Research into the biological causes of depressive disorder, such as its grounding in neurochemicals, receptors, genes, and the structure and function of the brain, holds great promise of contributing to our growing understanding of behavior, as well as of leading to new and more effective treatments. Such studies include, for example, those that use magnetic resonance imaging (MRI) to explore brain activity in depressed patients, examinations of neurotransmitters and their role in depression (bolstered by the success of medications in influencing the level of neurotransmitters), and research on the genetic influences on depressive disorder.
Around the same time as the publication of the DSM-III in 1980, biologically grounded models of depression began to dominate psychiatric theory and practice, and the influence of psychosocial models began to wane.1Moreover, a number of leading figures in the construction of the DSM were also leading biologically oriented psychiatrists. It is thus tempting to see the two as conceptually linked. Yet, as we have seen, the DSM definition was not in fact intended to imply any particular cause of depression. Instead, it was designed to be theory-neutral and compatible with social and psychological, as well as biological, causes of symptoms.
Nonetheless, the DSM criteria have played a prominent role in research studies on the biology of depression. The presence of agreed-on, theory-neutral criteria that could form a basis for communication among researchers has certainly been beneficial to biological research, as to all psychiatric research. However, on the other side of the ledger, we argue that the conflation of normal sadness and depressive disorder in DSM criteria has handicapped biological research and created confusion that can potentially lead researchers to draw misleading conclusions from their data.
The basic problem is simply that biological processes underlie nondisordered, as well as disordered, human traits. No doubt disordered sadness reactions