Vitamin D2 vs D3: Which Raises Your Levels More?

Vitamin D3 (cholecalciferol) raises blood vitamin D more than vitamin D2 (ergocalciferol) in most head-to-head trials: a meta-analysis of 24 studies in 1,277 healthy people found D3 raised total 25(OH)D by 15.69 nmol/L more¹. The gap is smaller at lower daily doses¹, and the two forms appear to cure rickets about equally well².

For most people buying a supplement, D3 is the sensible default^{1, 3}. If a clinician prescribed D2, take it as directed and ask about retesting rather than switching on your own. Our vitamin D page covers benefits, general dosing and safety.

The two forms differ chemically only in their side-chain structures, and both are well absorbed in the small intestine².

• D2 (ergocalciferol): made by irradiating ergosterol from yeast, and the form that UV-treated mushrooms contain².
• D3 (cholecalciferol): typically made by irradiating 7-dehydrocholesterol from the lanolin in sheep wool, though an animal-free D3 from lichen is also sold².

In nature, skin exposed to UVB sunlight makes D3, and the flesh of fatty fish such as trout, salmon, tuna and mackerel is among the best food sources. Mushrooms provide variable amounts of D2².

Most steps in the metabolism of the two forms are identical, and both appear equally able to treat rickets². A blood test reports either form as 25-hydroxyvitamin D, written 25(OH)D. Levels of 50 nmol/L (20 ng/mL) or more are generally considered adequate for bone health, and levels under 30 nmol/L (12 ng/mL) are linked to deficiency². For what low levels mean and how to correct them, see vitamin D deficiency.

Absorption is not the difference. After single 50,000 IU doses in 20 healthy men, both forms raised the blood level of the vitamin itself by similar amounts, which the authors took as equivalent absorption⁴. The difference is how much 25(OH)D you end up with, and three meta-analyses favor D3:

• 2012: D3 raised 25(OH)D more than D2 overall (P = 0.001). The edge was clear for single large doses (P = 0.0002) and lost with daily dosing⁵.
• 2021, 24 studies, 1,277 healthy participants: D3 raised total 25(OH)D by 15.69 nmol/L more (95% CI 9.46 to 21.93), with smaller differences at lower doses¹.
• 2024, 20 comparative studies: in 12 daily-dose comparisons measured by mass spectrometry, the D2 group gained 10.39 nmol/L (40%) less than the D3 group³.

Do individual trials agree?

Not all of them. Four trials favored D3^{6, 7, 8, 9}:

• 335 women, 15 mcg daily for 12 weeks in winter: D3 groups gained 15.3 to 16.9 nmol/L more 25(OH)D than D2 groups⁶.
• 95 adults, 1,000 IU daily for 25 weeks: total 25(OH)D ended 21 nmol/L lower on D2 (95% CI 14 to 30), while the D3 group stayed unchanged⁷.
• 33 adults, 50,000 IU weekly for 12 weeks: steady-state 25(OH)D rose 24 ng/mL on D2 and 45 ng/mL on D3⁸.
• 64 adults aged 65 and over, 1,600 IU daily or 50,000 IU monthly for 1 year: D3 was slightly but significantly more effective⁹.

Three found no meaningful difference^{10, 11, 12}:

• Healthy adults aged 18 to 84, 1,000 IU daily for 11 weeks: 25(OH)D rose from 16.9 to 26.8 ng/mL on D2 and from 19.6 to 28.9 ng/mL on D3. Neither lifted deficient participants above 30 ng/mL¹⁰.
• 40 infants and toddlers, 2,000 IU daily for 6 weeks: the D2 and D3 groups differed by 7% (P = 0.82), and both roughly tripled their 25(OH)D¹¹.
• 174 children with sickle cell anemia, 50,000 IU weekly for 6 weeks: median rises were 17.8 nmol/L on D2 and 15.3 nmol/L on D3, with no significant difference¹².

The pattern: the gap is widest with large, infrequent doses and narrower with modest daily doses^{5, 1}.

Does body weight change the answer?

It may. In the 2024 meta-analysis, body mass index was the strongest response modifier. The D2 versus D3 difference lost significance in people with a BMI above 25 kg/m² (P = 0.99), though BMI data existed for only 13 of 17 daily-dose comparisons³.

