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Updated: Mar 11, 2026

Author Spotlight: Studying the Impact of Maternal Dietary Deficiencies on Long-Term Offspring Health Outcomes
Published on: June 28, 2024
Maternal 25-hydroxyvitamin D is inversely correlated with foetal serotonin
Padma Murthi1,2, Miranda Davies-Tuck2,3, Martha Lappas4,5
1Department of Medicine, School of Clinical Sciences, Monash University, Melbourne, Vic., Australia.
Insights
Maternal vitamin D deficiency may increase fetal serotonin levels, potentially impacting infant neurodevelopment. This study found an inverse link between vitamin D and fetal serotonin, suggesting a mechanism for cognitive impairment.
Area of Science:
- Neuroscience
- Endocrinology
- Developmental Biology
Background:
- Maternal vitamin D deficiency is linked to impaired childhood neurocognitive development.
- The precise mechanism remains unclear but may involve serotonin, a key neurotransmitter in fetal brain development.
Purpose of the Study:
- To investigate the association between maternal and fetal vitamin D levels and fetal serotonin concentrations.
- To explore the role of vitamin D in regulating fetal serotonin.
Main Methods:
- Measured serum 25-hydroxyvitamin D (25(OH)D) and serotonin (5-HT) in maternal and umbilical cord blood (n=64).
- Utilized linear regression to analyze associations between vitamin D and serotonin.
- Assessed the in vitro effects of vitamin D receptor (VDR) modulation on serotonin secretion in human umbilical vein endothelial cells (HUVECs).
Main Results:
- An inverse relationship was observed between maternal and cord 25(OH)D concentrations and cord serotonin levels.
- In vitro, 1,25-dihydroxyvitamin D3 treatment decreased serotonin release in HUVECs.
- Inactivation of the VDR increased serotonin release in cultured HUVECs.
Conclusions:
- This study provides the first evidence of an inverse relationship between maternal 25(OH)D and fetal serotonin.
- Maternal vitamin D deficiency may lead to increased fetal serotonin, potentially contributing to neurocognitive impairments in infants and children.
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 foetal brain development. In this study, we aimed to explore associations between maternal and foetal vitamin D concentrations, and foetal serotonin concentrations at term.
Study Design And Measurements:
Serum 25-hydroxyvitamin 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 10 nm 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 foetal serotonin concentrations. We propose that maternal vitamin D deficiency increases foetal serotonin concentrations and thereby contributes to longer-term neurocognitive impairment in infants and children.
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