Introduction: In the UK, the number of comorbidities seen in children has increased along with the worsening obesity rate. These comorbidities worsen into adulthood. Genome-wide association studies have highlighted single nucleotide polymorphisms associated with the weight status of adults and offspring individually. To date, in the UK, parental genetic, lifestyle, and social determinants of health have not been investigated alongside one another as influencers of offspring weight status. A comprehensive obesity prevention scheme would commence prior to conception and involve parental intervention including all known risk factors. This current study aims to identify the proportion of overweight that can be explained by known parental risk factors, including genetic, lifestyle, and social determinants of health with offspring weight status in the UK. Methods: A cross-sectional study was carried out on 123 parents. Parental and offspring anthropometric data and parental lifestyle and social determinants of health data were self-reported. Parental genetic data were collected by use of GeneFiX saliva collection vials and genotype were assessed for brain-derived neurotrophic factor (BDNF) gene rs6265, melanocortin 4 receptor (MC4R) gene rs17782313, transmembrane protein 18 (TMEM18) gene rs2867125, and serine/threonine-protein kinase (TNN13K) gene rs1514175. Associations were assessed between parental data and the weight status of offspring. Results: Maternal body mass index modestly predicted child weight status (p < 0.015; R2 = 0.15). More mothers of overweight children carried the MC4R rs17782313 risk allele (77.8%; p = 0.007) compared to mothers of normal-weight children. Additionally, fathers who were not Caucasian and parents who slept for <7 h/night had a larger percentage of overweight children when compared to their counterparts (p = 0.039; p = 0.014, respectively). Conclusion: Associations exist between the weight status of offspring based solely on parental genetic, lifestyle, and social determinants of health data. Further research is required to appropriately address future interventions based on genetic and lifestyle risk groups on a pre-parent cohort.

中文翻译：

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父母遗传、生活方式和健康的社会决定因素与后代超重的关联

简介：在英国，儿童合并症的数量随着肥胖率的恶化而增加。这些合并症会恶化到成年。全基因组关联研究强调了与成人和后代个体体重状况相关的单核苷酸多态性。迄今为止，在英国，尚未对父母遗传、生活方式和健康的社会决定因素作为后代体重状况的影响因素进行调查。一个全面的肥胖预防计划将在受孕之前开始，并涉及包括所有已知风险因素在内的父母干预。目前的这项研究旨在确定可以由已知的父母风险因素解释的超重比例，包括遗传、生活方式、和英国后代体重状况的健康社会决定因素。方法：对 123 名父母进行横断面研究。父母和后代的人体测量数据以及父母的生活方式和健康数据的社会决定因素是自我报告的。使用 GeneFiX 唾液收集瓶收集父母遗传数据，并评估脑源性神经营养因子 (BDNF) 基因 rs6265、黑皮质素 4 受体 (MC4R) 基因 rs17782313、跨膜蛋白 18 (TMEM18) 基因 rs2867125 和丝氨酸/丝氨酸的基因型-蛋白激酶 (TNN13K) 基因 rs1514175。评估了父母数据与后代体重状况之间的关联。结果：母亲体重指数适度预测儿童体重状态（p < 0.015；R2 = 0.15）。更多超重儿童的母亲携带 MC4R rs17782313 风险等位基因 (77.8%; p = 0.007）与正常体重孩子的母亲相比。此外，与同龄人相比，非白种人的父亲和每晚睡眠时间小于 7 小时的父母的超重儿童比例更高（分别为 p = 0.039；p = 0.014）。结论：仅基于父母遗传、生活方式和健康数据的社会决定因素，后代的体重状况之间存在关联。需要进一步研究，以根据前父母队列中的遗传和生活方式风险群体适当地解决未来的干预措施。仅基于父母遗传、生活方式和健康数据的社会决定因素，后代的体重状况之间存在关联。需要进一步研究，以根据前父母队列中的遗传和生活方式风险群体适当地解决未来的干预措施。仅基于父母遗传、生活方式和健康数据的社会决定因素，后代的体重状况之间存在关联。需要进一步研究，以根据前父母队列中的遗传和生活方式风险群体适当地解决未来的干预措施。