Genetic Influences on Eating Disorders

Author(s):  
Tracey D. Wade ◽  
Cynthia Bulik

The current chapter reviews our progress in understanding how genes influence eating disorders by addressing the following areas: (1) how recognition of genetic influences on eating disorders emerged; (2) the complexities of gene environment interplay; (3) what twin studies can tell us about gene environment interplay, and (4) the current state of molecular genetic studies. It is concluded that both genes and nonshared environment play a critical role in the explanatory framework for the etiology of eating disorders. Shared environment is likely to contribute to the development of cognition and attitudes that may initiate disordered eating practices. Researchers are on the cusp of identifying specific genes that are implicated, and explication of the manner in which genes and the environment work together to increase risk for eating disorders hinges on the collection of larger samples.

Author(s):  
Tracey D. Wade

The current chapter reviews our progress in understanding how genes influence eating and eating disorders (EDs) by addressing the following areas: (1) how recognition of genetic influences on eating and EDs emerged; (2) the complex nature of genetic action; (3) what twin studies can tell us about genetic influences; and (4) the current state of linkage and association studies. It is concluded that genes are an important part of the explanatory framework for the etiology of EDs, with an important contribution of the shared environment to the development of cognition and attitudes that may initiate disordered eating practices, and a critical contribution of the environment in providing a context within which genetic risk is more likely to be expressed. We currently have a limited understanding of the specific genes that are implicated, and the ways in which genes and the environment work together to increase risk for disordered eating.


Author(s):  
Ted Reichborn-Kjennerud ◽  
Kenneth S. Kendler

This chapter reviews the evidence for genetic contributions to the etiology of personality disorders (PDs) as defined by the Diagnostic and Statistical Manual of Mental Disorders (DSM; 5th ed.). This approach and some of the controversial issues associated with its development are briefly described in the first section. The second section evaluates the evidence for genetic influence on DSM PDs from family and twin studies using quantitative genetic methods. Studies that move beyond individual PDs are also reviewed, together with studies on the extent to which common genetic factors influence PDs and normal personality traits and PDs and pathological personality trait domains. Stability of genetic influences on PDs over time are also examined. Molecular genetic studies are reviewed in the third section. The fourth section deals with gene environment interplay, and the final section discusses future directions in the exploration of genetic influences on PDs.


Author(s):  
Michael J. Lyons ◽  
Chandra A. Reynolds ◽  
William S. Kremen ◽  
Carol E. Franz

The rapidly increasing number of people age 65 and older around the world has important implications for public health and social policy, making it imperative to understand the factors that influence the aging process. Twin studies can provide information that addresses critical questions about aging. Twin studies capitalize on a naturally occurring experiment in which there are some pairs of individuals who are born together and share 100% of their segregating genes (monozygotic twins) and some pairs that share approximately 50% (dizygotic twins). Twins can shed light on the relative influence of genes and environmental factors on various characteristics at various times during the life course and whether the same or different genetic influences are operating at different times. Twin studies can investigate whether characteristics that co-occur reflect overlapping genetic or environmental determinants. Discordant twin pairs provide an opportunity for a unique and powerful case-control study. There are numerous methodological issues to consider in twin studies of aging, such as the representativeness of twins and the assumption that the environment does not promote greater similarity within monozygotic pairs than dizygotic pairs. Studies of aging using twins may include many different types of measures, such as cognitive, psychosocial, biomarkers, and neuroimaging. Sophisticated statistical techniques have been developed to analyze data from twin studies. Structural equation modeling has proven to be especially useful. Several issues, such as assessing change and dealing with missing data, are particularly salient in studies of aging and there are a number of approaches that have been implemented in twin studies. Twins lend themselves very well to investigating whether genes influence one’s sensitivity to environmental exposures (gene-environment interaction) and whether genes influence the likelihood that an individual will experience certain environmental exposures (gene-environment correlation). Prior to the advent of modern molecular genetics, twin studies were the most important source of information about genetic influences. Dramatic advances in molecular genetic technology hold the promise of providing great insight into genetic influences, but these approaches complement rather than supplant twin studies. Moreover, there is a growing trend toward integrating molecular genetic methods into twin studies.


