Association of vitamin D receptor gene polymorphisms with susceptibility to childhood asthma: A meta-analysis.
Pediatr Pulmonol. 2016 Aug 23. doi: 10.1002/ppul.23548. [Epub ahead of print]
Zhao DD1, Yu DD1, Ren QQ1, Dong B1, Zhao F1, Sun YH1,2.
1Department of Epidemiology and Health Statistics, Anhui Medical University, Hefei, China.
2Centre for Evidence-Based Practice, Anhui Medical University, Hefei, China.
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Vitamin D tests cannot detect Vitamin D Receptor (VDR) problems
A poor VDR restricts Vitamin D from getting in the cells
It appears that 30% of the population has a poor VDR (40% of the Obese )
VDR at-home test $29 - results not easily understood in 2016
There are hints that you may have inherited a poor VDR
Compensate for poor VDR by increasing one or more:
Increasing Increases 1) Vitamin D supplement
Sun, Ultraviolet -B
Vitamin D in the blood
and thus in the cells
2) Magnesium Vitamin D in the blood
AND in the cells
3) Omega-3 Vitamin D in the cells 4) Resveratrol Vitamin D Receptor 5) Intense exercise Vitamin D Receptor 6) Get prescription for VDR activator
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10) Essential oils e.g. ginger, curcumin Vitamin D Receptor 11) Progesterone Vitamin D Receptor 12) Infrequent high concentration Vitamin D
Increases the concentration gradient
Vitamin D in the cells
Note: If you are not feeling enough benefit from Vitamin D, you might try increasing VDR activation. You might feel the benefit within days of adding one or more of the above
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As for the association of vitamin D receptor (VDR) gene polymorphisms with susceptibility to pediatric asthma, results of published studies yielded conflicts. A systematic review was conducted on the relationship between childhood asthma and VDR gene polymorphisms, including ApaI (rs7975232), BsmI (rs1544410), FokI (rs2228570), and TaqI (rs731236).
PubMed, Web of Science, CBM (Chinese Biomedical Database), CNKI (China National Knowledge Infrastructure), and Wanfang (Chinese) database were searched for relevant studies. Pooled odds ratios (OR) with 95% confidence interval (CI) were calculated.
Overall results suggested that there was a statistically significant association between ApaI polymorphism and childhood asthma in homozygote model (OR = 1.674, 95%CI = 1.269-2.208, P < 0.001) and allele model (OR = 1.221, 95%CI = 1.084-1.375, P = 0.001). Stratification by ethnicity revealed a statistical association in Asians (OR = 1.389, 95%CI = 1.178-1.638, P < 0.001). There was some evidence of an association between BsmI polymorphism and childhood asthma in the homozygote (OR = 1.462, 95%CI = 1.016-2.105, P = 0.041) and allele models (OR = 1.181, 95%CI = 1.006-1.386, P = 0.042). This association reached significance only in the Caucasian group (OR = 1.236, 95%CI = 1.029-1.485, P = 0.023). For FokI, a statistical association was detected in dominant model (OR = 1.281, 95%CI = 1.055-1.555, P = 0.012); this association was significant in allele model (OR = 1.591, 95%CI = 1.052-2.405, P = 0.028) in Caucasian.
ApaI polymorphism plays a particular role in childhood asthma in Asians. FokI polymorphism may be connected with pediatric asthma in Caucasian population. And BsmI polymorphism marginally contributes to childhood asthma susceptibility, while there might be no association between TaqI polymorphism and childhood asthma risk.
Pediatr Pulmonol. 2016; 9999:XX-XX. © 2016 Wiley Periodicals, Inc.
PMID: 27551963 DOI: 10.1002/ppul.23548
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