Nearly half the world’s population has vitamin D levels below the threshold for deficiency, and the causes go well beyond not spending enough time outside. A pooled analysis of 7.9 million participants across studies from 2000 to 2022 found that 48% of people had serum vitamin D levels below 50 nmol/L, the cutoff the Endocrine Society uses to define deficiency. Understanding what drains your vitamin D helps explain why this number is so stubbornly high.
How Your Body Makes and Activates Vitamin D
To understand what depletes vitamin D, it helps to know the chain of events that produces it. When UVB rays hit your skin, they convert a cholesterol compound into a precursor form of vitamin D. That precursor travels to your liver, where an enzyme converts it into the circulating form your doctor measures on a blood test. From there, your kidneys perform a second conversion, turning it into the active hormone your body actually uses. A problem at any step in this chain, from sun exposure to skin production to liver conversion to kidney activation, can leave you deficient.
Limited Sun Exposure
The most straightforward cause of low vitamin D is simply not getting enough UVB radiation on your skin. Living at high latitudes (above roughly 37 degrees north or south), working indoors during daylight hours, and covering most of your skin with clothing all reduce the raw material your body needs to start the vitamin D production chain. Season matters too: during winter months at higher latitudes, the sun sits too low in the sky for enough UVB to reach the ground, even on clear days.
Darker skin contains more melanin, which acts as a natural sunscreen and slows UVB absorption. This means people with darker skin tones need significantly more sun exposure to produce the same amount of vitamin D as someone with lighter skin.
Sunscreen Use
A year-long randomized trial of 628 participants, published in the British Journal of Dermatology, put numbers to a long-debated question. Participants assigned to apply SPF 50+ sunscreen daily whenever the UV index reached 3 or higher had a vitamin D deficiency rate of 45.7%, compared to 36.9% in the group that used sunscreen at their own discretion. That’s a 33% higher likelihood of deficiency with routine use. Sunscreen is still important for skin cancer prevention, but regular users may need to get their vitamin D through food or supplements instead.
Air Pollution
Even if you spend time outdoors, the air above you can filter out UVB before it reaches your skin. Research published in Nature found that ozone, nitrogen dioxide, sulfur dioxide, benzene, and particulate matter all reduce UVB intensity at ground level. Particulate matter alone can cut UV radiation by over 25%. Atmospheric gases like carbon monoxide and nitrogen dioxide can reduce shorter-wavelength solar radiation by 20 to 40%. This helps explain why vitamin D deficiency tends to be more common in heavily polluted urban areas, independent of how much time residents spend outside.
Aging
Your skin becomes less efficient at producing vitamin D as you get older. The cholesterol compound in your skin that UVB converts into vitamin D declines with age. Research comparing skin samples from people in their teens and twenties with samples from people in their late seventies and eighties found that aging reduces the skin’s capacity to produce vitamin D by more than half. This means a 70-year-old standing in the same sunlight as a 20-year-old will produce less than half the vitamin D.
Obesity
Vitamin D is fat-soluble, which means it dissolves into fat tissue. In people with excess body fat, vitamin D gets pulled into adipose tissue and held there, effectively locking it away from the bloodstream where your body can use it. This happens through two overlapping mechanisms: the vitamin D is physically sequestered in fat cells, and it’s also diluted across a larger volume of tissue. Adipose tissue does release stored vitamin D slowly over time, acting as a kind of buffer, but in obesity the net effect is that circulating levels stay lower. Studies consistently show that people with higher BMIs have lower serum vitamin D, even when their intake is the same as leaner individuals.
Digestive Conditions That Block Absorption
Because vitamin D is fat-soluble, you need a functioning digestive system to absorb it from food and supplements. Several conditions interfere with this process.
Celiac disease, which affects roughly 0.7% of the global population, damages the lining of the small intestine. Vitamin D deficiency shows up in 20 to 59% of adults with celiac disease, and rates in children range from 9 to 52% depending on the study. Inflammatory bowel diseases like Crohn’s and ulcerative colitis carry similar risks. IBD patients have 64% higher odds of vitamin D deficiency compared to the general population, with overall deficiency rates reaching as high as 60%.
Bariatric surgery deserves special mention. In one study of 211 patients evaluated before surgery, a combined 100% had either insufficient or deficient vitamin D levels. Only about 6% of morbidly obese patients preparing for the procedure had levels in the normal range. After surgery, the shortened digestive tract makes absorption even harder, requiring lifelong supplementation for most patients.
Kidney Disease
Your kidneys perform the final activation step that turns circulating vitamin D into the hormone your cells can use. As kidney function declines, so does this conversion. The decline is progressive: it tracks directly with the drop in your kidneys’ filtration rate. Problems typically become measurable around stage 3 chronic kidney disease, when secondary effects like rising parathyroid hormone levels start appearing and continue worsening through later stages. By the time filtration drops below 20 mL per minute, nearly all patients show signs of disrupted vitamin D metabolism. The kidneys lose functional tissue, and rising phosphorus levels trigger a cascade that further suppresses the activating enzyme.
Liver Disease
The liver handles the first activation step, converting the raw vitamin D from your skin and diet into 25-hydroxyvitamin D, the form measured in standard blood tests. Conditions like non-alcoholic fatty liver disease can impair this conversion. Since the liver enzyme responsible for this step is essential to producing the circulating form, significant liver damage can lower your measurable vitamin D levels regardless of how much sun you get or how many supplements you take.
Medications
Several common drug classes accelerate the breakdown of vitamin D in your body. Certain anti-seizure medications, including carbamazepine, phenobarbital, and phenytoin, activate a receptor in the liver that ramps up the enzymes responsible for breaking down vitamin D. The result is a measurable drop in circulating vitamin D, lower calcium absorption, and over time, decreased bone density. This is well-documented enough that bone health monitoring is standard for long-term users of these drugs.
Corticosteroids like dexamethasone cause a similar problem through the same liver receptor, increasing the degradation of both circulating and active vitamin D. They also reduce calcium absorption in the gut and increase calcium loss through the kidneys, compounding the effect on bone health. If you take corticosteroids regularly, your vitamin D needs are likely higher than average.
Genetics
Some people are genetically predisposed to lower vitamin D levels. Variations in the GC gene, which codes for the protein that carries vitamin D through your bloodstream, are among the most studied. Specific variants of a gene called rs7041 have been identified as risk factors for deficiency, with certain forms of the gene appearing almost exclusively in people with low vitamin D levels in one study. Other genes involved in vitamin D metabolism can also influence how efficiently your body converts and uses the vitamin. These genetic differences help explain why two people with identical diets, sun exposure, and body composition can have meaningfully different vitamin D levels.