Biological suicide research: outcome and limitations.
Empirical study of suicide began early in this century from the sociological (Durkheim 1951) and psychological (Freud 1956) perspective. A decade ago, a biological dimension was added, focusing on two major issues, i.e., are disturbances in brain functioning instrumental in the occurrence of suicidal behavior and/or do such disturbances increase the likelihood of suicidal behavior in an individual exposed to stressful events? Biological suicide research has developed as an offshoot of biological depression research. This is a logical development, as depression is a major precursor of both attempted (Weissman et al. 1973; van Praag 1982a) and completed (Guze and Robins 1970; Miles 1977) suicide. The major biochemical research targets are similar: monoamines and hormones. This paper will review the main findings in suicidal behavior, discuss the methodological shortcomings of this research, and indicate ways of avoiding them.
D000374:Aggression / Q000502:physiology; D002395:Catecholamines / Q000378:metabolism; D003866:Depressive Disorder / Q000134:cerebrospinal fluid; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism; D006897:Hydroxyindoleacetic Acid / Q000134:cerebrospinal fluid; D008995:Monoamine Oxidase / Q000097:blood; D013405:Suicide; D013972:Thyrotropin / Q000378:metabolism
D002395:Catecholamines; D006897:Hydroxyindoleacetic Acid; D013972:Thyrotropin; D008995:Monoamine Oxidase; D006854:Hydrocortisone