General population survey data are used to disaggregate the associations of substance use disorders with suicide attempts in order to evaluate a number of hypotheses about the processes leading to these associations. Data are from the US National Comorbidity Survey (1990-1992). Discrete-time survival analysis is used to study the effects of retrospectively reported temporally prior substance use, abuse, and dependence in predicting first onset of suicidal behavior. Alcohol and drug use predict subsequent suicide attempts after controlling for sociodemographics and comorbid mental disorders. Previous use is not a significant predictor among current nonusers. Abuse and dependence are significant predictors among users for three of the 10 substances considered (alcohol, inhalants, and heroin). The number of substances used is more important than the types of substances used in predicting suicidal behavior. Disaggregation shows that the effects of use are largely on suicidal ideation and nonplanned attempts among ideators. In comparison, the effects of use on suicide plans and planned attempts among ideators are not significant. Clinicians need to be aware that current substance use, even in the absence of abuse or dependence, is a significant risk factor for unplanned suicide attempts among ideators.

Recent studies involved the pathways of kinases regulated by extracellular signal (ERK - extracellular signal regulated kinases), a broad range of key cellular processes, in the mechanisms of depression and consequently in the action of antidepressants. It is also known that the use of specific inhibitors of phosphorylation of ERKs1 / 2 showed to have antidepressant effect in animal models. Fluoxetina (SSRI) was recently discovered to be a potente inhibitor of phosphorylation of ERKs. The ERKs1 / 2 and recently the 3, are present in neurons and glia, these also engaged in biological mechanisms of depression.The authors propose to do, based on the current literature, the characterization of the type (s) of cell (s) where changes in activation of ERKs1 / 2, occur during depression, and during the administration of antidepressants, in order to understand, to what extent these kinases may be considered as biological markers of depression. Possibly also to examine the feasibility of using these markers in clinical use.

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