Bierer Linda M, Bader Heather N, Daskalakis Nikolaos P, Lehrner Amy L, Makotkine Iouri, Seckl Jonathan R, Yehuda Rachel
James J. Peters VA Medical Center, Bronx, NY, United States; Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, United States.
University of Edinburgh, Queen's Medical Research Institute, Edinburgh EH16 4TJ, UK.
Psychoneuroendocrinology. 2014 Oct;48:1-10. doi: 10.1016/j.psyneuen.2014.06.001. Epub 2014 Jun 7.
Adult offspring of Holocaust survivors comprise an informative cohort in which to study intergenerational transmission of the effects of trauma exposure. Lower cortisol and enhanced glucocorticoid sensitivity have been previously demonstrated in Holocaust survivors with PTSD, and in offspring of Holocaust survivors in association with maternal PTSD. In other work, reduction in the activity of the enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD-2), which inactivates cortisol, was identified in Holocaust survivors in comparison to age-matched, unexposed Jewish controls. Therefore, we investigated glucocorticoid metabolism in offspring of Holocaust survivors to evaluate if similar enzymatic decrements would be observed that might help to explain glucocorticoid alterations previously shown for Holocaust offspring.
Holocaust offspring (n=85) and comparison subjects (n=27) were evaluated with clinical diagnostic interview and self-rating scales, and asked to collect a 24-h urine sample from which concentrations of cortisol and glucocorticoid metabolites were assayed by GCMS. 11β-HSD-2 activity was determined as the ratio of urinary cortisone to cortisol.
Significantly reduced cortisol excretion was observed in Holocaust offspring compared to controls (p=.046), as had been shown for Holocaust survivors. However, 11β-HSD-2 activity was elevated for offspring compared to controls (p=.008), particularly among those whose mothers had been children, rather than adolescents or adults, during World War II (p=.032). The effect of paternal Holocaust exposure could not be reliably investigated in the current sample.
The inverse association of offspring 11β-HSD-2 activity with maternal age at Holocaust exposure is consistent with the influence of glucocorticoid programming. Whereas a long standing reduction in 11β-HSD-2 activity among survivors is readily interpreted in the context of Holocaust related deprivation, understanding the directional effect on offspring will require replication and further exploration.
大屠杀幸存者的成年后代构成了一个信息丰富的队列,可用于研究创伤暴露影响的代际传递。先前已在患有创伤后应激障碍(PTSD)的大屠杀幸存者以及与母亲患PTSD相关的大屠杀幸存者后代中发现较低的皮质醇水平和增强的糖皮质激素敏感性。在其他研究中,与年龄匹配的未暴露犹太对照相比,在大屠杀幸存者中发现使皮质醇失活的2型11β-羟基类固醇脱氢酶(11β-HSD-2)的活性降低。因此,我们调查了大屠杀幸存者后代的糖皮质激素代谢,以评估是否会观察到类似的酶活性下降,这可能有助于解释先前在大屠杀后代中显示的糖皮质激素改变。
对大屠杀后代(n = 85)和对照受试者(n = 27)进行临床诊断访谈和自评量表评估,并要求他们收集24小时尿液样本,通过气相色谱-质谱联用仪(GCMS)测定其中皮质醇和糖皮质激素代谢物的浓度。11β-HSD-2活性通过尿可的松与皮质醇的比率来确定。
与对照组相比,大屠杀后代的皮质醇排泄量显著降低(p = 0.046),这与大屠杀幸存者的情况一致。然而,与对照组相比,后代的11β-HSD-2活性升高(p = 0.008),特别是在那些母亲在第二次世界大战期间还是儿童而非青少年或成年人的后代中(p = 0.032)。在当前样本中无法可靠地研究父亲大屠杀暴露的影响。
后代11β-HSD-2活性与大屠杀暴露时母亲年龄的负相关与糖皮质激素编程的影响一致。虽然幸存者中11β-HSD-2活性的长期降低很容易在与大屠杀相关的剥夺背景下得到解释,但要理解对后代的定向影响还需要重复研究和进一步探索。