More maternal vitamin D increases child cognition (petri dish, serotonin)

Maternal 25-hydroxyvitamin D is inversely correlated with fetal serotonin.

Clin Endocrinol (Oxf). 2016 Nov 12. doi: 10.1111/cen.13281. [Epub ahead of print]

Murthi P1,2, Davies-Tuck M2,3, Lappas M4, Singh H2, Mockler J2,3, Rahman R2,3, Lim R2, Leaw B2, Doery J5, Wallace EM2,3, Ebeling PR1.

1Department of Medicine, School of Clinical Sciences, Monash University, Melbourne, VIC, Australia.

2The Ritchie Centre, Hudson Institute of Medical Research, Melbourne, VIC, Australia.

3Department of Obstetrics and Gynaecology, School of Clinical Sciences, Monash University, Melbourne, VIC, Australia.

4Department of Obstetrics and Gynaecology, University of Melbourne, and the Mercy Hospital for Women, Heidelberg, VIC, Australia.

5Monash Pathology, Monash Health, Clayton, VIC, Australia.

OBJECTIVE:

Maternal vitamin D deficiency during pregnancy has been linked to impaired neurocognitive development in childhood . The mechanism by which vitamin D affects childhood neurocognition is unclear but may be via interactions with serotonin, a neurotransmitter involved in fetal brain development. In this study we aimed to explore associations between maternal and fetal vitamin D concentrations, and fetal serotonin concentrations at term.

STUDY DESIGN AND MEASUREMENTS:

Serum 25-hydroxyitamin D (25(OH)D, nmol/L) and serotonin (5-HT, nmol/L) concentrations were measured in maternal and umbilical cord blood from mother-infant pairs (n=64). Association between maternal 25(OH)D, cord 25(OH)D and cord serotonin was explored using linear regression, before and after adjusting for maternal serotonin levels. We also assessed the effects of siRNA knockdown of the vitamin D receptor (VDR) and administration of 10nM 1,25-dihydroxyvitamin D3 on serotonin secretion in human umbilical vein endothelial cells (HUVECs) in vitro.

RESULTS:

We observed an inverse relationship between both maternal and cord 25(OH)D concentrations with cord serotonin concentrations. The treatment of HUVECs with 1,25- dihydroxyvitamin D3 in vitro decreased the release of serotonin (193·9±14·8 nmol/L vs. 458·9±317·5 nmol/L, control, p<0·05). Conversely, inactivation of VDR increased serotonin release in cultured HUVECs.

CONCLUSIONS:

These observations provide the first evidence of an inverse relationship between maternal 25(OH)D and fetal serotonin concentrations. We propose that maternal vitamin D deficiency increases fetal serotonin concentrations and thereby contributes to longer-term neurocognitive impairment in infants and children. This article is protected by copyright. All rights reserved.

PMID: 27862146 DOI: 10.1111/cen.13281 Publisher rents PDF for $6