Let's Get Personal: These 10 Factors Mediate Your Individual Response To Vitamin D

We are unique individuals with the DNA to prove it. As it turns out, your response to vitamin D can be influenced by a variety of personal factors, from our genes and sex to age, dietary pattern, and much more. I think it's time to get personal, for the sake of our nation's vitamin D health.

If you're providing your body with sufficient vitamin D3 (5,000 I.U. plus per day) from a high-quality D3 supplement (or via a combination of food, sunshine, and supplement) to overcome personal nuance in vitamin D metabolism and response, then you're probably fine [you can know for sure by having your doc test your 25(OH)D level].* 

Where you start affects where you'll end up. I'm talking about your baseline nutrition status. The more pronounced your hypovitaminosis D dilemma (i.e., how insufficient or deficient you are) is to start, the more effective and responsive you will be to supplementation.* 

Vitamin D is an essential fat-soluble micronutrient. It's essential today, tomorrow, and always and thus requires daily input. Because vitamin D is truly scant in naturally occurring and fortified foods, and sun exposure is variable at best (and carries certain obvious risks), supplementation with a high-quality, high-potency D3 supplement is the most prudent approach to guarantee reliable, daily D3 input. 

I'd like to start off by saying I am 100% pro-body-positivity and think overall health is a holistic concept that cannot and should not be boiled down to a singular feature of someone's body composition. With that said, vitamin D is a fat-soluble nutrient. That's its chemical makeup. As such, it is attracted to and sequestered in adipose (fat) tissue. Research indicates that there may also be a dilution factor and even metabolic differences for key vitamin D pathways when higher adiposity is involved.

When it comes to age, the mechanisms for depressed vitamin D levels are more lucid. First, cutaneous synthesis (i.e., when sunshine hits exposed skin and creates vitamin D3) is reduced as we age into older adulthood and beyond. Next, conversion of the circulating 25(OH)D form to its active, doubly hydroxylated 1,25(OH)2D form (the active hormone version of vitamin D) is blunted. 

If you're not taking a vitamin D supplement (or vitamin-D-containing supplements, like a multivitamin, bone, or immune complex), your likelihood of vitamin D deficiency is high. Perhaps this compelling science will inspire you to reconsider vitamin D supplementation. 

The next two factors may seem obvious but actually merit attention. If your vitamin D intake from your diet plus sunshine isn't cutting it (see here for why it probably isn't), then your need for vitamin D supplementation (and likely your response to it) will be heightened.

If you're "sun challenged" (um, most of us these days), that means less vitamin D3 production via your skin. And when I say relying on sun exposure for vitamin D sufficiency throughout life is dicey at best, hear me out. 

Stat: 93% of U.S. adults6 aren't consuming a measly 400 I.U. of this fat-soluble nutrient per day (even counting fortified foods). While "food first" genuinely fails us with this particular nutrient, dietary pattern also comes into play with opportunities (or lack of) to consume vitamin D.

Just like many health-related issues, our DNA comes into play. Our unique genotype includes genetic polymorphisms7 specific to vitamin D's metabolism, transport, and receptor binding. This DNA variability8 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 rs22826799. (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 research10 and is not yet commonly measured in clinical settings.

Two key SNPs related to 25-hydroxylase (rs1075165711, CYP2R1) and 1α-hydroxylase (rs1087701212, 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 (rs222857013), BsmI (rs154441014), ApaI (rs797523215), and TaqI (rs73123616) 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.*

Last but certainly not least are any individual differences or anomalies in physiology that affect the gastrointestinal tract (i.e., vitamin D's absorption starting point17), liver [where vitamin D is converted to 25(OH)D], or kidneys [where 25(OH)D is predominantly converted to its active form of 1,25(OH)2D].