Your body converts D2 into 25(OH)D2, the D2 version of the blood marker¹³. In trials, D2 also lowers the D3 version, 25(OH)D3. A 2025 meta-analysis of randomized trials found that people taking D2 had 25(OH)D3 that was 17.99 nmol/L lower at the end of the trial than controls (95% CI -25.86 to -10.12)¹⁴.

• 8 weeks of 50 mcg daily in winter: 25(OH)D3 rose from 41.5 to 88.0 nmol/L on D3 but fell from 36.4 to 16.6 nmol/L on D2¹⁵.
• 6 weeks of UV-treated mushrooms in 38 adults: servings providing 8.8 and 17.1 mcg of D2 daily raised 25(OH)D2 by 13.8 and 12.7 nmol/L. At 17.1 mcg, and with a 28.2 mcg D2 supplement, 25(OH)D3 fell significantly more than in controls (by 20.6 and 29.5 nmol/L), and the authors concluded D2 did not change vitamin D status¹³.

Whether this is specific to D2 is unclear. In a trial of 279 adults, the drop in 25(OH)D3 on D2 tracked the rise in 25(OH)D2, and in the one participant with measurable baseline 25(OH)D2, D3 caused a similar fall. The authors suggested D2 may be converted faster¹⁶.

Nobody knows yet whether a lower 25(OH)D3 harms health. The 2013 trial that measured it saw no change in parathyroid hormone (PTH), and called the functional consequence worth studying⁷. In the 2021 meta-analysis, D3 lowered PTH more than D2¹.

No trial in the sources we read compared the two forms on disease outcomes directly. The closest evidence is indirect: trials of each form against placebo, grouped by form.

• Cochrane review, 56 trials, 95,286 participants: vitamin D lowered all-cause mortality (RR 0.97, 95% CI 0.94 to 0.99). By form, only D3 did (RR 0.94, 38 trials, 75,927 participants). D2 had no significant effect¹⁷.
• BMJ 2019 meta-analysis, 52 trials, 75,454 participants: vitamin D was not associated with all-cause mortality (RR 0.98, 95% CI 0.95 to 1.02). Mortality was lower in D3 trials than D2 trials (P for interaction = 0.04), but neither form reached significance alone¹⁸.

So the mortality case for D3 is weaker than the blood-level case. The Cochrane authors warned of dropout and reporting bias, and said a D2 signal of higher mortality in high-risk-of-bias trials could be chance¹⁷. These are comparisons across different trials, not a randomized D2 versus D3 test.

The 2024 Endocrine Society guideline covers both forms. It suggests empiric supplementation for ages 1 to 18, for adults 75 and older, in pregnancy and for high-risk prediabetes, but not above the Dietary Reference Intakes in healthy adults under 75. For nonpregnant people over 50 who need vitamin D, it suggests daily dosing over intermittent high doses¹⁹.

No source we read states prescribers' reasons. The prescription 50,000 IU capsules on DailyMed are ergocalciferol (1.25 mg each), indicated for hypoparathyroidism, refractory rickets and familial hypophosphatemia²⁰. A 2004 trial described D2 as the only high-dose calciferol then available in the US market, and found its potency was less than one third that of D3 in a single-dose test⁴. Habit and availability are plausible reasons, but that is our inference.

That matters if you are repleting a deficiency. On weekly 50,000 IU, D2 produced about half the 25(OH)D rise of D3 in 33 adults⁸, and after a single dose it fell back to baseline by day 14 while D3 peaked then⁴. Retesting after a D2 course is reasonable. Ask your prescriber about D3 rather than substituting a supplement dose yourself.

Only under medical direction. The prescription label warns that the range between therapeutic and toxic doses is narrow and that dosage must be individualized under close medical supervision²⁰. For scale, the tolerable upper intake level is 25 to 100 mcg (1,000 to 4,000 IU) a day depending on age, and signs of toxicity are unlikely below 250 mcg (10,000 IU) a day².

The label requires blood calcium and phosphorus checks every 2 weeks during treatment²⁰. The one-year trial data are for a lighter schedule: in 64 adults aged 65 and over, 50,000 IU monthly (about 1,600 IU a day on average) or 1,600 IU daily produced no toxicity and no change in serum or urinary calcium⁹. The highest 25(OH)D there was 72.5 ng/mL, above the 50 ng/mL level that ODS links to potential adverse effects^{9, 2}. That trial does not show that weekly 50,000 IU is safe without monitoring.

