Dalle Molle Roberta, Fatemi Hajar, Dagher Alain, Levitan Robert D, Silveira Patricia P, Dubé Laurette
Desautels Faculty of Management, McGill Center for the Convergence of Health and Economics, McGill University, Bronfman Building, 1001 Sherbrooke St. W., Montreal, QC H3A 1G5, Canada; McConnell Brain Imaging Centre, Montreal Neurological Institute, McGill University, 3801 University Street, Montreal, QC H3A 2B4, Canada.
Desautels Faculty of Management, McGill Center for the Convergence of Health and Economics, McGill University, Bronfman Building, 1001 Sherbrooke St. W., Montreal, QC H3A 1G5, Canada.
Neurosci Biobehav Rev. 2017 Feb;73:326-339. doi: 10.1016/j.neubiorev.2016.12.028. Epub 2016 Dec 23.
The differential susceptibility model states that a given genetic variant is associated with an increased risk of pathology in negative environments but greater than average resilience in enriched ones. While this theory was first implemented in psychiatric-genetic research, it may also help us to unravel the complex ways that genes and environments interact to influence feeding behavior and obesity. We reviewed evidence on gene vs. environment interactions that influence obesity development, aiming to support the applicability of the differential susceptibility model for this condition, and propose that various environmental "layers" relevant for human development should be considered when bearing the differential susceptibility model in mind. Mother-child relationship, socioeconomic status and individual's response are important modifiers of BMI and food intake when interacting with gene variants, "for better and for worse". While only a few studies to date have investigated obesity outcomes using this approach, we propose that the differential susceptibility hypothesis is in fact highly applicable to the study of genetic and environmental influences on feeding behavior and obesity risk.
差异易感性模型指出，特定的基因变异在负面环境中与病理风险增加相关，但在丰富环境中则具有高于平均水平的恢复力。虽然这一理论最初应用于精神遗传学研究，但它或许也能帮助我们揭示基因与环境相互作用影响进食行为和肥胖的复杂方式。我们综述了关于基因与环境相互作用影响肥胖发生的证据，旨在支持差异易感性模型对这种情况的适用性，并提出在考虑差异易感性模型时，应考虑与人类发育相关的各种环境“层面”。母婴关系、社会经济地位和个体反应在与基因变异相互作用时，无论好坏，都是体重指数和食物摄入量的重要调节因素。虽然迄今为止只有少数研究采用这种方法调查肥胖结果，但我们认为差异易感性假说实际上非常适用于研究基因和环境对进食行为及肥胖风险的影响。
