Vitamin D against atopic dermatitis: correlation or real help?

Nutrients published a large review of recent years (2019–2025) on whether vitamin D is useful in atopic dermatitis (AD). The answer is neat: vitamin D can be a useful addition to standard therapy, especially in children with moderate-to-severe AD and laboratory-confirmed deficiency, but it is not a universal “pill.” The effect is not the same in different groups, and some randomized studies do not find clear advantages over placebo. Larger and more accurate clinical trials are needed, taking into account “responders” and baseline 25(OH)D levels .

Background

• Why vitamin D in AD at all? Vitamin D affects immunity and the skin barrier (cathelicidin, filaggrin; modulation of Th2/Th17 inflammation), so its deficiency is often considered a factor in the more severe course of AD. A review in Nutrients summarizes these mechanisms and clinical data.
• What clinical trials show. Randomized trials give a mixed picture:
  • In children with moderate-severe AD, supplementation with 1600 IU/day D₃ for 12 weeks increased EASI-75 incidence and reduced severity compared with placebo (a signal in favor of D-deficient “responders”).
  • In other RCTs (including those with weekly high doses), improvement in 25(OH)D status was not always accompanied by a reduction in SCORAD/EASI.
  • In children with "winter" worsening of blood pressure in Mongolia, vitamin D alleviated symptoms - a population at high risk of deficiency.
• What do the pooled reviews say? Recent meta-analyses of RCTs suggest modest reductions in AD severity with vitamin D supplementation, but highlight heterogeneity and the need for larger, longer studies stratified by baseline 25(OH)D.
• Who potentially benefits more. Signals are stronger in children, with moderate-to-severe AD and laboratory vitamin D deficiency; genetic response modifiers (VDR/CYP variants) are discussed, supporting the idea of a “vitamin D response endotype.” (See Nutrients for summary and examples.)
• Perinatal context: In a large pregnancy study (MAVIDOS), maternal cholecalciferol reduced the risk of offspring eczema at 12 months, but the effect waned by 24–48 months—another hint of an age/context relationship.

Why Consider Vitamin D for BP at All?

AD is a chronic inflammatory skin disease: up to 20% of children and up to 10% of adults suffer from it, itching and dry skin seriously affect the quality of life; asthma, sleep disorders and depression often coexist. The biology of AD includes a defect in the skin barrier and Th2 inflammation (IL-4/IL-13, etc.). Vitamin D affects immunity and barrier proteins (e.g. filaggrin), so researchers have long had a hypothesis “vitamin D → milder course of AD”.

What clinical studies have shown

• Children with severe AD. In a double-blind RCT, adding 1600 IU cholecalciferol/day for 12 weeks to standard hydrocortisone resulted in a greater reduction in EASI (−56.4% vs. −42.1% placebo; p =0.039) and more EASI-75 responders (38.6% vs. 7.1%). The improvement correlated with the increase in 25(OH)D, suggesting a dose-response relationship and benefit in deficiency.
• High doses and biomarkers. In a weight-based dose RCT of 8,000–16,000 IU/week, 25(OH)D levels increased significantly over 6 weeks, but total SCORAD did not change versus placebo. Post-hoc analysis identified a subgroup of participants who had greater symptom improvement with 25(OH)D levels >20 ng/mL, a possible “vitamin D response endotype.”
• Infants <1 year: D vs synbiotic. In a three-arm RCT of 81 infants, both vitamin D3 (1000 IU/day) and a multistrain synbiotic significantly reduced SCORAD compared with standard care; there was no difference in the magnitude of effect between the interventions. The authors conclude that the interventions likely affect overlapping immune pathways (gut-skin axis, SCFA, regulatory T cells).

What observational and preclinical data say

Many observational studies find: low 25(OH)D ↔ more severe AD; in a number of meta-analyses of RCTs, vitamin D supplementation in children and in moderate-to-severe cases is associated with clinical improvement. But there are also studies without significant differences - seasonality, insolation, nutrition, age and other confounding factors interfere. In mouse models, calcifediol suppressed STAT3/AKT/mTOR signaling, reduced AQP3 (associated with TEWL) and increased VDR/VDBP expression; in experiments, combinations of vitamin D + crisaborole reduced proinflammatory cytokines more than either alone.

Genetics and pregnancy: who benefits more

• VDR/CYP24A1 polymorphisms may influence AD risk and response to therapy: for example, the C allele of rs2239182 is associated with a ~66% reduction in risk, whereas rs2238136 is associated with a more than two-fold increase in risk. This is an argument for personalized supplementation.
• In a study of pregnant women (MAVIDOS), cholecalciferol intake reduced the risk of AD in the child at 12 months (OR 0.57), but the effect disappeared by 24–48 months; the benefit was greater in children breastfed for >1 month.

Practical conclusion

• Vitamin D is not a substitute for basic therapy (emollients, topical steroids/calcineurin inhibitors, phototherapy, biological/UC inhibitors when indicated), but can be an adjuvant - if there is a deficiency and/or moderate-severe course (especially in children). Before starting, it makes sense to take a 25(OH)D test and discuss the dose with a doctor, so as not to go into hypervitaminosis/hypercalcemia.
• There are no universal patterns: some patients appear to belong to the “vitamin D-responder” endotype. Future studies should stratify participants by 25(OH)D levels, immune profile, and VDR variants and look for biomarkers of response (including skin/gut microbiome).

Review conclusion

The totality of clinical and experimental data suggests that vitamin D has immunomodulatory and barrier-restoring potential (↓Th2/Th17, ↑barrier proteins, local anti-inflammatory activity). For now, its place is personalized support as part of standard therapy, not a “magic wand.” Large RCTs with long-term observation and smart stratification of “responders” are needed.

Source: Przechowski K., Krawczyk MN, Krasowski R., Pawliczak R., Kleniewska P. Vitamin D and Atopic Dermatitis—A Mere Correlation or a Real Supportive Treatment Option? Nutrients. 2025;17(16):2582. doi:10.3390/nu17162582.