Abstract

Vitamin D deficiency and elevated pro-inflammatory cytokines have each been associated individually with postpartum depression (PPD). African American women are at increased risk for prenatal vitamin D deficiency, inflammation, and prenatal and postpartum depressive symptoms, but biological risk factors for PPD in this population have rarely been tested. This prospective study tested whether low prenatal vitamin D status (serum 25-hydroxyvitamin D, 25[OH]D) predicted PPD symptomatology in pregnant African American women and whether high levels of prenatal inflammatory cytokines interacted with low 25(OH)D in effects on PPD symptoms. Vitamin D status was measured in the first trimester in a sample of 91 African American pregnant women who had a second trimester blood sample assayed for inflammatory markers. Depressive symptoms were assessed at a postpartum visit. An inverse association between prenatal log 25(OH)D and PPD symptomatology approached significance (β = -0.209, p = 0.058), and interleukin-6 and IL-6/IL-10 ratio significantly moderated the effect. Among women with higher levels of inflammatory markers, lower prenatal log 25(OH)D was associated with significantly higher PPD symptoms (p < 0.05). These preliminary results are intriguing because, if replicable, easy translational opportunities, such as increasing vitamin D status in pregnant women with elevated pro-inflammatory cytokines, may reduce PPD symptoms.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.