, composite measure of global anxiety symptoms in boys (c2 = .33). In contrast to the failure to find appreciable shared environmental influences on mood and anxiety, disorder symptoms in adults, the results from several twin studies suggest that shared environmental influences, as well as additive genetic influences and nonshared environmental influences, contribute moderately to anxiety and mood symptoms in children (collectively termed the childhood internalizing disorders).

The finding of shared environmental influences on children’s internalizing symptoms is not entirely consistent, however, with heterogeneity across diagnostic categories, parent versus child informant, and variables such as age and sex. An important caveat is also that rater effects, such as the tendency for parents to contrast their DZ twins when rating their characteristics, may lead to biased heritability and shared environmental influence estimates in children and adolescents.

In future studies, these methodological issues and discrepant findings will need to be addressed by using models that incorporate information from multiple raters. With respect to the generalizability of the findings reviewed, it is worth nothing that few studies of anxiety and mood disorders in children have employed DSM diagnoses based upon strict diagnostic criteria (although most of the studies reported here assessed DSM-III or DSM-III-R symptoms), and most have been based on self- or parent-report questionnaires rather than on diagnostic interviews

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