Association of vitamin D receptor gene FokI polymorphism and susceptibility to CAP in Egyptian children: a multicenter study
Pediatric Research (2018) https://doi.org/10.1038/s41390-018-0149-y
Heba Abouzeid, NourEldin M. Abdelaal, Mohammed A. Abdou, Amira A. A. Mosabah, Mervat T. Zakaria, Mohammed M. Soliman, Ashraf M. Sherif, Mohammed E. Hamed, Attia A. Soliman, Maha A. Noah, Atef M. Khalil, Mohamed S. Hegab, Alsayed Abdel-Aziz, Shaimaa S. A. Elashkar, Rehab M. Nabil, Adel M. Abdou, Ghada M. Al-Akad & Hany A. A. Elbasyouni
- Children with pneumonia in Ethiopia were 22X more likely to have rickets – 1997
- Pneumonia - elderly and children
- Hospital-acquired pneumonia treated by vitamin D if person was deficient – RCT Sept 2018
- Fewer children died of pneumonia after 100,000 IU Vitamin D injection – RCT March 2021
Vitamin D Receptor category has the following
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 have a poor VDR (40% of the Obese )
Several diseases protect themselves by deactivating the Vitamin D receptor. Example: Breast Cancer
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The Vitamin D Receptor is associated with many health problems
Some health problems, such as Breast Cancer, Diabetes, and COVID protect themselves by reducing VDR activation
55 health problems associated with poor VDR
A poor VDR is associated with the risk of 55 health problems click here for details
The risk of 48 diseases at least double with poor VDR as of Jan 2023 click here for details
Some health problem, such as Breast Cancer reduce the VDR
VDR at-home test $29 - results not easily understood in 2016
There are hints that you may have inherited a poor VDR
How to increase VDR activation
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 paricalcitol, maxacalcitol? | Vitamin D Receptor |
7) Quercetin (flavonoid) | Vitamin D Receptor |
8) Zinc is in the VDR | Vitamin D Receptor |
9) Boron | Vitamin D Receptor ?, etc |
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 Receptor |
13) Sulfroaphane and perhaps sulfur | Vitamin D Receptor |
14) Butyrate especially gut | Vitamin D Receptor |
15) Berberine | Vitamin D Receptor |
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
Far healthier and stronger at age 72 due to supplements Includes 6 supplements that help the VDR
Increased risk of diseases if poor VDR
Increased risk associated with a poor Vitamin D Receptor
Note: Some diseases reduce VDR activation
those with a * are known to decrease activation
Breathing problems often associated with Poor Vitamin D Receptors
- Asthma by age 7 if wheezing before preschools and poor vitamin D Receptor - May 2023
- 2X increase risk of Asthma if a particular Vitamin D Receptor mutation – meta-analysis Feb 2022
- Atopies (allergy, asthma, rhinitis, etc.) variously associated with low Vitamin D and poor Vitamin D Receptor – Aug 2021
- Mucosal membranes (mouth, lungs, nose, intestines, etc) can activate Vitamin D – July 2020
- Respiratory problems in Children 1.4X more likely if poor Vitamin D receptor – April 2020
- Poor response to Asthma inhaler if poor Vitamin D Receptor – Dec 2019
- Microbiomes of both gut and airway are affected by Vitamin D and Vitamin D Receptor – Nov 2018
- Asthma 3.7X higher risk of poor Vitamin D Receptor (teens in Taiwan in this case) – Nov 2019
- Asthma is 20 percent more likely with a poor Vitamin D Receptor gene – meta-analysis Oct 2019
- Asthmatic children 5X more likely to have a poor Vitamin D Receptor – June 2019
- Best supplements for hay fever (Quercetin, which activates the Vitamin D receptor) - June 2019
- Upper respiratory infection associated with poor Vitamin D Receptor – Oct 2018
- Respiratory Distress Syndrome in preemies 5 X more likely if poor vitamin D receptor – Feb 2019
- Gut and airway bionome are affected by Vitamin D and Vitamin D Receptor – Nov 2018
- Pneumonia in Egyptian Children 3.6 X more likely if poor Vitamin D Receptor – Aug 2018
- Respiratory Tract Infections in children 7.4 X more likely if poor Vitamin D Receptor – 2008
- Inflammation and immune responses to Vitamin D (perhaps need to measure active vitamin D) – July 2017
- Vitamin D Receptor problems occur 5 times for often with Nasal polyposis – Nov 2016
- Vitamin D effects on lung immunity and respiratory diseases – 2011
- Childhood asthma about 1.3 times more likely if poor Vitamin D Receptor – meta-analysis Aug 2016
- Severe Pertussis is 1.5 times more likely if poor vitamin D receptor – Feb 2016
- 2X higher risk of wheezing and asthma if modified receptor genes, even if vitamin D levels OK – Sept 2015
- 2.8X higher risk of osteoporosis if COPD and modified vitamin D receptor genes – Sept 2015
- Strong Vitamin D deficiency associations in Asthma patients – Nov 2014
- Epigenetics and Vitamin D – many studies
Background
Community-acquired pneumonia (CAP) is the leading cause of child deaths around the world. Recently, the vitamin D receptor (VDR) gene has emerged as a susceptibility gene for CAP.