Toxicity is almost always caused by supplements. It raises blood calcium (hypercalcemia), usually with 25(OH)D above 375 nmol/L (150 ng/mL). Hypercalcemia can cause²:

• nausea, vomiting and loss of appetite;
• muscle weakness and pain;
• excessive thirst and urination, with dehydration;
• neuropsychiatric changes;
• kidney stones.

In extreme cases it leads to kidney failure, calcium deposits in soft tissues, heart rhythm problems and death². The fact sheet does not separate D2 from D3 here.

The same cautions apply to D2 and D3, as far as the sources say. The ergocalciferol label lists these contraindications: hypercalcemia, malabsorption syndrome, abnormal sensitivity to the toxic effects of vitamin D, and hypervitaminosis D. It also notes that mineral oil interferes with vitamin D absorption, and that people with high phosphate from kidney bone disease need it controlled to prevent calcification²⁰. Thiazide diuretics lower urinary calcium, so combining them with vitamin D might lead to hypercalcemia, especially in older adults, kidney impairment or hyperparathyroidism².

Pregnancy and breastfeeding

The label says vitamin D above the recommended dietary allowance should be avoided in normal pregnancy unless a physician judges the benefit to outweigh the hazards, and that safety above 400 IU a day in pregnancy has not been established. In a breastfeeding mother given large doses, the vitamin passed into milk and caused hypercalcemia in her child²⁰. The ODS upper limit is 100 mcg (4,000 IU) a day in pregnancy and lactation².

Infants and children

Upper limits are lower: 25 mcg (1,000 IU) a day from birth to 6 months, 38 mcg (1,500 IU) at 7 to 12 months, 63 mcg (2,500 IU) at 1 to 3 years and 75 mcg (3,000 IU) at 4 to 8 years². The label says pediatric doses must be individualized and that vitamin D must be strictly restricted in infants with idiopathic hypercalcemia²⁰. The infant trial above also gave every child 50 mg/kg of calcium daily¹¹. Do not copy trial or adult doses for a child.

Kidney stones

In the Cochrane review, D3 combined with calcium raised the risk of kidney stones (RR 1.17, 95% CI 1.02 to 1.34, 4 trials)¹⁷. Our guide to calcium and vitamin D supplements covers taking them together.

Probably a little, while treatment is running. In a randomized trial of 44 people with stage 3 to 5 non-dialysis kidney disease, 50,000 IU weekly for 12 weeks raised total 25(OH)D by 45.0 ng/mL on D3 versus 30.7 ng/mL on D2 (P < 0.01), partly because 25(OH)D3 fell on D2²¹.

Six weeks after stopping, the difference was no longer significant (22.4 versus 17.6 ng/mL, P = 0.17), and levels dropped substantially in both groups. PTH and 1,25-dihydroxyvitamin D did not differ²¹. A retrospective analysis of 57 patients agreed on direction²².

Dose and form in kidney disease are a nephrologist's decision. For background, see chronic kidney disease and kidney health.

D2 is the form made from yeast and found in UV-treated mushrooms, but it is not the better one for raising levels. People who avoid animal products can ask supplement makers about sourcing, and an animal-free D3 from lichen is available². Our search found no trial testing lichen D3 itself, so the case for it rests on its being D3.

UV-treated mushrooms may not change total status much: in the 38-adult trial above, extra 25(OH)D2 was offset by lower 25(OH)D3¹³. Fortified foods also favor D3⁶.

You can, but there is no benefit in mixing. In one trial, splitting 1,000 IU into 500 IU of D2 plus 500 IU of D3 daily for 11 weeks raised 25(OH)D from 20.2 to 28.4 ng/mL, about the same as 1,000 IU of either form alone¹⁰. In a 279-adult trial, 25(OH)D3 did not increase in the combined D2 and D3 group¹⁶.

The practical risk is double counting. Doses from both forms, multivitamins and fortified foods all add toward the upper limit of 100 mcg (4,000 IU) for adults². A "vitamin D" label may mean either form, so check the supplement facts for cholecalciferol (D3) or ergocalciferol (D2).

