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Schizophrenia epigenesis: past, present, and future
Author(s) -
Gottesman Irving I.
Publication year - 1994
Publication title -
acta psychiatrica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.849
H-Index - 146
eISSN - 1600-0447
pISSN - 0001-690X
DOI - 10.1111/j.1600-0447.1994.tb05887.x
Subject(s) - schizophrenia (object oriented programming) , disease , genetic discrimination , etiology , epigenesis , psychosis , genetic epidemiology , schizophrenia research , epidemiology , psychiatry , psychology , genetics , biology , medicine , gene , genetic testing , pathology , gene expression , dna methylation
Sociopolitical and ideological attacks on the various genetically oriented programs of research into the causes of schizophrenia, even when well‐motivated to prevent genetic discrimination in all its forms, endangers the enterprise. Although there have been no replicated successes in finding genes linked or associated to markers for schizophrenia yet, the solid foundation for the fact that genetic factors are importantly involved in the etiology of schizophrenia derives from replicated studies using the strategies of genetic epidemiology ‐ families, twins, adoptees. The models to emulate in schizophrenia research should follow the paths of researchers on coronary artery disease, diabetes, and Alzheimer's disease. All are complex diseases with multifactorial and multigenic components. Even when the necessary genotype is present, it may not be expressed as clinical disease at the phenotypic level.