sponse may also contribute to symptoms of depression by triggering sickness behaviors, including disruptions in appetite, sleep, and social activity. These processes may be involved in depression in general, or only in those individuals in which depression is comorbid with a medical condition, such as heart disease. Alternatively, depression may be involved in provoking inflammation. A recent meta-analysis reports some support for three causal models: depression to inflammation, inflammation to depression, and bidirectional associations (Howren, Lamkin, and Suls, 2009). Further research using prospective longitudinal designs is needed to clarify the directions of the relations among stress, depression, and inflammation.
Evidence from one longitudinal study has shed some additional light on the possible role of inflammatory processes in depression. Danese et al. (2008) examined the role of early life stress (childhood maltreatment) and later depression and inflammatory response processes (as measured by levels of CRP) as part of the longitudinal study of a birth cohort in Dunedin, New Zealand, followed into young adulthood. Specifically, they were able to compare young adults with no history of childhood maltreatment and no current depression, those with current depression and no maltreatment history, those with a positive history of maltreatment but no current depression, and those with both current depression and a history of maltreatment. It appeared that depressed individuals with a history of maltreatment were more likely to have high levels of CRP when compared to depressed-only individuals. Thus, maltreatment history seems to be an important modifier of the association between depression and inflammatory markers.
Although in its early stages, research on inflammatory responses suggests an additional biological process that may help to explain the link between stress and depression. And inflammatory processes may be especially important in elucidating important medical comorbidities of depression, most notably coronary heart disease.
Depression is commonly construed as a reaction to negative environmental circumstances. Etiological models are largely diathesis-stress perspectives. A diathesis is a risk factor or vulnerability process, such as people’s biological, personality, or cognitive characteristics, that accounts for individual differences in how they respond to similar stressful challenges. In order to illustrate key points—as well as to draw attention to circumstances that help to identify populations at particular risk for depression—in this section we focus on three kinds of stressful (environmental)