Pub Date : 2018-06-07DOI: 10.1093/oxfordhb/9780190681777.013.25
R. Uher
Both genetic variation and environmental exposures play key roles in the development of mental health or psychopathology. Their roles are interdependent: The effects of genetic variants depend on environment, and the impact of environment depends on the genetic variants. This chapter will explain and critically review the most important models of gene–environment interplay, including gene–environment correlation, gene–environment interaction, and epigenetics. Gene–environment correlation describes a mechanism where genetic variants influence the likelihood of environmental exposure. Gene–environment interactions refer to a mechanism where genetic variants influence the impact of an environmental exposure on the individual. Finally, epigenetics provides a molecular mechanism through which environmental exposures affect the function of genes for long periods of time. The chapter concludes with a discussion of the limits of current knowledge, its implications for treatment and prevention, and directions for further research.
{"title":"Genetic and Epigenetic Models","authors":"R. Uher","doi":"10.1093/oxfordhb/9780190681777.013.25","DOIUrl":"https://doi.org/10.1093/oxfordhb/9780190681777.013.25","url":null,"abstract":"Both genetic variation and environmental exposures play key roles in the development of mental health or psychopathology. Their roles are interdependent: The effects of genetic variants depend on environment, and the impact of environment depends on the genetic variants. This chapter will explain and critically review the most important models of gene–environment interplay, including gene–environment correlation, gene–environment interaction, and epigenetics. Gene–environment correlation describes a mechanism where genetic variants influence the likelihood of environmental exposure. Gene–environment interactions refer to a mechanism where genetic variants influence the impact of an environmental exposure on the individual. Finally, epigenetics provides a molecular mechanism through which environmental exposures affect the function of genes for long periods of time. The chapter concludes with a discussion of the limits of current knowledge, its implications for treatment and prevention, and directions for further research.","PeriodicalId":375662,"journal":{"name":"The Oxford Handbook of Stress and Mental Health","volume":"23 9","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2018-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132679650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-06-07DOI: 10.1093/OXFORDHB/9780190681777.013.16
Catherine B. Stroud
The stress sensitization model was developed to explain the mechanism through which the relationship between stress and affective disorder onsets changes across the course of the disorder. The model posits that individuals become sensitized to stress over time, such that the level of stress needed to trigger episode onsets becomes increasingly lower with successive episodes. The stress sensitization model has accrued empirical support in the context of major depression and to a lesser extent in bipolar spectrum disorders. Furthermore, expanding upon the original stress sensitization model, research also indicates that early adversity (i.e., early childhood experiences) sensitizes individuals to subsequent proximal stress, increasing risk for psychopathology. In this chapter, the theoretical background underlying the stress sensitization model is reviewed, and research evidence investigating stress sensitization is evaluated. In addition, moderators and mechanisms of stress sensitization effects are reviewed, and recommendations for future research are provided.
{"title":"The Stress Sensitization Model","authors":"Catherine B. Stroud","doi":"10.1093/OXFORDHB/9780190681777.013.16","DOIUrl":"https://doi.org/10.1093/OXFORDHB/9780190681777.013.16","url":null,"abstract":"The stress sensitization model was developed to explain the mechanism through which the relationship between stress and affective disorder onsets changes across the course of the disorder. The model posits that individuals become sensitized to stress over time, such that the level of stress needed to trigger episode onsets becomes increasingly lower with successive episodes. The stress sensitization model has accrued empirical support in the context of major depression and to a lesser extent in bipolar spectrum disorders. Furthermore, expanding upon the original stress sensitization model, research also indicates that early adversity (i.e., early childhood experiences) sensitizes individuals to subsequent proximal stress, increasing risk for psychopathology. In this chapter, the theoretical background underlying the stress sensitization model is reviewed, and research evidence investigating stress sensitization is evaluated. In addition, moderators and mechanisms of stress sensitization effects are reviewed, and recommendations for future research are provided.","PeriodicalId":375662,"journal":{"name":"The Oxford Handbook of Stress and Mental Health","volume":"28 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2018-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126759098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}