The importance of developmental mechanisms in understanding adolescent depression

The risk for developing depression markedly increases during the second decade of life [1]. Over the past two decades, considerable research has examined the unique characteristics of adolescence that confer risk for depression, spanning neurobiological, genetic, hormonal, behavioral and psychosocial domains. Identifying etiological mechanisms to guide effective prevention and intervention has proved challenging for many reasons, including the necessary reliance on observational rather than experimental studies, the high cost and attrition problems associated with longitudinal investigations and the integration of rapidly emerging fields, often accompanied with highly technical methods, such as genomics and functional neuroimaging. The heterogeneous classification of depressionrelated disorders, combined with high levels of comorbidity, has presented additional challenges to the study of contributing mechanisms, particularly if depression is a disorder with multiple underlying causes. In ‘‘The ROOTS study ten years on: a review of findings on adolescent depression and future directions, challenges, and recommendations for longitudinal research’’ [2] the authors describe a multi-wave and multimodal population study of teenagers tracked from 14 to 21 years of age, involving assessment of psychosocial, biological and childhood adversity measures. The study has made a number of noteworthy contributions. The nuanced characterization of the relationship between adversity and mental health helps identify sub-populations at greater risk and suggests unique risk pathways. Evidence that cognitive biases contribute to associations between genetic variation, stress exposure and mental health problems, as well as failure to show physical activity is an effective intervention for depression during adolescence, contributes to the search for modifiable targets for intervention. Description of developmental pathways to depression—for example, that elevated cortisol and moderate depressive symptoms in early adolescence predict later onset of clinical disorder, is useful for identifying underlying mechanisms and biomarkers for early detection. Finally, identification of an underlying transdiagnostic risk factor for mental disorders may assist in identifying common mechanisms that increase general susceptibility for psychiatric disorders and contribute to co-morbidity. Methodological strengths of the study that address the aforementioned challenges are the overall prospective design, use of nested studies to study distinctive subgroups, and data analysis techniques that integrate both person-centered and variable-centered perspectives, which allow observation of underlying mechanisms that may not initially appear intuitive. Although epidemiological evidence [1] and neurodevelopmental changes [3] provide the impetus to focus on the period of adolescence as the crucible for mood disorders, it is unlikely that all contributing factors emerge only during this period of development. Instead, for many youth, it is likely that by adolescence the twig is bent, so is the tree inclined. For example, structural differences in the hippocampus are already observable among 12-year-old children who subsequently develop first-onset depression in adolescence [4]. Within the ROOTS study, elevated morning cortisol combined with sub-threshold depression symptoms already present at 14 years predicted clinical depression at 17 years. This discovery has immense This comment refers to the article available at doi: 10.1007/s00127015-1150-y