School of Epidemiology, Public Health and Preventive Medicine, University of Ottawa, Ottawa, Canada.
School of Social and Community Medicine, University of Bristol, Bristol, UK.
J Am Acad Child Adolesc Psychiatry. 2016 Aug;55(8):709-716.e2. doi: 10.1016/j.jaac.2016.05.014. Epub 2016 Jun 2.
The fetal programming hypothesis posits that in utero exposure to stress can alter prenatal brain development and lifelong stress response. However, human studies linking objective prenatal stressors to offspring mental illness, especially depression, are rare. The purpose of this study was to examine the association between mothers' exposure to prenatal stressful life events (SLEs) and offspring depression.
The sample comprised 10,569 members of a prospective population-based cohort, the Avon Longitudinal Study of Parents and Children (ALSPAC). Mothers reported on the occurrence and impact of 42 prenatal SLEs. Offspring depressive symptoms were assessed using a computerized version of the Clinical Interview Schedule-Revised (CIS-R) at age 17 to 18, as well as 13 self-report statements from the Short Mood and Feelings Questionnaire (SMFQ) at 6 time points from ages 10 to 11 to 18 to 19. Latent class growth analysis (LCGA) was used to identify trajectories of depressive symptoms across adolescence.
After adjusting for potential confounders, a 1-unit increase in maternal SLE scores (range, 0-168) during gestation was associated with increased offspring depressive symptoms (β = 0.07, p < .01) and major depression (odds ratio [OR] = 1.03, 95% CI 1.01, 1.06) at age 17 to 18. LCGA revealed 4 trajectories of depressive symptoms. High maternal SLEs (fourth quartile) were associated with membership in the trajectory characterized by stable, high levels of depression from age 10 to 11 to 18 to 19 years (OR = 1.72, 95% CI = 1.09, 2.71).
These results provide support for the fetal programming hypothesis, demonstrating that prenatal exposure to acute stress is associated with offspring depression in adolescence. Stress management may be of benefit for expectant mothers.
胎儿编程假说认为，子宫内暴露于压力会改变产前大脑发育和终生应激反应。然而，将客观的产前压力源与后代精神疾病（尤其是抑郁症）联系起来的人类研究很少。本研究旨在探讨母亲产前应激性生活事件（SLE）暴露与后代抑郁症之间的关联。
该样本包括前瞻性人群队列——阿冯纵向父母与子女研究（ALSPAC）的 10569 名成员。母亲报告了 42 项产前 SLE 的发生和影响。在 17 至 18 岁时，使用计算机化的临床访谈量表修订版（CIS-R）评估后代的抑郁症状，在 10 至 11 岁至 18 至 19 岁的 6 个时间点使用简短情绪和感觉问卷（SMFQ）的 13 个自我报告陈述评估抑郁症状。使用潜在类别增长分析（LCGA）来确定青少年期抑郁症状的轨迹。
在调整了潜在的混杂因素后，妊娠期间母体 SLE 评分（范围为 0-168）增加 1 个单位与后代抑郁症状增加（β=0.07，p<.01）和 17 至 18 岁时的主要抑郁症（比值比[OR]为 1.03，95%CI 为 1.01，1.06）相关。LCGA 显示出 4 种抑郁症状轨迹。母体 SLE 较高（四分位间距）与从 10 至 11 岁到 18 至 19 岁期间具有稳定、高水平抑郁的轨迹成员身份相关（OR=1.72，95%CI=1.09，2.71）。
这些结果为胎儿编程假说提供了支持，表明产前暴露于急性应激与青春期后代的抑郁症有关。应激管理可能对孕妇有益。
