Abstract Introduction Sleep problems are highly prevalent in the early postpartum period and often reflect the dynamic interplay of biopsychosocial influences. Inflammation, particularly the cytokine TNF-α, plays a regulatory role in sleep, with human studies linking higher TNF-α to alterations in sleep quality and rodent models demonstrating its somnogenic effects on NREM sleep. However, inflammatory pathways may also be shaped by developmental context, like early adversity. Although associations between threat-related early adversity and alterations in stress- and immune-system functioning have been identified, no research has examined whether such adversity moderates associations between inflammation and postpartum sleep. The current study examined whether threat-related adversity moderated the association between TNF-α and sleep problems at 6 weeks postpartum. Methods Participants included 151 pregnant women (49.7% white) who completed questionnaires on demographics and childhood adversity (MACE5) at 35 weeks gestation. Following prior work6, severity scores from seven subscales were summed to create a threat composite. At 6-weeks postpartum, mothers reported on their sleep (WHIIRS7) and provided serum samples assayed for TNF-α. Results Linear regression analysis showed threat-related adversity moderated the association between maternal inflammation and sleep problems (b = -0.074, SE = 0.038, p = .050). Follow-up simple slope analyses probed the association between TNF-α and sleep problems at low (-1 SD), mean-centered, and high (+1 SD) levels of threat. The association between TNF-α and postpartum sleep problems was significant at mean (b = -1.27, SE = 0.49, p = .010) and high (b = -2.36, SE = 0.74, p = .001) levels of threat, but not at low levels. Among mothers with higher threat-related adversity, elevated TNF-α was associated with fewer postpartum sleep problems. Conclusion Elevated TNF-α was associated with fewer sleep problems, consistent with evidence that TNF-α promotes NREM sleep, although only among women with moderate-to-high adversity. TNF-α’s sleep-promoting effects may be most evident under physiological strain, including postpartum recovery, and early threat may similarly heighten sensitivity to cytokine variation, calibrating immune responsivity in ways that make inflammatory signals more consequential for sleep. These patterns highlight the value of considering adversity when modeling perinatal biological risk and identifying mothers at elevated sleep-related risk. Support (if any)
Hinckley et al. (Fri,) studied this question.