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Schizophrenia: A critical view on genetic effects

机译:精神分裂症:对遗传效应的批判性观点

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The main justification for molecular genetics studies of enduring psychosis (schizophrenia) are high heritability estimates obtained from classical twin studies. The classical twin method rests upon the equal environment assumption (EEA), which holds that reared-together identical and fraternal twin pairs grow up experiencing equally similar environmental exposures. However, a review of prior twin studies shows that identical twins are more similar than fraternal twins on childhood exposures that are central to the etiology of psychosis. Such exposures include bullying, sexual abuse, physical maltreatment, emotional neglect and abuse, and general trauma. An additional assumption presented by twin researchers, that the differential intraclass correlation for child social adversities can be explained by evocative gene-environment covariation, is not consistent with the available evidence. Moreover, due to an array of methodological problems and questionable assumptions, adoption studies provide misleading indications in support of genetic effects. As a result, direct studies of DNA variations in schizophrenia must stand on their own ground. Possible minor findings from such molecular genetics studies, when combined with the available evidence of environmental effects, support a stress-based sociopsychobiological model of schizophrenia etiology.
机译:持久性精神病(精神分裂症)的分子遗传学研究的主要理由是从经典双生子研究获得的高遗传力估计值。经典的双胞胎方法基于平等的环境假设(EEA),该假设认为,饲养在一起的同卵双胞胎和异卵双胞胎对成长时会经历同样相似的环境暴露。然而,对先前双胞胎研究的回顾表明,在儿童期暴露中,同卵双胞胎比异卵双胞胎更相似,而这对精神病的病因至关重要。此类暴露包括欺凌,性虐待,身体虐待,情感疏忽和虐待以及一般性创伤。双胞胎研究人员提出的另一种假设是,儿童社交逆境的差异性群体内相关性可以通过令人回味的基因-环境协变来解释,这与现有证据不一致。此外,由于一系列方法学问题和可疑的假设,采用研究为支持遗传效应提供了误导性迹象。因此,对精神分裂症中DNA变异的直接研究必须站在自己的立场上。从此类分子遗传学研究中得出的可能的次要发现,与现有的环境影响证据相结合,支持了基于压力的精神分裂症病因的社会心理生物学模型。

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