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

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/m(2)) were genotyped for the 5-HTTLPR polymorphism S'/S' (S/S, S/L(G), L(G)/L(G)), S'/L' (S/L(a), L(a)/Lg) and L'/L' (L(A)/L(A)) 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.