Mikhail Megan E, Pascoe Laura A, Burt S Alexandra, Culbert Kristen M, Klump Kelly L
Department of Psychology, Michigan State University, East Lansing, Michigan, USA.
Department of Psychiatry and Behavioral Sciences, University of California, San Francisco, California, USA.
Int J Eat Disord. 2025 Mar;58(3):564-582. doi: 10.1002/eat.24360. Epub 2024 Dec 25.
Accumulating research suggests both eating disorders (EDs) and internalizing disorders (e.g., anxiety, depression) are associated with gastrointestinal disease (e.g., irritable bowel syndrome, inflammatory bowel disease). However, the mechanisms underlying comorbidity with gastrointestinal disease-and whether they may differ for eating and internalizing disorders-remain poorly understood. Addressing these gaps is a critical first step to refining etiologic models of comorbidity and identifying potential targets for intervention.
Participants included female and male twins ages 18-65 from the population-based MSU Twin Registry (N = 5883). Lifetime history of EDs, internalizing disorders, and gastrointestinal disease was assessed via questionnaire. We first examined whether EDs and internalizing disorders were independently associated with gastrointestinal disease phenotypically. We then used trivariate Cholesky decomposition twin models to investigate whether EDs and internalizing disorders were related to gastrointestinal disease through overlapping or distinct genetic/environmental pathways.
Eating (OR = 2.54, p = 0.009) and internalizing (OR = 2.14, p < 0.001) disorders were independently associated with gastrointestinal disease. Conclusions were unchanged after adjusting for important covariates (e.g., body mass index, age) and did not significantly differ across sex. Twin models suggested genetic influences shared by all three conditions explained their co-occurrence, with 31% of the variance in EDs and 12% of the variance in gastrointestinal disease attributable to genetic influences shared with internalizing disorders.
Shared genetic mechanisms may contribute to comorbidity between EDs, internalizing disorders, and gastrointestinal disease. Identifying overlapping molecular pathways could potentially lead to novel interventions that simultaneously address all three conditions.
越来越多的研究表明,饮食失调(EDs)和内化性障碍(如焦虑、抑郁)都与胃肠道疾病(如肠易激综合征、炎症性肠病)有关。然而,与胃肠道疾病共病的潜在机制——以及这些机制在饮食失调和内化性障碍中是否可能不同——仍知之甚少。填补这些空白是完善共病病因模型和确定潜在干预靶点的关键第一步。
参与者包括来自基于人群的密歇根州立大学双胞胎登记处的18 - 65岁的男性和女性双胞胎(N = 5883)。通过问卷调查评估饮食失调、内化性障碍和胃肠道疾病的终生病史。我们首先从表型上检查饮食失调和内化性障碍是否与胃肠道疾病独立相关。然后,我们使用三变量Cholesky分解双胞胎模型来研究饮食失调和内化性障碍是否通过重叠或不同的遗传/环境途径与胃肠道疾病相关。
饮食失调(OR = 2.54,p = 0.009)和内化性障碍(OR = 2.14,p < 0.001)与胃肠道疾病独立相关。在调整重要协变量(如体重指数、年龄)后结论不变,且在性别间无显著差异。双胞胎模型表明,这三种情况共有的遗传影响解释了它们的共现,饮食失调中31%的变异和胃肠道疾病中12%的变异可归因于与内化性障碍共有的遗传影响。
共同的遗传机制可能导致饮食失调、内化性障碍和胃肠道疾病之间的共病。识别重叠的分子途径可能会带来同时解决所有这三种情况的新干预措施。