Serotonin transporter gene polymorphism in eating disorders: Data from a new biobank and META-analysis of previous studies

Solmi, Marco; Gallicchio, Davide; Collantoni, Enrico; Correll, Christoph U.; Clementi, Maurizio; Pinato, Claudia; Forzan, Monica; Cassina, Matteo; Fontana, Francesca; Giannunzio, Valeria; Piva, I.; Siani, Roberta; Salvo, Pierandrea; Santonastaso, Paolo; Tenconi, Elena; Veronese, Nicola; Favaro, Angela

doi:10.3109/15622975.2015.1126675

Cited by 23 publications

(14 citation statements)

References 46 publications

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“…Conversely, there were no main effects of 5-HTTLPR genotype in any analyses, contrary to some past findings (Calati et al, 2011; Lee & Lin, 2010), although aligned with others (Castellini et al, 2012; Solmi et al, 2016). …”

Section: Introductioncontrasting

confidence: 99%

A systematic review and secondary data analysis of the interactions between the serotonin transporter 5-HTTLPR polymorphism and environmental and psychological factors in eating disorders

Rozenblat

Ong

Fuller‐Tyszkiewicz

et al. 2017

Journal of Psychiatric Research

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Objectives To summarize and synthesize the growing gene x environment (GxE) research investigating the promoter region of the serotonin transporter gene (5-HTTLPR) in the eating disorders (ED) field, and overcome the common limitation of low sample size, by undertaking a systematic review followed by a secondary data meta-analysis of studies identified by the review. Method A systematic review of articles using PsycINFO, PubMed, and EMBASE was undertaken to identify studies investigating the interaction between 5-HTTLPR and an environmental or psychological factor, with an ED-related outcome variable. Seven studies were identified by the systematic review, with complete data sets of five community (n=1750, 64.5% female) and two clinical (n=426, 100% female) samples combined to perform four secondary-data analyses: 5-HTTLPR x Traumatic Life Events to predict ED status (n=909), 5-HTTLPR x Sexual and Physical Abuse to predict bulimic symptoms (n=1097), 5-HTTLPR x Depression to predict bulimic symptoms (n=1256), and 5-HTTLPR x Impulsiveness to predict disordered eating (n=1149). Results Under a multiplicative model, the low function (s) allele of 5-HTTLPR interacted with traumatic life events and experiencing both sexual and physical abuse (but not only one) to predict increased likelihood of an ED and bulimic symptoms, respectively. However, under an additive model there was also an interaction between sexual and physical abuse considered independently and 5-HTTLPR, and no interaction with traumatic life events. No other GxE interactions were significant. Conclusion Early promising results should be followed-up with continued cross-institutional collaboration in order to achieve the large sample sizes necessary for genetic research.

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Section: Introductioncontrasting

confidence: 99%

A systematic review and secondary data analysis of the interactions between the serotonin transporter 5-HTTLPR polymorphism and environmental and psychological factors in eating disorders

Rozenblat

Ong

Fuller‐Tyszkiewicz

et al. 2017

Journal of Psychiatric Research

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“…The fact that less studies investigated COMT polymorphisms in BN, compared with AN, is consistent with the more limited neurobiological characterization of BN and with a less homogeneous description of its neuropsychological functioning (Degortes, Tenconi, Santonastaso, & Favaro, ; Van den Eynde et al, ). Moreover, the absence of an association between COMT Val158Met genotype and ED mirrors similar results for the serotonin transporter 5‐HTTLPR polymorphism, another monoamine modulating single polymorphism as previously reported (Rozenblat et al, ; Solmi et al, ).…”

Section: Discussionsupporting

confidence: 88%

“…However, since then, additional studies have explored the potential association between EDs and COMT, and studies evaluating the relevance of COMT genotype in BN have not been meta‐analysed to date. Therefore, the aim of the present meta‐analysis was to test whether COMT Val158Met polymorphism is associated with ED as a broad category, or specifically with AN or BN, summarizing all published evidence and adding novel data from the ‘ Biobanca Veneta per i Disturbi Alimentari ’ biobank (BIO.VEDA; Solmi et al, ).…”

Section: Introductionmentioning

confidence: 99%

Catechol‐O‐Methyltransferase (COMT) Val158Met Polymorphism and Eating Disorders: Data From a New Biobank and Meta‐Analysis of Previously Published Studies

Collantoni

Solmi

Gallicchio

et al. 2017

Euro Eating Disorders Rev

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“…Two meta-analyses also indicated that the short allele of 5-HTTLPR, a 5-HTT polymorphism, increased risk for AN compared with long allele carriers [14, 15]. However, a meta-analysis conducted in 2016 did not replicate these results [*16]. Although some candidate gene studies showed a significant association between Val158Met and Val66Met and AN, meta-analyses indicated no significant association between these polymorphisms and AN risk [17, 18].…”

Section: Historical Genetic Findingsmentioning

confidence: 99%

Genetics of Anorexia Nervosa

Baker

Schaumberg

Munn‐Chernoff

2017

Curr Psychiatry Rep

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Purpose of review: Genetic factors contribute to the etiology of anorexia nervosa (AN). This review synthesizes the current state of knowledge about the genetic etiology of AN, provides directions for future research, and discusses clinical implications for this research. Recent findings: Candidate gene meta-analyses indicate serotonin genes may be involved in the genetic etiology of AN. Three genome-wide association studies have been conducted and one genome-wide significant locus was identified. Cross-disorder analyses suggest shared genetic risk between AN and several psychiatric, educational, and medical phenotypes. Summary: Much has been learned about the genetic etiology of AN over the past three decades. However, to fully understand the genetic architecture, we must consider all aspects including common variation, cross-disorder analysis, rare variation, copy number variation, and gene-environment interplay. Findings have important implications for the development of treatment and prevention approaches and for how AN, and psychiatric and medical diseases in general, are conceptualized.

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Serotonin transporter gene polymorphism in eating disorders: Data from a new biobank and META-analysis of previous studies

Cited by 23 publications

References 46 publications

A systematic review and secondary data analysis of the interactions between the serotonin transporter 5-HTTLPR polymorphism and environmental and psychological factors in eating disorders

A systematic review and secondary data analysis of the interactions between the serotonin transporter 5-HTTLPR polymorphism and environmental and psychological factors in eating disorders

Catechol‐O‐Methyltransferase (COMT) Val158Met Polymorphism and Eating Disorders: Data From a New Biobank and Meta‐Analysis of Previously Published Studies

Genetics of Anorexia Nervosa

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