JAMA Dermatol. 2017;153(10):983-989. doi:10.1001/jamadermatol.2017.1976
Erin M. Burns, MS, PhD, MSPH1; Purushotham Guroji, MS, PhD1; Israr Ahmad, MS, PhD1; et al Hana M. Nasr, MPH1; Yingxue Wang, MPH2; Iman A. Tamimi, MD1; Elijah Stiefel, MD1; Mohammad S. Abdelgawwad, MD1; Abdullah Shaheen, BS1; Anum F. Muzaffar, BS1; Lisa M. Bush, MS, GCC3; Christina B. Hurst, MS, GCC3; Russell L. Griffin, MPH, PhD2; Craig A. Elmets, MD1; Nabiha Yusuf, MS, PhD1
- Non-melanoma skin cancer varies with latitude, melanoma does not – April 2017
- Decreased risk of non-melanoma skin cancer by working outdoors in Europe – April 2013
- The Protective Role of Vitamin D Signaling in Non-Melanoma Skin Cancer - Nov 2013
- Overview Suntans melanoma and vitamin D - also, non-melanoma
- Book: Sunlight, UV, Vitamin D and Receptor, Skin and other Cancers - Dec 2020
- Melanoma cancer growth slowed by increased Vitamin D Receptor (yet again) – Oct 2019
- Nonmelanoma Skin Cancer 2X more likely if poor Vitamin D Receptor – Oct 2017
- UVB improvements to Vitamin D receptor appear to improve melanoma survival – Oct 2017
- Skin Cancers, Vitamin D, Vitamin D Receptor and Genes – Jan 2015
- Malignant melanoma may be reduced by skin-activated vitamin D – Nov 2016
- Skin cancer 20 percent more likely with some Vitamin D receptor gene polymorphisms – Oct 2015
- Death from melanoma (without ulcers) greatly decreased if have lots of vitamin D receptors – May 2014
- Melanoma risk 2X to 4X higher if Vitamin D receptor genes had morphed – March 2014
- Vitamin D receptor may suppress skin cancer – Dec 2013
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 )
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:
|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|
|Vitamin D Receptor|
|7) Quercetin (flavonoid)||Vitamin D Receptor|
|8) Zinc is in the VDR||Vitamin D Receptor|
|9) Boron||Vitamin D Receptor ?, |
|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|
|13) Sulfroaphane and perhaps sulfur||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
If poor Vitamin D Receptor
- Question Is there an association between vitamin D receptor single-nucleotide polymorphisms and the risk of nonmelanoma skin cancer?
- Findings This case-control study involving 100 case patients and 100 control patients proposed a model for predicting the incidence of skin cancer and found that individuals with the BsmI single-nucleotide polymorphism were twice as likely to develop nonmelanoma skin cancer than those with no mutation.
- Meaning A screening for the BsmI single-nucleotide polymorphism may emphasize the need for skin cancer prevention for individuals with this polymorphism.
Importance Protective effects of UV-B radiation against nonmelanoma skin cancer (NMSC) are exerted via signaling mechanisms involving the vitamin D receptor (VDR). Recent studies have examined single-nucleotide polymorphisms (SNPs) in the VDR, resulting in contradictory findings as to whether these polymorphisms increase a person’s risk for NMSC.
Objective To examine whether the polymorphisms in the VDR gene are associated with the development of NMSC and the demographic characteristics of the participants.
Design, Setting, and Participants This case-control study recruited 100 individuals who received a diagnosis of and were being treated for basal cell carcinoma or squamous cell carcinoma (cases) and 100 individuals who were receiving treatment of a condition other than skin cancer (controls) at the dermatology clinics at the Kirklin Clinic of the University of Alabama at Birmingham Hospital between January 1, 2012, and December 31, 2014. All participants completed a questionnaire that solicited information on skin, hair, and eye color; skin cancer family history; and sun exposure history, such as tanning ability and number of severe sunburns experienced throughout life. Blood samples for DNA genotyping were collected from all participants.
Main Outcomes and Measures Polymorphisms in the VDR gene (ApaI, BsmI, and TaqI) were assessed to determine the association of polymorphisms with NMSC development and demographic characteristics. χ2 Analysis was used to determine whether genotype frequencies deviated significantly from Hardy-Weinberg equilibrium. Logistic regression was used to calculate odds ratios (ORs) and associated 95% CIs for the identification of factors associated with NMSC diagnosis. A model was created to predict NMSC diagnoses using known risk factors and, potentially, VDR SNPs.
Results A total of 97 cases and 100 controls were included. Of the 97 cases, 68 (70%) were men and 29 (30%) were women, with a mean (SD) age of 70 (11) years. Of the 100 controls, 46 (46%) were men and 54 (54%) were women, with a mean (SD) age of 63 (9) years. All participants self-identified as non-Hispanic white. A model including age, sex, and skin color was created to most effectively predict the incidence of skin cancer.
Risk factors that significantly increased the odds of an NMSC diagnosis were
- light skin color (OR, 5.79 [95% CI, 2.79-11.99]),
- greater number of severe sunburns (OR, 2.59 [95% CI, 1.31-5.10]),
- light eye color (OR, 2.47 [95% CI, 1.30-4.67]), and
- less of an ability to tan (OR, 2.35 [95% CI, 1.23-4.48]).
The risk factors of family history of NMSC (OR, 1.66 [95% CI, 0.90-3.07]) and light hair color (OR, 1.17 [95% CI, 0.51-2.71]) did not reach statistical significance.
Participants with the BsmI SNP were twice as likely to develop NMSC than participants with no mutation (OR, 2.04 [95% CI, 1.02-4.08]; P = .045).
Conclusions and Relevance The results of this study are especially useful in the early treatment and prevention of NMSC with chemopreventive agents (for those with the BsmI SNP). A screening for the BsmI SNP may emphasize the importance of sun protection and facilitate skin cancer prevention and, therefore, decrease the skin cancer burden.
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