Objectives
To evaluate the association of the VDR gene Fok I polymorphism with susceptibility to CAP in Egyptian children.
Methods
This was a multicenter case-control study of 300 patients diagnosed with CAP, and 300 well-matched healthy control children. The VDR Fok I (rs2228570) polymorphism was genotyped by PCR-restriction fragment length polymorphism (RFLP), meanwhile serum 25-hydroxy vitamin D (25D) level was assessed using ELISA method.
Results
The frequencies of the VDR FF genotype and F allele were more common in patients with CAP than in our control group (OR = 3.6; (95% CI: 1.9–6.7) for the FF genotype; P = 0.001) and (OR: 1.8; (95% CI: 1.4–2.3) for the F allele; P = 0.01). Patients carrying the VDR FF genotype had lower serum (25D) level (mean; 14.8 ± 3.6 ng/ml) than Ff genotype (20.6 ± 4.5 ng/ml) and the ff genotype (24.5 ± 3.7 ng/ml); P < 0.01.
Conclusion
The VDR gene Fok I (rs2228570) polymorphism confers susceptibility to CAP in Egyptian children.
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Acknowledgements
We thank the staff of Pediatric Pulmonology and Outpatient Clinics in Zagazig University, Ain-Shams and Cairo University hospitals for their collaboration in sampling as well as our patients who participated in the study.
Author contributions
H.A.Z. submitted the manuscript. M.A.A. designed the study. A.M.K. collected clinical data and coordinated the sample collection (Zagazig University). N.M.A. collected clinical data and coordinated the sample collection (Ain-Shams University). M.M.S. collected clinical data and coordinated the sample collection (Cairo University). M.S.H. and H.A.A.E. performed the statistical analysis. M.A.N. and A.A.S. helped to draft the manuscript. A.M.S., A.A.M., and M.E.H. wrote the manuscript. A.A.A., M.T.Z., and S.S.A.E. critically revised the final version. A.M.A., R.M.N., and G.M.A. performed laboratory analysis and genotyping. All authors read and approved all the manuscript.
Author information
Affiliations
Department of Pediatrics, Faculty of Medicine, Zagazig University, Zagazig, Egypt
Heba Abouzeid, Mohammed A. Abdou, Mohammed E. Hamed, Attia A. Soliman, Maha A. Noah, Atef M. Khalil, Mohamed S. Hegab, Alsayed Abdel-Aziz & Shaimaa S. A. Elashkar
Department of Pediatrics, Faculty of Medicine, Ain-Shams University, Cairo, Egypt
NourEldin M. Abdelaal
Department of Pediatrics, Faculty of Medicine, Cairo University, Cairo, Egypt
Amira A. A. Mosabah, Mervat T. Zakaria, Mohammed M. Soliman & Ashraf M. Sherif
Department of Clinical pathology, Faculty of Medicine, Zagazig University, Zagazig, Egypt
Rehab M. Nabil & Ghada M. Al-Akad
Department of Clinical pathology, Al Azhar Faculty of Medicine, Cairo, Egypt
Adel M. Abdou
Department of Internal Medicine, Faculty of Medicine, Menoufia University, Monufia, Egypt
Hany A. A. Elbasyouni
Competing interests
The authors declare no competing interests.
Corresponding author
Correspondence to Heba Abouzeid.
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