Psychiatric epidemiology is becalmed. Since mid-century, there has been substantial progress in
finding risk factors for the common mental disorders of anxiety and depression. This has been
almost entirely within a social paradigm. Much has been learned about the effects of interpersonal
and other social exposures across the lifespan in contributing to these disorders (Brown & Harris,
1978, 1989; Paykel, 1992; Blazer, 1995; Henderson, 1988, 1999). But the range of possibly causal
variables has been narrow: demography, socio-economic status, childhood experiences, recent
exposure to adversity and the availability of social support. The dominant paradigm has been
environmental exposure, examining how experiences that arise outside the individual may have an
enduring impact on mental health. The environment in question has been interpersonal or social.
Within this paradigm, no new hypotheses of major significance have emerged in recent years.Epidemiologists have known that the biological domain might be important in aetiology, but for
the common mental disorders it has been largely passed over. Properties of the adult brain, whether
innate or moulded by environmental exposures, have only rarely been accessible. With the advances
in molecular genetics, this is changing (Rutter & Plomin, 1997). For epidemiology, there is now the
possibility of bringing molecular genetics into studies of aetiology. Because of the significance of this
development, we present a critical assessment of the prospects for population-based research using
molecular genetics, the work already reaching publication and the methodological issues that are
arising.
Molecular genetics in psychiatric epidemiology: the promise and challenge