PLoS One, 15 (1), e0227193 2020 Jan 29 eCollection 2020, DOI: 10.1371/journal.pone.0227193
Aishwarya P Yadama 1, Hooman Mirzakhani 1, Thomas F McElrath 2, Augusto A Litonjua 3, Scott T Weiss 1
- Hypertension during pregnancy: low Vitamin D, poor Vit. D genes – June 2022
- After lactation Vitamin D levels are low, increased risk of Breast Cancer, vitamin D should decrease risk – Aug 2021
- Gestational Diabetes – increased risk if poor Vitamin D Receptor – 2 Meta-Analyses 2021
- Higher risk of Recurrent Pregnancy Loss if poor Vitamin D Receptor – Feb 2021
- Spontaneous Miscarriage strongly associated with 2 vitamin D genes – March 2020
- Preterm birth associated with many genes, including the Vitamin D Receptor again – Jan 2020
- Preterm birth 8X more likely if poor Vitamin D Receptor – Dec 2019
- Preterm birth 9 X more likely if fetus had a poor Vitamin D Receptor and previous miscarriage – Aug 2017
- Recurrent miscarriage occurs 2.2 more often if poor Vitamin D Receptor – Aug 2019
- Gestational Diabetes 2.4X more likely if poor Vitamin D Receptor (region in China) – June 2019
- Gestational Diabetes 3 X more likely if poor Vitamin D receptor (Turkey) – May 2019
- Preeclampsia 2X more likely if poor Vitamin D Receptor – April 2019
- Preterm births 12 X more likely if poor Vitamin D Receptor (white infants in Italy) – meta-analysis Aug 2018
- UV at time of conception associated with Vitamin D Receptor activation 65 years later – Sept 2017
- A good Vitamin D Receptor (or perhaps more vitamin D) protects against lead during pregnancy
- Vitamin D Receptor is associated with preeclampsia, gestational diabetes and preterm birth – Nov 2017
- Gestational Diabetes Mellitus associated with 4 Vitamin D genes – Oct 2015
- Frequent miscarriage associated with both lower vitamin D and poor Vitamin D receptor – Sept 2017
- Vitamin D genes and pregnancy – 7th study - Sept 2017
- Preterm births strongly related to Vitamin D, Vitamin D Receptor, Iodine, Omega-3, etc
- Recurrent miscarriage associated with half as much vitamin D getting to fetus – Sept 2016
- Progesterone activates vitamin D receptor - many studies
PRETERM was in the title of 78 VitaminDWiki pages as of Feb 2022
Vitamin D Receptor is associated in over 58 autoimmune studies
The risk of 44 diseases at least double with poor Vitamin D Receptor as of Oct 2019
Vitamin D Receptor Activation can be increased by any of: Resveratrol, Omega-3, Magnesium, Zinc. Quercetin, non-daily Vit D. Curcumin, intense exercise, Ginger, Essential oils, etc Note: The founder of VitaminDWiki uses 10 of the 12 known VDR activators
- Miscarriages strongly associated with poor placental, decidua gene which locally activates Vitamin D – Dec 2016
Background: We conducted a literature review on the studies that investigated the relationship of preterm birth, including spontaneous preterm birth (sPTB), with vitamin D status. Overall, these studies demonstrated that the incidence of sPTB was associated with maternal vitamin D insufficiency in early pregnancy. However, the potential mechanisms and biological pathways are unknown.
Objectives: To investigate early pregnancy gene expression signatures associated with both vitamin D insufficiency and sPTB. We further constructed a network of these gene signatures and identified the common biological pathways involved.
Study design: We conducted peripheral blood transcriptome profiling at 10-18 weeks of gestation in a nested case-control cohort of 24 pregnant women who participated in the Vitamin D Antenatal Asthma Reduction Trial (VDAART). In this cohort, 8 women had spontaneous preterm delivery (21-32 weeks of gestation) and 17 women had vitamin D insufficiency (25-hydroxyvitamin D < 30 ng/mL). We separately identified vitamin D-associated and sPTB gene signatures at 10 to 18 weeks and replicated the overlapping signatures in the mid-pregnancy peripheral blood of an independent cohort with sPTB cases.
Result: At 10-18 weeks of gestation, 146 differentially expressed genes (25 upregulated) were associated with both vitamin D insufficiency and sPTB in the discovery cohort (FDR < 0.05). Of these genes, 43 (25 upregulated) were replicated in the independent cohort of sPTB cases and controls with normal pregnancies (P < 0.05). Functional enrichment and network analyses of the replicated gene signatures suggested several highly connected nodes related to inflammatory and immune responses.
Conclusions: Our gene expression study and network analyses suggest that the dysregulation of immune response pathways due to early pregnancy vitamin D insufficiency may contribute to the pathobiology of sPTB.