未经证实:儿童时期较高的BMI与情绪和行为问题有关,但是这些关联可能不是因果关系。先前的遗传研究结果暗示了因果关系,但可能反映了人口统计学和家庭环境的影响。
UNASSIGNED:这项研究使用了来自挪威母亲的40,949名8岁儿童及其父母的数据,父亲和儿童队列研究(MoBa)和挪威医学出生登记处(MBRN)。我们调查了BMI对抑郁症状的影响,焦虑,和8岁时的注意力缺陷多动障碍(ADHD)。我们应用了家庭内孟德尔随机化,通过控制亲本基因型来解释家族效应。
UNASSIGNED:使用与成人BMI相关的遗传变异进行的家庭内孟德尔随机化估计表明,儿童自身的BMI增加了他们的抑郁症状(BMI每增加5kg/m2,β=0.26S.D.,CI=-0.01,0.52,p=0.06)和ADHD症状(β=0.38S.D.,CI=0.09,0.63,p=0.009)。这些估计还表明母亲的BMI,或相关因素,可能独立影响儿童的抑郁症状(每增加5kg/m2的母亲BMI,β=0.11S.D.,CI:0.02,0.09,p=0.01)。然而,使用与回顾性报道的儿童体型相关的遗传变异进行的家庭内孟德尔随机化不支持BMI对这些结局的影响.几乎没有证据表明父母的BMI会影响孩子的ADHD症状,或者孩子或父母的BMI影响了孩子的焦虑症状。
未经评估:我们发现不一致的证据表明儿童的BMI影响他们的抑郁和多动症症状,很少有证据表明儿童的BMI会影响他们的焦虑症状。父母BMI的影响证据有限。无关个体样本的遗传研究,或者使用与成人BMI相关的遗传变异,可能高估了孩子自身BMI的因果效应。
UNASSIGNED:这项研究由健康基金会资助。这是“收获”合作的一部分,由挪威研究委员会支持。个人共同作者资助:欧洲研究理事会,挪威东南部地区卫生局,挪威研究理事会,她的背心,诺和诺德基金会,卑尔根大学,挪威东南部地区卫生局,TrondMohn基金会,挪威西部地区卫生局,挪威糖尿病协会英国医学研究委员会。医学研究理事会(MRC)和布里斯托尔大学支持MRC综合流行病学部门。
一些研究表明,肥胖儿童更有可能被诊断为抑郁症,焦虑,或注意力缺陷多动障碍(ADHD)。但这并不一定意味着肥胖会导致这些疾病。抑郁症,焦虑,或多动症可能导致肥胖。一个孩子的环境,包括家庭收入或父母的心理健康,也会影响孩子的体重和心理健康。了解这些关系的性质可以帮助科学家针对肥胖和精神健康状况制定更好的干预措施。遗传研究可以帮助科学家更好地了解环境在这些条件下的作用,但在这些分析中,考虑孩子和他们父母的基因是很重要的。这是因为父母和孩子不仅共享基因,还有环境条件。例如,携带与较高体重相关的遗传变异的家庭也可能收入较低,如果父母受到社会和工作场所对较重人群的偏见的影响。由于父母体重的影响,这些家庭中的孩子可能会有更糟糕的心理健康,而不是自己的体重。研究儿童和成人的遗传学可以帮助解开这些过程。休斯等人。显示孩子自己的体重指数,体重和身高的比率,与孩子的心理健康症状没有强烈关联。他们分析了基因,体重,以及约41,000名8岁儿童及其父母的健康调查数据。结果表明,儿童自身的BMI对他们的焦虑症状没有很大影响。也没有明确的证据表明儿童的BMI影响他们的抑郁症或ADHD症状。这些结果与以前的研究相矛盾,这并没有解释父母的遗传学。休斯等人。建议,至少对8岁的孩子来说,与成人体重相关的因素以及家庭之间的差异可能比儿童自身的体重对儿童的心理健康更为重要。对于年龄较大的儿童和青少年,可能不是这样,个人的体重可能更重要。因此,旨在减少儿童中期肥胖的政策不太可能大大改善儿童的心理健康。另一方面,针对导致较高体重的环境或社会因素的政策,对体重较高的人有偏见,和不良儿童心理健康直接可能更有益。
Higher BMI in childhood is associated with emotional and behavioural problems, but these associations may not be causal. Results of previous genetic studies imply causal effects but may reflect influence of demography and the family environment.
