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The last decades have witnessed remarkable developments in the behavioral neurosciences, but without commensurate improvements in the provision of mental health care. Several explanations have been proposed. Some have pointed to gaps in our knowledge that require more translational research before laboratory findings can be brought to the clinic. Others see a lag in adopting new treatments that require more implementation research so proven practices can be brought into wider use. Without discounting these possibilities, I would suggest an alternative explanation. There are limits to what the behavioral neurosciences can explain. What lies within these limits is not necessarily relevant and what lies beyond them is not necessarily irrelevant to clinical practice. Therefore, these scientific developments, although important in their own right, may have little bearing on clinical practice. In contrast, there are areas of knowledge dealing with society, culture, and meaning (Moerman and Jonas, 2002) that are intimately related to the practice of psychiatry and should remain a focus for clinicians. With this in mind, I will first focus on the management of affective disorders, and review several areas of research to make the case that current and continued progress in the behavioral neurosciences should not (at least in the foreseeable future) be expected to address relevant clinical concerns. Subsequently, I will widen the scope to highlight areas in which knowledge that lies outside these sciences remains essential for our field.Perhaps our most notable scientific advances have been in molecular genetics. It had been hoped that developments, including the elucidation of the human genome, would clarify the nosology, unravel the pathophysiology, and lead to novel treatments of affective disorders. To date none of these hopes have been fulfilled. Beginning with DSM-III, psychiatric nosology has been based on clinical presentation and not on any etiological theory. But this etiological agnosticism had been directed at distinctions based on psychoanalytic or behavioral theory. It was assumed that diagnoses would someday be revised based on genetic information; that similar phenotypes could be distinguished by differences in genotype. But, despite 40 years of genetic research; DSM V will no more rely on genetic information than did DSM-III. There is as well good reason to believe that this will continue into the foreseeable future. Similar genes (i.e., for glutamic acid decarboxylase) are associated with multiple conditions (i.e., anxiety disorders, major depression, and neuroticism (Hettema et al., 2006) whereas the same condition may involve multiple genes. Recent findings that bipolar illness and schizophrenia share a common genetic predisposition (Lichtenstein et al., 2009) that involves thousands of common alleles (International Schizophrenia Consortium, 2009) would suggest that knowledge about any gene or even a panel of genes will not differentiate these illnesses. This point has been forcefully stated by Weinberger 2010 “Finding specific genes for mental illness now seems a pipe dream... Many of hundreds of genes may contribute to raised vulnerability, and such defects may affect brain development and function independently of any psychiatric diagnosis.”I would argue that the same skepticism should apply toward the hope of soon elucidating the pathophysiologic processes that would differentiate affective disorders, distinguish them from nonaffective states, or inform the development of new treatments. Forty years ago it was assumed that the synaptic action of antidepressants on neurotransmitters provided insight into the pathophysiology of depression. Depression was seen as a “chemical imbalance.” But antidepressants have proven effective in multiple psychiatric conditions (generalized anxiety, phobic disorders, panic attacks, eating disorders, etc) whereas the various types (tricyclic, SSRI, SNRI etc) have identical efficacy despite their action on different neurotransmitters (Freemantle et al., 2000).