Arch Gynecol Obstet. 2017 Aug;296(2):215-222. doi: 10.1007/s00404-017-4412-y. Epub 2017 Jun 13.
Rosenfeld T1,2, Salem H1, Altarescu G2, Grisaru-Granovsky S2, Tevet A2, Birk R3.
1 Department of Nutrition, School of Health Sciences, Ariel University, Ariel, Israel.
2 Genetics Unit and Department of Obstetrics and Gynecology, Shaare Zedek Medical Center, Jerusalem, Israel.
3 Department of Nutrition, School of Health Sciences, Ariel University, Ariel, Israel. ruthb at ariel.ac.il.
Pages listed in BOTH the categories Pregnancy and Vitamin D Receptor
- 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 4 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
- Preterm birth far more likely if previous miscarriage and poor Vitamin D receptor – Aug 2017
- 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 birth (PTB) is a complex trait with strong genetic background, whose etiology is not fully understood. It was recently suggested that pregnancy duration is affected by fetal genetic variation even more than by the maternal genome. Vitamin D receptor (VDR) is involved in embryonic implantation and fertility. We studied the association between both maternal and neonatal vitamin D receptor (VDR) genetic variation and PTB.
Maternal and fetal (umbilical cord) DNA was isolated from Jewish Israeli idiopathic preterm newborns (24-36 weeks, n = 146) and control term newborns (>37 weeks, n = 229). Maternal and fetal VDR polymorphisms (FokI, ApaI, BsmI, TaqI) were analyzed by restriction fragment length polymorphism analysis. Using SPSS analysis to correlate VDR genotypes with phenotypic variation: pregnancy duration, preterm birth and spontaneous miscarriages, adjusted for gravidity, parity and gender of newborn.
- Women homozygous to VDR ApaI (AA) genotype had significant twofold increase risk for PTB
[OR 1.973, (CI) 1.183-3.289, p = 0.009] compared to heterozygous women.
- Male newborns had significant (p < 0.05) 1.73-fold increase of PTB.
- Women with history of previous (≥1) spontaneous miscarriage had a significant increased risk for PTB if their newborn carried
either of the VDR BsmI homozygous (BB or bb) genotypes compared to the heterozygous (Bb) genotype
[OR 6.857, (CI) 1.273-36.934, p = 0.018 and OR 9.231, (CI) 1.753-48.618, p = 0.008, respectively], or
VDR ApaI homozygous (AA or aa) genotype compared to heterozygous (Aa) genotype
[OR 4.33, (CI) 1.029-18.257, p = 0.046 and OR 7.2, (CI) 1.34-38.917, p = 0.021, respectively].
We show association between maternal and fetal VDR genotype variants with PTB.
PMID: 28612095 DOI: 10.1007/s00404-017-4412-y
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