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Contribution of the 5-HTTLPR gene by neuroticism on weight gain in male and female participants

Markus, C. Rob; Capello, Aimee E.M.

doi: 10.1097/YPG.0b013e328358632a
Original Articles

Introduction: Reduced brain serotonin (5-HT) function is believed to increase the risk for eating-related disturbances. Differences in 5-HT vulnerability are genetically determined, including a short (S) allele polymorphism in the serotonin transporter gene (5-HTTLPR) that is associated with serotonin dysfunction and is therefore believed to increase the risk for obesity. However, considerable variability has been apparent to replicate these findings.

Objective: Because reduced control of energy intake often results from distress and negative mood (emotional eating) and because brain 5-HT controls stress adaptation and mood changes, the aim of the current study was to investigate whether the S-allele may particularly contribute toward weight gain in cognitive stress-vulnerable individuals with high neuroticism.

Methods: A total of 857 healthy young male and female college students (21.0±2.1 years; BMI 19–25 kg/m2) were genotyped for the 5-HTTLPR polymorphism S′/S′ (S/S, S/LG, LG/LG), S′/L′ (S/La, La/Lg) and L′/L′ (LA/LA) and trait neuroticism. The interaction of 5-HTTLPR by neuroticism was assessed on BMI.

Results: BMI increased significantly as a function of the presence of the S-allele of 5-HTTLPR only in high neurotic individuals.

Conclusion: These results indicate that cognitive stress vulnerabilities are critical mediators of the association between 5-HTTLPR and body weight.

Department of Neuropsychology and Psychopharmacology, Faculty of Psychology and Neuroscience, Maastricht University, Maastricht, The Netherlands

Correspondence to C. Rob Markus, PhD, Department of Neuropsychology and Psychopharmacology, Faculty of Psychology and Neuroscience, Maastricht University, Room 2.773, Universiteitssingel 40, 6229 ER Maastricht, The Netherlands Tel: +31 43 3882474; fax: +31 43 3884196; e-mail: r.markus@psychology.unimaas.nl

Received October 17, 2011

Accepted May 3, 2012

© 2012 Lippincott Williams & Wilkins, Inc.