Prenatal and early postnatal stress and later life inflammation

Evidence suggests that maternal psychological and social stress during the prenatal period and in childhood represent an important condition that may adversely impact the anatomy and physiology of the developing child with implications for a number of health-related conditions and disorders. In a large prospective study, we aim to address if social stressors in the prenatal and early postnatal periods, as individual exposures as well as their accumulation, are associated with a range of inflammatory markers in late middle-aged offspring.

The study sample includes Danish men and women born between 1959 and 1961 (n = 1206) who were members of the Copenhagen Perinatal Cohort and participated in the Copenhagen Aging and Midlife Biobank in 2009-2011 (age 49-52). Information on social stressors was collected through an interview with the mothers at the first antenatal visit and postnatal stressor data was collected at year one follow-up. A series of ordinary least square regression models were performed with the stress measures as the exposures and C-reactive protein (CRP), Interleukin-6 (IL-6), Interleukin-10 (IL-10), and Tumor necrosis factor α (TNF-α) separately as the outcomes.

The individual prenatal maternal stressors (being unmarried and having an unwanted pregnancy) and the prenatal index were associated with higher levels of CRP and IL-6 among offspring but not with IL-10 or TNF-α. Low social status, but not living away from parents or having an unmarried mother in the first year of life, was associated with higher levels of CRP and IL-6. The accumulation of social stressors in the early postnatal period was associated with higher levels of CRP and IL-6 but not IL-10 and TNF-α. The accumulation of stressors in the prenatal and postnatal periods combined was associated with higher levels of CRP and IL-6, but not with IL-10 or TNF-α.

The findings suggest that exposure to the accumulation of prenatal and early life stressors, is associated with higher levels of CRP and IL-6 in later life. This may indicate that the effects of early stressors on later inflammation operate through pathways with clear links to cardiovascular disease.