Just like many health-related issues, our DNA comes into play. Our unique genotype includes genetic polymorphisms specific to vitamin D’s metabolism, transport, and receptor binding. This DNA variability sprinkles individual differences into our response to vitamin D supplementation.
For example, we know that single nucleotide polymorphisms (SNPs) affect vitamin D metabolism. Serum 25(OH)D levels can be influenced by genetic differences in the vitamin D binding protein (VDBP) per gene rs2282679. (The G allele is tied to lower vitamin D levels.)
If your VDBP levels are higher, more 25(OH)D will be bound and less available to do its job. Thus, your supplementation needs may be higher. You can ask your health care provider to measure “free 25(OH)D” to quantify the unbound vitamin D in your blood, but this test is used more in research and is not yet commonly measured in clinical settings.
Two key SNPs related to 25-hydroxylase (rs10751657, CYP2R1) and 1α-hydroxylase (rs10877012, CYP27B1) have also been identified. These are the enzymes that convert vitamin D into its circulating form and active hormone form, respectively.
And then FokI (rs2228570), BsmI (rs1544410), ApaI (rs7975232), and TaqI (rs731236) are genetic polymorphisms linked to the vitamin D receptor (VDR) and thus the ability of vitamin D to bind and do its many critical jobs in the body.*
These genetic differences (and their risk associations for key health pathways) are still in the rapidly growing clinical research stage, with everyday implications for clinical practice forthcoming. With that said, an integrative-minded health care practitioner on the cutting edge may consider SNPs in a personalized nutrition assessment and treatment approach.
This article was originally published by mindbodygreen.com. Read the original article here.