Does magnesium help vitamin D absorption?

The trial evidence is on vitamin D metabolites in the blood, not absorption, and the effect depended on baseline level. In a randomized trial of 180 adults aged 40 to 85 (nested in a colorectal cancer prevention trial), magnesium raised 25(OH)D3 when baseline 25(OH)D was close to 30 ng/mL and lowered it when baseline was higher, about 30 to 50 ng/mL²³. Our guide to taking magnesium with vitamin D covers timing.

What depletes vitamin D?

• Obesity: people with a BMI of 30 or more have lower serum 25(OH)D than people without obesity².
• Orlistat: with a reduced-fat diet it can cut absorption from food and supplements².
• Corticosteroids: drugs such as prednisone can reduce calcium absorption and impair vitamin D metabolism².
• Statins: they may reduce vitamin D synthesis, and high supplement doses might weaken some statins².
• Low dietary fat: fat in the gut enhances absorption, so take it with a meal containing some fat².

Supplements in this guide

• Vitamin D
• Magnesium
• Calcium
• Vitamin K2

• Buying vitamin D for general use: choose D3, since it raises levels more^{1, 3}. Adult RDAs are 15 to 20 mcg (600 to 800 IU) a day², and the Endocrine Society suggests against going above the DRI in healthy adults under 75¹⁹.
• Prescribed 50,000 IU of D2: take it as directed and ask when to retest. Levels may fall back sooner than with D3⁴.
• Vegan: choose lichen-derived D3 where available, or D2 with a recheck of your level^{2, 6}.
• Kidney disease: let your nephrologist pick the form and dose²¹.
• Already taking D2 or D3: pick one form and count all sources toward the upper limit². See what to take with vitamin D for companions that do matter.

For low levels, see vitamin D for vitamin D deficiency. For food sources, read our vitamin D foods guide. For pairings, see our guides to calcium and vitamin D supplements and to vitamin D and vitamin K supplements.

Related conditions

• Vitamin D Deficiency
• Chronic Kidney Disease
• Rickets

We searched PubMed-indexed literature in several framings (D2 versus D3 trials, meta-analyses, mortality reviews, kidney disease, vegan sources, safety and magnesium) and read the abstracts of 22 studies and cited 21 of them. We also read the NIH Office of Dietary Supplements vitamin D fact sheet and a prescription ergocalciferol label on DailyMed on 2026-11-01. We prioritized meta-analyses and randomized trials in adults.

Limits: most trials measured blood levels over weeks to months, not disease outcomes, and the mortality comparison between forms is indirect. We found no trial of lichen-derived D3 specifically.

