Social support, depressed mood, and adjustment to stress: a genetic epidemiologic investigation.

A survey of 821 same-sex female twin pairs from a population-based registry assessed 8 dimensions of social support and social integration. Twin analyses documented significant common environmental influences on 5 of these 8 measures and significant genetic influences on 5 of the 8. A decomposition of the multiplicative association between support and a measure of stressful life experiences in predicting depressed mood--an association typically interpreted as providing evidence for a stress-buffering effect of social support--shows clearly that it is the environmental and genetic factors that cause support, rather than support itself, that buffer the effects of stress on mood in most cases. We discuss the implications of this result for future research on the relationship between social support and psychopathology.     

A personal encounter with psychology (1937-2002)

An undergraduate assistantship with Abraham Maslow, research with Solomon Asch, and an indirect exposure to Ernest Nagel's philosophy of science encouraged Howard H. Kendler to become involved with methodological issues in psychology. Graduate training with Kenneth Spence led to an active research career that was initially immersed in the latent learning controversy and later, with the collaboration of his wife Tracy Kendler, in the extension of the Hull-Spence model of cognitive development. Methodological concerns from a variety of sources encouraged Kendler to express his ideas on the methodology and history of psychology as well as its role in ethical and social policy issues. A productive symbiotic relationship is created from the interaction of democracy, natural-science psychology, and moral pluralism.     

Genetic and environmental contributions to the co-occurrence of depressive personality disorder and DSM-IV personality disorders

One of the main controversies with regard to depressive personality disorder (DPD) concerns the co-occurrence with the established DSM-IV personality disorders (PDs). The main aim of this study was to examine to what extent DPD and the DSM-IV PDs share genetic and environmental risk factors, using multivariate twin modeling. The DSM-IV Structured Interview for Personality was applied to 2,794 young adult twins. Paranoid PD from Cluster A, borderline PD from Cluster B, and all three PDs from Cluster C were independently and significantly associated with DPD in multiple regression analysis. The genetic correlations between DPD and the other PDs were strong (.53-.83), while the environmental correlations were moderate (.36-.40). Close to 50% of the total variance in DPD was disorder specific. However, only 5% was due to disorder-specific genetic factors, indicating that a substantial part of the genetic vulnerability to DPD also increases the vulnerability to other PDs.