2007 ◽  
Vol 38 (1) ◽  
pp. 29-39 ◽  
Author(s):  
T. M. M. Button ◽  
J. Y. F. Lau ◽  
B. Maughan ◽  
T. C. Eley

BackgroundTo investigate the extent to which three putative ‘environmental’ risk factors, maternal punitive discipline (MPD), paternal punitive discipline (PPD) and negative life events (NLEs), share genetic influences with, and moderate the heritability of, externalizing behavior.MethodThe sample consisted of 2647 participants, aged 12–19 years, from the G1219 and G1219Twins longitudinal studies. Externalizing behavior was measured using the Youth Self-Report, MPD, PPD and exposure to NLEs were assessed using the Negative Sanctions Scale and the Life Event Scale for Adolescents respectively.ResultGenetic influences overlapped for externalizing behavior and each ‘environmental’ risk, indicating gene–environment correlation. When controlling for the gene–environment correlation, genetic variance decreased, and both shared and non-shared environmental influences increased, as a function of MPD. Genetic variance increased as a function of PPD, and for NLEs the only interaction effect was on the level of non-shared environment influence unique to externalizing behavior.ConclusionThe magnitude of the influence of genetic risk on externalizing behavior is contextually dependent, even after controlling for gene–environment correlation.


Author(s):  
Michael Windle

This chapter provides an introduction and overview of important issues that served as motivations for this book. For many complex phenotypes (e.g., depression, diabetes, obesity, substance use), there is substantial evidence that while genetic influences are important, so are environmental influences; moreover, there is substantial evidence from both behavior genetic studies (e.g., twin and adoptee studies) and molecular genetic studies (both human and infrahuman) that genes commonly interact with environmental factors in predicting complex phenotypes. The fields of genomics and other –omics (e.g., proteomics, metabolomics) provide exciting opportunities to advance science and foster the goals of public health and a more individualized intervention approach (e.g., precision medicine). The goals of these more individualized approaches would benefit greatly not only by advances in genomics and other –omics, but also by incorporating information both on environments and their interactions with genomic and other biological material and regulatory processes (e.g., environmental signal to biological pathway responses). Such findings would thereby offer more flexible guidance to a broader range of prevention, intervention, and treatment targets, and facilitate more tailored programs based on a fuller complement of G and E influences.


2021 ◽  
pp. 164-186
Author(s):  
Benjamin B. Lahey

This chapter summarizes the basic biology of inheritance, including chromosomes, genes, nucleotides, genotype, and gene expression. It uses these concepts and the logic of studies of the two kinds of twins—monozygotic and dizygotic—to define the concept of heritability as the proportion of differences on the dimension among people in the population that is attributable to genetic factors. The genetic variance in the phenotypes of psychological problems, such as depression, is never encoded in a single allele or genetic variant. Rather, every dimension of psychological problems is polygenic, meaning that many genetic variants have very small genetic influences on each dimension of psychological problems that must be combined to meaningfully measure the genetic component of risk at the molecular level. Often, single variations in individual nucleotides—the molecules arranged on DNA that serve as the letters of the genetic code—known as single nucleotide polymorphisms are summed to quantify the molecular genetic risk in a polygenic risk score. The nonspecific genetic influences at the top of the hierarchy of genetic influences result from some genetic variants being pleiotropic in the sense of directly or indirectly influencing essentially all dimensions of psychological problems. Identifying the specific genetic and environmental influences on dimensions of psychological problems at each level of the hierarchy is complicated because they operate together through the crucially important gene–environment correlations and interactions described in this chapter.


2016 ◽  
Vol 27 (8) ◽  
pp. 827-847 ◽  
Author(s):  
Catherine Winsper ◽  
Steven Marwaha ◽  
Suzet Tanya Lereya ◽  
Andrew Thompson ◽  
Julie Eyden ◽  
...  

