Vitamin D deficiency has a surprisingly long list of causes, and most people have more than one working against them at the same time. Your body gets vitamin D from two places: your skin (which produces it when exposed to sunlight) and your diet. Anything that limits either source, or interferes with how your body processes the vitamin, can push your levels too low.
How Your Body Makes Vitamin D
Understanding the causes of deficiency starts with understanding the supply chain. When UVB rays from the sun hit your skin, they convert a cholesterol compound in the outer layer of skin into a precursor of vitamin D3. That precursor then transforms into vitamin D3 (cholecalciferol), enters your bloodstream, and travels to your liver and kidneys, where it’s converted into the active hormone your body actually uses.
This process is efficient under ideal conditions, but it’s sensitive to disruption at every step. Block the UV light, reduce the cholesterol compound in the skin, slow the liver or kidney conversions, or trap the vitamin D before it circulates, and you end up deficient.
Where You Live and When You Go Outside
Geography is one of the biggest factors. If you live north of the 37th parallel in the United States (roughly a line from Richmond, Virginia, to Santa Cruz, California), UVB sunlight is too weak to trigger meaningful vitamin D production from late October through late April. That’s about six months of the year when your skin simply can’t make the vitamin, no matter how long you stay outside. The same applies to equivalent latitudes in Europe and Asia.
Even in sunnier months, the window is narrow. UVB rays strong enough for vitamin D synthesis are only available between roughly 10 a.m. and 3 p.m. Cloud cover, air pollution, and window glass all filter out UVB. If you work indoors during those peak hours, commute before and after them, or consistently apply sunscreen (which blocks UVB by design), your skin gets little opportunity to produce vitamin D regardless of season.
Skin Tone and Age
Melanin, the pigment that gives skin its color, acts as a natural sunscreen. People with darker skin still produce vitamin D, but the process is slower. Research comparing the lightest and darkest skin types found melanin reduces vitamin D synthesis efficiency by a factor of roughly 1.3 to 1.4. That difference sounds modest, but over months of limited sun exposure it can be enough to explain the significantly higher deficiency rates seen in people with darker skin tones, especially those living at northern latitudes.
Age also matters. As you get older, the amount of the cholesterol precursor in your skin declines, and your skin becomes less efficient at the conversion process. Older adults who spend less time outdoors face a double hit: less raw material in the skin and less sun exposure to work with. The kidneys also become less effective at activating vitamin D with age, compounding the problem.
Too Few Dietary Sources
Very few foods naturally contain meaningful amounts of vitamin D, which makes diet alone a difficult way to maintain adequate levels. A 3-ounce serving of cooked sockeye salmon provides about 570 IU, which is close to a full day’s recommended intake for most adults. But after salmon, the numbers drop steeply. A large scrambled egg has only 44 IU. Three ounces of braised beef liver contain about 42 IU.
Fortified foods like milk, orange juice, and some cereals help bridge the gap, but people who follow vegan diets, are lactose intolerant, or simply don’t eat fish regularly may fall short. If you’re also not getting much sun, dietary shortfall becomes a primary driver of deficiency.
Body Weight and Fat Storage
Carrying excess body fat changes how vitamin D moves through your system. Vitamin D is fat-soluble, meaning it dissolves in and gets absorbed by fat tissue. In people with obesity, vitamin D is pulled into expanded fat stores and held there, reducing the amount available in the bloodstream for the rest of the body to use. Fat tissue doesn’t lock it away permanently. It functions more like a slow-release storage compartment, but the release is too gradual to keep circulating levels where they need to be.
On top of this sequestration effect, vitamin D is also diluted across a larger body volume in people who weigh more. Both mechanisms together mean that people with obesity often show lower blood levels of vitamin D even when they get the same amount of sun exposure or take the same supplement dose as someone at a lower weight. Higher supplementation doses are frequently needed to reach the same blood concentration.
Digestive Conditions That Block Absorption
Because dietary and supplemental vitamin D are absorbed through the small intestine along with fats, any condition that impairs fat absorption can cause deficiency. Crohn’s disease, ulcerative colitis, and celiac disease all inflame or damage the intestinal lining in ways that reduce nutrient uptake. Celiac disease, when undiagnosed and untreated, can be particularly insidious because the damage to intestinal villi may be extensive before symptoms become obvious.
Gastric bypass surgery creates a similar problem mechanically. The procedure reroutes food past a portion of the small intestine, which is exactly where vitamin D would normally be absorbed. People who have had this surgery need lifelong monitoring and typically require higher-dose supplementation to compensate for the reduced absorptive surface.
Liver and kidney diseases also interfere with deficiency, though at a different stage. These organs handle the two chemical conversions that turn inactive vitamin D into its usable form. If either organ is compromised, you can have adequate vitamin D entering your bloodstream but still end up functionally deficient because it never gets activated.
Medications That Deplete Vitamin D
Several common prescription drugs accelerate the breakdown of vitamin D in your body. Corticosteroids (often prescribed for autoimmune conditions, asthma, or joint inflammation) impair vitamin D metabolism and reduce calcium absorption. One mechanism involves increasing the activity of an enzyme in the kidneys that degrades vitamin D’s active forms.
Certain anti-seizure medications, including phenytoin, phenobarbital, and carbamazepine, are also well-documented offenders. These drugs ramp up liver enzymes that break vitamin D down into inactive byproducts. People on long-term anti-seizure therapy often develop deficiency if their vitamin D levels aren’t monitored and supplemented proactively. Cholestyramine (used for high cholesterol) and some antifungal medications can have similar effects.
Multiple Causes Often Overlap
What makes vitamin D deficiency so common is that these risk factors rarely exist in isolation. A person with darker skin living in Chicago who works indoors, avoids dairy, and takes a corticosteroid for an autoimmune condition has five separate forces pushing their levels down simultaneously. Each factor on its own might only cause a modest dip, but stacked together they can drive levels well below the deficiency threshold. If you recognize several of these factors in your own life, a simple blood test measuring your circulating vitamin D level can tell you exactly where you stand and how aggressively you might need to supplement.