Maternal-fetal vitamin D receptor polymorphisms significantly associated with preterm birth.
Arch Gynecol Obstet. 2017 Aug;296(2):215-222. doi: 10.1007/s00404-017-4412-y
- Poor VDR ==> less vitamin D to tissue (fetal tissue in this study)
- Previous miscarriage associated with low maternal or fetal Vitamin D
- Preterm births strongly related to Vitamin D, Vitamin D Receptor, Iodine, Omega-3, etc
- Preterm births 12 X more likely if poor Vitamin D Receptor (white infants in Italy) – meta-analysis Aug 2018
- Maternal VDR in the above study, not the fetal VDR as in study on the page
- Preterm birth rate reduced by vitamin D – 78 percent if non-white, 39 percent if white – July 2017
- Appears that increasing the activation of fetal/materanl VDR is far more important than just raising Vitamin D levels
- Using VDR activators might increase both maternal and fetal VDR
- 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, non-daily Vitamin D dosing, curcumin, intense exercise, etc
Note: The founder of VitaminDWiki uses 10 of the 12 known VDR activators
Study PDF can be viewed on Deepdyve
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.
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.