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Pneumonia in Egyptian Children 3.6 X more likely if poor Vitamin D Receptor – Aug 2018

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

VitaminDWiki

Vitamin D Receptor category has the following

234 items in Vitamin D Receptor category

Vitamin D tests cannot detect Vitamin D Receptor (VDR) problems
A poor VDR restricts Vitamin D from getting in the cells

A poor VDR increases the risk of 45 health problems  click here for details

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:

IncreasingIncreases
1) Vitamin D supplement
  Sun, Ultraviolet -B
Vitamin D in the blood
and thus to the cells
2) MagnesiumVitamin D in the blood
 AND to the cells
3) Omega-3 Vitamin D to the cells
4) Resveratrol Vitamin D to the cells
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
Costs less than 1 cent per day
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


See chart at the bottom of VDR page for Magnesium, Omega-3 and Resveratrol

If poor Vitamin D Receptor

Risk
increase
Health Problem
28Leprosy
13Sepsis
9.6Chronic Periodontitis
   and smoke
8Juvenile Rheumatoid Arthritis
7.6Crohn's disease
7.5Respiratory Tract Infections
5.8Low back pain in athletes
5Ulcerative Colitis
5Coronary Artery Disease
4.6Breast Cancer
4.1Vitiligo
4polycystic ovary syndrome
3.6 Pneumonia - children
3.3 Pre-term birth
3.1 Colon Cancer survival
3 Multiple Sclerosis
3Dengue
3 Waist size
3 Ischemic Stroke
3Alzheimer’s
2.8Osteoporosis & COPD
2.7Gastric Cancer
2.6Lupus in children
2.5 Lumbar Disc Degeneration
2.4Lung Cancer
2.3Autism
2.2Juvenile idiopathic arthritis
2.1Adolescent idiopathic scoliosis in Asians
2Diabetic Retinopathy
2Parkinson's
2 Wheezing/Asthma
2 Melanoma   Non-melanoma Skin Cancers
2Myopia
1.9Uterine Fibroids
1.9Early tooth decay
1.8Diabetic nephropathy
1.6Diabetes - Type I
1.6Prostate Cancer while black
1.5 Diabetes -Type II
1.5Pertusus
1.5Obesity
1.4 Rheumatoid arthritis
1.3Childhood asthma
1.3Tuberculosis

Publisher rents PDF for $9

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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