1. Balachandar R, et al. Relative Efficacy of Vitamin D2 and Vitamin D3 in Improving Vitamin D Status: Systematic Review and Meta-Analysis. Nutrients. 2021;13(10). doi:10.3390/nu13103328
2. National Institutes of Health, Office of Dietary Supplements. Vitamin D: Fact Sheet for Health Professionals. https://ods.od.nih.gov/factsheets/VitaminD-HealthProfessional/
3. van den Heuvel EG, et al. Comparison of the Effect of Daily Vitamin D2 and Vitamin D3 Supplementation on Serum 25-Hydroxyvitamin D Concentration (Total 25(OH)D, 25(OH)D2, and 25(OH)D3) and Importance of Body Mass Index: A Systematic Review and Meta-Analysis. Adv Nutr. 2024;15(1):100133. doi:10.1016/j.advnut.2023.09.016 Our study summary.
4. Armas LA, et al. Vitamin D2 is much less effective than vitamin D3 in humans. J Clin Endocrinol Metab. 2004;89(11):5387-91. doi:10.1210/jc.2004-0360
5. Tripkovic L, et al. Comparison of vitamin D2 and vitamin D3 supplementation in raising serum 25-hydroxyvitamin D status: a systematic review and meta-analysis. Am J Clin Nutr. 2012;95(6):1357-64. doi:10.3945/ajcn.111.031070 Our study summary.
6. Tripkovic L, et al. Daily supplementation with 15 μg vitamin D2 compared with vitamin D3 to increase wintertime 25-hydroxyvitamin D status in healthy South Asian and white European women: a 12-wk randomized, placebo-controlled food-fortification trial. Am J Clin Nutr. 2017;106(2):481-490. doi:10.3945/ajcn.116.138693
7. Logan VF, et al. Long-term vitamin D3 supplementation is more effective than vitamin D2 in maintaining serum 25-hydroxyvitamin D status over the winter months. Br J Nutr. 2013;109(6):1082-8. doi:10.1017/S0007114512002851
8. Heaney RP, et al. Vitamin D(3) is more potent than vitamin D(2) in humans. J Clin Endocrinol Metab. 2011;96(3):E447-52. doi:10.1210/jc.2010-2230
9. Binkley N, et al. Evaluation of ergocalciferol or cholecalciferol dosing, 1,600 IU daily or 50,000 IU monthly in older adults. J Clin Endocrinol Metab. 2011;96(4):981-8. doi:10.1210/jc.2010-0015
10. Holick MF, et al. Vitamin D2 is as effective as vitamin D3 in maintaining circulating concentrations of 25-hydroxyvitamin D. J Clin Endocrinol Metab. 2008;93(3):677-81. doi:10.1210/jc.2007-2308
11. Gordon CM, et al. Treatment of hypovitaminosis D in infants and toddlers. J Clin Endocrinol Metab. 2008;93(7):2716-21. doi:10.1210/jc.2007-2790
12. Adekunle MO, et al. Comparative Effectiveness of a Six-Week Treatment Course of Vitamin D2 and D3 in Children With Sickle Cell Anemia in Steady State With Hypovitaminosis D: A Randomized Clinical Trial. J Hematol. 2021;10(3):114-122. doi:10.14740/jh817
13. Stephensen CB, et al. Ergocalciferol from mushrooms or supplements consumed with a standard meal increases 25-hydroxyergocalciferol but decreases 25-hydroxycholecalciferol in the serum of healthy adults. J Nutr. 2012;142(7):1246-52. doi:10.3945/jn.112.159764
14. Brown EIG, et al. Effect of Vitamin D2 Supplementation on 25-Hydroxyvitamin D3 Status: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Nutr Rev. 2025. doi:10.1093/nutrit/nuaf166
15. Lehmann U, et al. Bioavailability of vitamin D(2) and D(3) in healthy volunteers, a randomized placebo-controlled trial. J Clin Endocrinol Metab. 2013;98(11):4339-45. doi:10.1210/jc.2012-4287
16. Hammami MM, et al. Differential effects of vitamin D2 and D3 supplements on 25-hydroxyvitamin D level are dose, sex, and time dependent: a randomized controlled trial. BMC Endocr Disord. 2017;17(1):12. doi:10.1186/s12902-017-0163-9
17. Bjelakovic G, et al. Vitamin D supplementation for prevention of mortality in adults. Cochrane Database Syst Rev. 2014;2014(1):CD007470. doi:10.1002/14651858.CD007470.pub3
18. Zhang Y, et al. Association between vitamin D supplementation and mortality: systematic review and meta-analysis. BMJ. 2019;366:l4673. doi:10.1136/bmj.l4673
19. Demay MB, et al. Vitamin D for the Prevention of Disease: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2024;109(8):1907-1947. doi:10.1210/clinem/dgae290
20. U.S. National Library of Medicine, DailyMed. Ergocalciferol capsules, USP 1.25 mg (50,000 IU): prescription drug label. https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=4ae38744-020d-4c37-a6f1-88f55c2f1047
21. Wetmore JB, et al. Cholecalciferol v. ergocalciferol for 25-hydroxyvitamin D (25(OH)D) repletion in chronic kidney disease: a randomised clinical trial. Br J Nutr. 2016;116(12):2074-2081. doi:10.1017/S000711451600427X
22. Mangoo-Karim R, et al. Ergocalciferol versus Cholecalciferol for Nutritional Vitamin D Replacement in CKD. Nephron. 2015;130(2):99-104. doi:10.1159/000430813
23. Dai Q, et al. Magnesium status and supplementation influence vitamin D status and metabolism: results from a randomized trial. Am J Clin Nutr. 2018;108(6):1249-1258. doi:10.1093/ajcn/nqy274 Our study summary.