Vitamin D (25-Hydroxy): Normal Range, Deficiency, How Much to Take

The 25-hydroxy vitamin D test combines D2 (from plant supplements and fortified foods) and D3 (from sunlight, animal foods, and most supplements). It is the right test for vitamin D status — not the active form (1,25-dihydroxy vitamin D), which is regulated by the parathyroid and reflects different physiology.

Reported in either ng/mL (United States) or nmol/L (most of the rest of the world). Conversion: 1 ng/mL = 2.5 nmol/L. This page uses ng/mL.

The Endocrine Society and Institute of Medicine give slightly different cutoffs:

• Below 12 ng/mL: severe deficiency. Risk of rickets in children, osteomalacia in adults, secondary hyperparathyroidism.
• 12–20 ng/mL: deficient. Bone health affected; supplementation indicated.
• 20–30 ng/mL: insufficient by Endocrine Society criteria, sufficient by IOM criteria. Practically, most experts treat this range with at least modest supplementation.
• 30–60 ng/mL: sufficient. The target range for most adults.
• 60–100 ng/mL: high but not toxic. No proven additional benefit.
• Above 100 ng/mL: potentially toxic at sustained levels — risk of hypercalcemia.

Genuinely high vitamin D — above 100 ng/mL — is almost always supplement-induced. Sun exposure does not cause vitamin D toxicity because the skin self-regulates production. Common patterns:

• High-dose supplementation (10,000+ IU/day for months) without monitoring.
• Mistakenly taking 50,000 IU capsules daily instead of weekly.
• Granulomatous diseases (sarcoidosis, tuberculosis, lymphoma) that activate vitamin D pathologically — usually presents with high calcium more than high 25-OH-D.

Toxicity manifests as hypercalcemia: nausea, kidney stones, confusion, and renal injury. Stop the supplement, recheck in 4–6 weeks, and check serum calcium.

Low vitamin D is common. About 25–40% of adults globally are deficient or insufficient depending on the cutoff used. Risk factors:

• Limited sun exposure — northern latitudes, indoor work, sunscreen use, dark skin in low-sun environments.
• Older adults — skin produces vitamin D less efficiently with age.
• Obesity — vitamin D is sequestered in adipose tissue, lowering circulating levels.
• Malabsorption — celiac disease, inflammatory bowel disease, post-bariatric surgery.
• Liver or kidney disease — affects vitamin D activation.
• Some medications — anticonvulsants (especially older ones), glucocorticoids, antiretrovirals, cholestyramine.

How to correct deficiency:

• Mild deficiency (20–30 ng/mL): 1,000–2,000 IU D3 daily.
• Moderate deficiency (12–20 ng/mL): 4,000–5,000 IU D3 daily for 2–3 months, then maintenance.
• Severe deficiency (under 12 ng/mL): 50,000 IU D3 weekly for 6–8 weeks, then daily maintenance.
• Recheck 25-OH-D after 8–12 weeks.

D3 (cholecalciferol) is more effective than D2 (ergocalciferol) at raising blood levels. Take with the largest meal of the day for better absorption — vitamin D is fat-soluble.

Vitamin D varies seasonally. Levels in late summer can be 30–50% higher than in late winter at the same latitude. A November test in Boston is not directly comparable to a July test. If your level looks borderline, the time of year matters.

The other under-appreciated point: low vitamin D is a marker as much as a cause. People with chronic illness, obesity, low sun exposure, and poor diet tend to have low vitamin D — but supplementing alone often does not improve those underlying conditions. This is one reason large randomized supplementation trials have been disappointing for endpoints like cancer and cardiovascular disease.

Where supplementation does clearly help: bone health and fracture prevention in deficient older adults, fall risk reduction in deficient older adults, pregnancy outcomes, and severe deficiency in any age group.

• Below 12 ng/mL — treat aggressively; check parathyroid hormone and calcium.
• 12–20 ng/mL — supplement and recheck in 8–12 weeks.
• Persistently low despite supplementation — consider malabsorption (celiac, IBD), obesity-related sequestration, or medication interaction.
• Above 100 ng/mL — stop the supplement, check calcium, recheck in 4–6 weeks.

• Calcium and parathyroid hormone (PTH) — together with 25-OH-D, these clarify whether deficiency has caused secondary hyperparathyroidism.
• Phosphorus, alkaline phosphatase — bone metabolism context.
• Magnesium — required for vitamin D activation; deficiency interferes with response to supplementation.
• Albumin — most calcium is bound to albumin; correct calcium for albumin level.