Etiologies, Environments, and Genes—Challenges for Psychiatric Diagnosis During an Era of Scientific Transition

Abstract

The article by Dr. Krishnan 1 comes at an auspicious time, as the Diagnostic and Statistical Manual of Mental Disorders (DSM)—and our understanding of psychopathology and its related diseases and conditions—constantly needs rethinking. There is no better way to get the blood flowing than to stimulate discussion and controversy! However, I am of two minds about this article. At once I applaud its aims and agree with its drive toward enhancing the validity of psychiatric diagnoses even while I have concerns about its approach and what I see as an inadvertent potential for stifling the science that it proposes to fortify and promote. More specifically, I explore the following issues. 1) Is this newly proposed approach to classification really new? Although Dr. Krishnan calls for moving from “nominalist” (descriptive) to “essentialist” (etiologic) diagnoses, he proposes a two-axis approach that basically recapitulates what already is included in DSM. 2) What are the central concerns? The crux of his proposal requires a determination of causation, yet there is no standard, valid method now used to make such a determination, a vexing challenge, especially given that the bulk of psychiatric conditions likely reflect the influence of multiple and very diverse genetic, developmental, environmental, and incident life and exposure-related determinants. 3) If not this proposal, what? Dr. Krishnan’s proposal may have the effect of inadvertently constraining the processes of exploration and discovery. It is time to explicitly test the predictive validity of current DSM constructs. Several general caveats are in order before addressing the three major points of this commentary. Dr. Krishnan uses “diagnosis” and “disease” as if they are the same thing. I do not. To me, “disease” gets at the fundamental pathologic processes that lead to the systemic expression of signs (objectively detected and measured) and symptoms (subjectively experienced and expressed); the latter can be especially susceptible to individual and culturally based variations, and the former are not immune from these influences. “Illness” gets at the broader individual and social processes that are linked to having a disease. “Disease” has a somewhat fuzzy boundary too, because someone may be infected with an organism but not show any manifestations (thus, “latent disease”). Given this context, the definition of disease cited by Dr. Krishnan caught my attention. Read literally, it could include most adolescents; just ask their parents! Moreover, it is a leap of faith to lump the apparent cause of disease in small numbers of individuals drawn from extensively studied pedigrees with presenile dementia together with conditions solely labeled on the basis of the appearance of having a “dominant pattern of inheritance” (see page 1). The author notes that the latter are “more common in