Aim The bidirectional association between obesity and depression seen in adults is not clearly established in adolescents. The aim of this study was to investigate the longitudinal association between body mass index (BMI), depressive symptoms and interactions between bullying victimization and BMI, taking gender differences into account. Subjects and methods In a Swedish county, self-reported bullying victimization, BMI and depressive symptoms from 1729 adolescents ($$ \overline{y} $$ y ¯ = 14.4, 56% females) were collected in 2012 (wave 1), in 2015 (wave 2) ($$ \overline{y}=17.3 $$ y ¯ = 17.3 ) and in 2018 (wave 3) ($$ \overline{y} $$ y ¯ = 19.9). Longitudinal associations were assessed using binary logistic regression models controlling for confounding factors. Interaction effects between BMI and victimization on depressive symptoms were also assessed. Results Wave 1 obese males had approximately six times increased odds ratio compared to normal weight, for wave 2 depressive symptoms. W1 overweight was associated with an odds ratio of 1.5 in all participants for wave 3 depressive symptoms. Victimization was consistently associated with higher odds ratio for future depressive symptoms. We found interaction effects between bullying victimization and BMI for future depressive symptoms with different patterns depending on sex. Conclusion Given the present findings, bullying needs to be prevented, and, if it occurs, it needs to be stopped at an early stage to prevent future depressive symptoms.

The severity of symptoms as well as efficacy of antidepressants in major depressive disorder (MDD) is modified by single nucleotide polymorphisms (SNPs) in different genes, which may contribute in an additive or synergistic fashion. We aimed to investigate depression severity in participants with MDD under treatment with antidepressants in relation to the combinatory effect of selected genetic variants combined using a genetic risk score (GRS). The sample included 150 MDD patients on regular AD therapy from the population‐based Swiss PsyCoLaus cohort. We investigated 44 SNPs previously associated with antidepressant response by ranking them with regard to their association to the Center for Epidemiologic Studies Short Depression Scale (CES‐D) score using random forest. The three top scoring SNPs (rs12248560, rs878567, rs17710780) were subsequently combined into an unweighted GRS, which was included in linear and logistic regression models using the CES‐D score, occurrence of a major depressive episode (MDE) during follow‐up and regular antidepressant treatment during the 6 months preceding follow‐up assessment as outcomes. The GRS was associated with MDE occurrence (p = .02) and ln CES‐D score (p = .001). The HTR1A rs878567 variant was associated with ln CES‐D after adjustment for demographic and clinical variables [p = .02, lower scores for minor allele (G) carriers]. Additionally, rs12248560 (CYP2C19) CC homozygotes showed a six‐fold higher likelihood of regular AD therapy at follow‐up compared to minor allele homozygotes [TT; ultrarapid metabolizers (p = .03)]. Our study suggests that the cumulative consideration of pharmacogenetic risk variants more reliably reflects the impact of the genetic background on depression severity than individual SNPs.

Depression affects one in five persons at 18 years of age. Allele A of the brain-derived neurotrophic factor (BDNF) rs6265 is considered to be a risk factor for depression. Previous studies of the interaction between BDNF rs6265, early adversity, and/or physical activity have shown mixed results. In this study, we explored the relation between BDNF rs6265 polymorphism and childhood stress, as well as the moderating effect of physical activity in relation to depressive symptoms using binary logistic regressions and process models 1, 2 and 3 applied to data obtained at three times (waves 1, 2 and 3) from the Survey of Adolescent Life in Västmanland cohort study (SALVe). Results revealed that both childhood stress and physical activity had a moderation effect; physical activity in wave 1 with an R2 change = 0.006, p = 0.013, and the Johnson–Neyman regions of significance (RoS) below 1.259, p = 0.05 for 11.97%; childhood stress in wave 2 with the R2 change = 0.008, p = 0 002, and RoS below 1.561 with 26.71% and >4.515 with 18.20%; and a three-way interaction in wave 1 in genotype AA carriers. These results suggest that allele A is susceptible to physical activity (positive environment) and childhood stress (negative environment).

Objective: Breastfeeding, which is important for early growth, is a possible moderator of genetic influence, such as the effect of the fat mass and obesityassociated gene (FTO) on body mass index (BMI). The aim of this study was to assess the moderating effect of breastfeeding duration on the relationship between FTO rs9939609 and BMI in a Caucasian sample. Methods: Adolescents born in 1997 and in 1999, who were living in the Swedish county Västmanland in 2012, were invited to participate in the Survey of Adolescent Life in Västmanland. The adolescents and their parents completed self-reported questionnaires in 2012, 2015, and 2018. Genotyping of rs9939609 T > A polymorphism was conducted from saliva DNA samples. Interaction effects of parental reported breastfeeding duration in months, including regions of significance, on the relationship between rs9939609 and BMI plus overweight were assessed.Results: Considering physical activity levels, parental reported breastfeeding duration was a moderator of the relationship between rs9939609 and BMI for the younger (regions of significance = <1.6 and >28.1 months) and older adolescents (region of significance = >19.9 months), but not for the young adults. Plots of the association between breastfeeding duration and BMI showed higher BMI for AA with short breastfeeding, but lower BMI with longer breastfeeding than AT and TT.Longer breastfeeding lowered the odds for overweight among the younger adolescents, especially among AA individuals. Conclusion:Rs9939609 AA individuals were more susceptible than AT and TT individuals to both short and long breastfeeding durations, which is consistent with the differential susceptibility hypothesis. FTO rs9939609 AA might be a plasticityThis is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.