This study used data on 40,949 8-year-old children and their parents from the Norwegian Mother, Father and Child Cohort Study (MoBa) and Medical Birth Registry of Norway (MBRN). We investigated the impact of BMI on symptoms of depression, anxiety, and attention-deficit hyperactivity disorder (ADHD) at age 8. We applied within-family Mendelian randomization, which accounts for familial effects by controlling for parental genotype.
Within-family Mendelian randomization estimates using genetic variants associated with BMI in adults suggested that a child\'s own BMI increased their depressive symptoms (per 5 kg/m2 increase in BMI, beta = 0.26 S.D., CI = -0.01,0.52, p=0.06) and ADHD symptoms (beta = 0.38 S.D., CI = 0.09,0.63, p=0.009). These estimates also suggested maternal BMI, or related factors, may independently affect a child\'s depressive symptoms (per 5 kg/m2 increase in maternal BMI, beta = 0.11 S.D., CI:0.02,0.09, p=0.01). However, within-family Mendelian randomization using genetic variants associated with retrospectively-reported childhood body size did not support an impact of BMI on these outcomes. There was little evidence from any estimate that the parents\' BMI affected the child\'s ADHD symptoms, or that the child\'s or parents\' BMI affected the child\'s anxiety symptoms.
We found inconsistent evidence that a child\'s BMI affected their depressive and ADHD symptoms, and little evidence that a child\'s BMI affected their anxiety symptoms. There was limited evidence of an influence of parents\' BMI. Genetic studies in samples of unrelated individuals, or using genetic variants associated with adult BMI, may have overestimated the causal effects of a child\'s own BMI.
This research was funded by the Health Foundation. It is part of the HARVEST collaboration, supported by the Research Council of Norway. Individual co-author funding: the European Research Council, the South-Eastern Norway Regional Health Authority, the Research Council of Norway, Helse Vest, the Novo Nordisk Foundation, the University of Bergen, the South-Eastern Norway Regional Health Authority, the Trond Mohn Foundation, the Western Norway Regional Health Authority, the Norwegian Diabetes Association, the UK Medical Research Council. The Medical Research Council (MRC) and the University of Bristol support the MRC Integrative Epidemiology Unit.
Some studies show that children with obesity are more likely to receive a diagnosis of depression, anxiety, or attention-deficit hyperactivity disorder (ADHD). But this does not necessarily mean obesity causes these conditions. Depression, anxiety, or ADHD could cause obesity. A child\'s environment, including family income or their parents\' mental health, could also affect a child\'s weight and mental health. Understanding the nature of these relationships could help scientists develop better interventions for both obesity and mental health conditions. Genetic studies may help scientists better understand the role of the environment in these conditions, but it\'s important to consider both the child\'s and their parents’ genetics in these analyses. This is because parents and children share not only genes, but also environmental conditions. For example, families that carry genetic variants associated with higher body weight might also have lower incomes, if parents have been affected by biases against heavier people in society and the workplace. Children in these families could have worse mental health because of effects of their parent’s weight, rather than their own weight. Looking at both child and adult genetics can help disentangle these processes. Hughes et al. show that a child\'s own body mass index, a ratio of weight and height, is not strongly associated with the child’s mental health symptoms. They analysed genetic, weight, and health survey data from about 41,000 8-year-old children and their parents. The results suggest that a child\'s own BMI does not have a large effect on their anxiety symptoms. There was also no clear evidence that a child\'s BMI affected their symptoms of depression or ADHD. These results contradict previous studies, which did not account for parental genetics. Hughes et al. suggest that, at least for eight-year-olds, factors linked with adult weight and which differ between families may be more critical to a child\'s mental health than a child’s own weight. For older children and adolescents, this may not be the case, and the individual’s own weight may be more important. As a result, policies designed to reduce obesity in mid-childhood are unlikely to greatly improve the mental health of children. On the other hand, policies targeting the environmental or societal factors contributing to higher body weights, bias against people with higher weights, and poor child mental health directly may be more beneficial.