Objective – The paper discusses conceptual, methodological and clinical issues of comorbidity from the perspective of more recent epidemiological studies. Further the potential causal and pathogenic role of temporally primary disorders for the onset of secondary disorders is evaluated. Results – The available data suggest so far that comorbidity (a) is not an artefact of assessment strategies, sampling or design features, (b) is specific in different disorders, (c) is particularly frequent in anxiety and affective disorders, (d) affects systematically the course of the comorbid conditions and (0 might be related to symptom progression models. Conclusions – Furthermore, evidence is presented that specific forms of primary anxiety disorders affect the risk for secondary depressive disorders, increase the likelihood of non-remission as well as the number of subsequent depressive episodes.

Aim – To describe the rationale for introducing molecular genetic analyses to psychiatric epidemiology. This offers new possibilities for aetiological research on common mental disorders. Method – In addition to the traditional variables used in field surveys, it is now possible to include molecular genetic information. This is currently done by looking for allelic associations rather than by linkage analysis, and can be directed either at traits conferring susceptibility or at states. The purpose is to identify quantitative trait loci (QTLs) by examining candidate genes. An alternative strategy is genome scanning, which can identify genes by their chromosomal position with increasing resolution. Results – Some associations have already been reported in the literature, linking personality traits with particular alleles: extraversion or novelty-seeking with a polymorphism of the dopamine DRD4 receptor gene; and neuroticism with a polymorphism of the serotonin transporter gene. Conclusions – These findings are of major interest, but cannot yet be looked upon as confirmed. What is significant for epidemiology is the opportunity to link behavioural and psychiatric variables with genes influencing biochemical and physiological processes in the brain, and to do so at the population level. For further allelic association studies, there are four principal requirements: valid measures of phenotypes; replication of findings across diverse populations; more candidate genes; and exploration of the interaction between genotype and environmental exposures from conception to late life. Through such research, psychiatric epidemiology can now investigate biopsychosocial phenomena.

El desarrollo de agentes farmacológicos en el tratamiento del alcoholismo representa una de las muchas maneras diferentes de suprimir la ingesta de alcohol. Se han examinado sustancias específicas con respecto a la hipotética participación de sistemas neuroquímicos diferentes en el «ansia de alcohol” en modelos animales (especialmente ratas) y cada vez más en el ser humano. Se han descrito resultados prometedores en la reducción del «ansia de alcohol » con el uso de diferentes clases de sustancias químicas. Por tanto, difícilmente se puede explicar el «ansia» sobre la base de un déficit en un solo sistema (neurotransmisor) neuroquímico. Los datos apoyan esta conclusión. La eficacia de muchas sustancias contra el ansia, descrita en estudios más pequeños, se debe confirmar primero en trabajos clínicos en una escala más amplia.