Objectives. To investigate whether there is an association between adolescent obesity and depression in a nonclinical population and whether psychosocial and economic status and subjective experiences of shame (defined as experiences of being degraded or ridiculed by others) may account for such an association. Method.We examined associations between self-reported body mass index (BMI) and depression, controlling for gender, shame, parental employment, parental separation, and economy. The study was performed on a sample of 4703 adolescents (71% of the target population of 15- and 17-year-old students in 1 Swedish County) who answered the Survey of Adolescent Life in Vestmanland 2004. Results.Obesity was significantly related to depression and depressive symptoms among 15- and 17-year-olds. Obesity was also significantly related to experiences of shame. All significant association between BMI grouping and depression according to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition disappeared when shaming experiences, parental employment, and parental separation were controlled for. Adolescents who reported many experiences of shame had an increased risk (odds ratio: 11.3; confidence interval: 8.3–14.9) for being depressed. Conclusions.There is a significant statistical association between adolescent obesity and depression. Effects of experiences of shame, parental separation, and parental employment explain this association. These results suggest that clinical treatment of obesity may sometimes not just be a matter of diet and exercise but also of dealing with issues of shame and social isolation.

Previous research has demonstrated that a polymorphism in the serotonin transporter gene (5-HTTLPR) and adverse psychosocial circumstances interact t

A functional VNTR polymorphism in the promoter of the monoamine oxidase A gene (MAOA-LPR) has previously been shown to be an important predictor of antisocial behavior in men. Testosterone analogues are known to interact with the MAOA promoter in vitro to influence gene transcription as well as in vivo to influence CSF levels of the MAO metabolite 3-methoxy-4-hydroxyphenylglycol (MHPG) in human males. We examined the possible joint effects of testosterone (measured in CSF) and MAOA-LPR genotype on antisocial personality disorder and scores on the Brown–Goodwin Aggression scale in 95 unrelated male criminal alcoholics and 45 controls. The results confirm that MAOA genotype and CSF testosterone interact to predict antisocial behaviors. The MAOA/testosterone interaction also predicted low levels of CSF MHPG, which tentatively suggests the possibility that the interaction may be mediated by a direct effect on gene transcription. If replicated these findings offer plausible explanations for previous inconsistencies in studies of the relationship between testosterone and male human aggression, as well as for how MAOA genotype may influence aggressive behavior in human males.