Was sind Ursachen von Depressionen?

Improved methods of assessment and research design have established a robust and causal association between stressful life events and major depressive episodes. The chapter reviews these developments briefly and attempts to identify gaps in the field and new directions in recent research. There are notable shortcomings in several important topics: measurement and evaluation of chronic stress and depression; exploration of potentially different processes of stress and depression associated with first-onset versus recurrent episodes; possible gender differences in exposure and reactivity to stressors; testing kindling/sensitization processes; longitudinal tests of diathesis-stress models; and understanding biological stress processes associated with naturally occurring stress and depressive outcomes. There is growing interest in moving away from unidirectional models of the stress-depression association, toward recognition of the effects of contexts and personal characteristics on the occurrence of stressors, and on the likelihood of progressive and dynamic relationships between stress and depression over time-including effects of childhood and lifetime stress exposure on later reactivity to stress.

Stressful life events are associated with the onset of episodes of major depression. However, exposure to stressful life events is influenced by genetic factors, and these factors are correlated with those that predispose to major depression. The aim of this study was to clarify the degree to which stressful life events cause major depression.

A central phrase in the new "GeneTalk" is "X is a gene for Y," in which X is a particular gene on the human genome and Y is a complex human disorder or trait. This article begins by sketching the historical origins of this phrase and the concept of the gene-phenotype relationship that underlies it. Five criteria are then proposed to evaluate the appropriateness of the "X is a gene for Y" concept: 1) strength of association, 2) specificity of relationship, 3) noncontingency of effect, 4) causal proximity of X to Y, and 5) the degree to which X is the appropriate level of explanation for Y. Evidence from psychiatric genetics is then reviewed that address each of these criteria. The concept of "a gene for..." is best understood as deriving from preformationist developmental theory in which genes-like preformationist anlagen-"code for" traits in a simple, direct, and powerful way. However, the genetic contribution to psychiatric disorders fails to meet any of the five criteria for the concept of "X is a gene for Y." The impact of individual genes on risk for psychiatric illness is small, often nonspecific, and embedded in complex causal pathways. The phrase "a gene for..." and the preformationist concept of gene action that underlies it are inappropriate for psychiatric disorders.