The Associations Between the Polymorphisms of Vitamin D Receptor and Coronary Artery Disease: A Systematic Review and Meta-Analysis.
Medicine (Baltimore). 2016 May;95(21):e3467. doi: 10.1097/MD.0000000000003467.
Lu S1, Guo S, Hu F, Guo Y, Yan L, Ma W, Wang Y, Wei Y, Zhang Z, Wang Z wuxiaohongtian at 163.com
1From the Department of Cardiology (SL, FH, LY, WM, YW, YW, ZW), Union Hospital, Huazhong University of Science and Technology, Wuhan; Department of Endocrinology and Metabolism (SG, ZZ), Huashan Hospital, Fudan University, Shanghai; and Department of Health Management (YG), Hangzhou Normal University, Hangzhou, People's Republic of China.
- Magnesium prevents cardiovascular events – Meta-analysis March 2013
- Cardiovascular disease 50 % more likely if low vitamin D - meta-analysis Nov 2012
- Health problems that run in families are often associated with low vitamin D
- 2X more Parkinson's disease if modified vitamin D receptor genes – meta-analysis Aug 2014
- Vitamin D Receptor Activator might help treat or prevent various diseases
The items in Cardiovascular and VDR are listed here:
- 4 Cardiovascular diseases are associated with little vitamin D getting to cells – May 2023
- Cardiovascular disease 2.3 X more-likely if poor Vitamin D Receptor – Aug 2022
- Resveratrol and Cardiovascular Diseases – May 2016
- Heart Failure 15X more likely if poor VDR, even if good level of vitamin D (China) – March 2019
- Coronary Artery Disease without diabetes 5 times more likely if VDR gene problems – meta-analysis May 2016
- Potential for vitamin D receptor agonists in the treatment of cardiovascular disease
Download the PDF from VitaminDWiki
Vitamin D receptor (VDR) polymorphisms were indicated to be associated with coronary artery disease (CAD); however, published studies reported inconsistent results. The aim of this meta-analysis is to reach a more accurate estimation of the relationship between VDR genetic polymorphisms and CAD risk. Eligible studies were retrieved by searching PubMed, Embase, VIP, Wanfang and China National Knowledge Infrastructure databases. Included and excluded criteria were formulated. The case group was patients with CAD, and the control group was healthy subjects. Summary odds ratios (ORs) and 95% confidence intervals (CIs) were used to evaluate VDR polymorphisms associations with CAD risk. Heterogeneity was evaluated by Q statistic and I statistic. Seven studies of a total of 2306 CAD patients and 4151 control subjects met the inclusion criteria. The pooled results from Taq1 showed increased risk in allelic model (OR?=?1.14, 95% CI?=?1.02-1.28), dominant model (OR=1.21, 95% CI=1.02-1.43), heterozygote model (OR?=?1.19, 95% CI?=?1.00-1.1.42), and homozygote model (OR?=?1.27, 95% CI?=?1.01-1.61). Besides, Fok1 T?>?C showed decreased risk in allelic model (OR?=?0.81, 95% CI?=?0.65-1.00) and Fok1 A?>?G also showed decreased risk in allelic model (OR?=?0.67, 95% CI?=?0.45-1.00) and recessive model (OR?=?0.55, 95% CI?=?0.31-0.97). In Caucasian subgroup, Bsm1 showed increased risk in allelic model (OR?=?1.23, 95% CI?=?1.02-1.47), heterozygote model (OR?=?1.20, 95% CI?=?1.00-1.44), and homozygote model (OR?=?1.22, 95% CI?=?1.02-1.45).
In CAD patients with type 2 diabetes mellitus (T2DM), Apa1 showed a decreased risk in heterozygote model (OR=0.80, 95% CI=0.66-0.98); however, increased risk in recessive model (OR=5.00, 95% CI=2.74-9.13) was discovered in CAD patients without T2DM. The Fok1 polymorphism may play a protective role in CAD, and the possible protective role in Apa1 CA genotype in CAD patients with T2DM needs further studies. The Taq1 polymorphism is found to be associated with a significant increase in CAD risk based on our analysis; moreover, increased risk in Apa1 polymorphism in CAD patients without T2DM and Bsm1 polymorphism in Caucasian group is also detected.
PMID: 27227912