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Adverse life experiences, particularly those in childhood, contribute to disease morbidity and mortality [1, 2, 3, 4, 5, 6, 7]. There is considerable interest in understanding the mechanisms through which they do so, as it remains unclear how illness becomes apparent decades after the presumed initiating event. Long-standing hypotheses include chronic activation of the hypothalamic-pituitary-adrenal axis [8, 9, 10] and alterations of neuroimmune function [11]. Molecular signatures of stressful life experiences and their relation to disease are therefore of special interest to clarify the causal relationship between signature, disease, and stress.

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