AbstractContemporary theories for the aetiology of borderline personality disorder (BPD) take a lifespan approach asserting that inborn biological predisposition is potentiated across development by environmental risk factors. In this review, we present and critically evaluate evidence on the neurobiology of BPD in childhood and adolescence, compare this evidence to the adult literature, and contextualise within a neurodevelopmental framework. A systematic review was conducted to identify studies examining the neurobiological (i.e. genetic, structural neuroimaging, neurophysiological, and neuropsychological) correlates of BPD symptoms in children and adolescents aged 19 years or under. We identified, quality assessed, and narratively summarised 34 studies published between 1980 and June 2016. Similar to findings in adult populations, twin studies indicated moderate to high levels of heritability of BPD, and there was some evidence for gene-environment interactions. Also consistent with adult reports is that some adolescents with BPD demonstrated structural (grey and white matter) alterations in frontolimbic regions and neuropsychological abnormalities (i.e. reduced executive function and disturbances in social cognition). These findings suggest that neurobiological abnormalities observed in adult BPD may not solely be the consequence of chronic morbidity or prolonged medication use. They also provide tentative support for neurodevelopmental theories of BPD by demonstrating that neurobiological markers may be observed from childhood onwards and interact with environmental factors to increase risk of BPD in young populations. Prospective studies with a range of repeated measures are now required to elucidate the temporal unfurling of neurobiological features and further delineate the complex pathways to BPD.


Author(s):  
Jennifer A. Sumner ◽  
Angela C. Bustamante ◽  
Karestan C. Koenen ◽  
Monica Uddin

Trauma exposure and PTSD are heritable. However, the mechanisms of risk and resilience following trauma exposure are not yet well understood, suggesting that investigations into the genetic architecture of PTSD have much to contribute. This chapter reviews the rapidly growing literature on molecular genetic risk factors for PTSD, including findings from candidate gene and genome-wide association studies. Given the critical role of trauma exposure in the onset of PTSD, it also discusses gene-environment interplay, and highlights some recent findings from epigenetic studies. The chapter concludes by summarizing considerations for the field as it continues to move forward, and discusses exciting new developments in the search for genetic markers for PTSD.


2005 ◽  
Vol 8 (5) ◽  
pp. 467-482 ◽  
Author(s):  
Margarita C. T. Slof-Op ‘t Landt ◽  
Eric F. van Furth ◽  
Ingrid Meulenbelt ◽  
P. Eline Slagboom ◽  
Meike Bartels ◽  
...  

AbstractSubstantial effort has been put into the exploration of the biological background of eating disorders, through family, twin and molecular genetic studies. Family studies have shown that anorexia (AN) and bulimia nervosa (BN) are strongly familial, and that familial etiologic factors appear to be shared by both disorders. Twin studies often focus on broader phenotypes or subthreshold eating disorders. These studies consistently yielded moderate to substantial heritabilities. In addition, there has been a proliferation of molecular genetic studies that focused on Diagnostic and Statistical Manual of Mental Disorders (4th ed.; DSM-IV; American Psychiatric Association, 1994) AN and BN. Seven linkage regions have been identified in genome-wide screens. Many genetic association studies have been performed, but no consistent association between a candidate gene and AN or BN has been reported. Larger genetic association studies and collaborations are needed to examine the involvement of several candidate genes and biological pathways in eating disorders. In addition, twin studies should be designed to assist the molecular work by further exploring genetic determinants of endophenotypes, evaluating the magnitude of contribution to liability of measured genotypes as well as environmental risk factors related to eating disorders. In this manner twin and molecular studies can move the field forward in a mutually informative way.


2004 ◽  
Vol 13 (2) ◽  
pp. 91-98 ◽  
Author(s):  
Cynthia M. Bulik ◽  
Federica Tozzi

SummaryObjective – To review recent literature documenting how family, twin and molecular genetic studies of eating disorders have revolutionized our conceptualizations of anorexia and bulimia nervosa. Methods – We summarized extant litera-ture on genetic epidemiology of eating disorders. Results – Results of extant studies highlight the underlying biological vulnera- bilities associated with these conditions. Genetic research has also opened up new avenues and approaches for exploring how the environment exerts its influence on risk. Conclusions – We discuss state-of-the-science findings in the genetics of eating disorders, explore various mechanisms of gene-environment interplay, and discuss implications of this research for science, practice, families and individuals with eating disorders.


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