Vitamin D

Vitamin D is a secosteroid hormone that regulates over 200 genes. In skin specifically, it promotes keratinocyte differentiation (essential for barrier formation), stimulates production of cathelicidin (an antimicrobial peptide important for innate immunity), modulates inflammatory T-cell responses, and supports wound healing.

The skin is both a source and target of vitamin D. UVB radiation converts 7-dehydrocholesterol in the epidermis to pre-vitamin D3, but diligent sunscreen use (correctly applied at SPF 30+) reduces cutaneous vitamin D synthesis by over 95%. This creates a paradox for skin-health-conscious people: the best UV protection practice for preventing photoageing simultaneously reduces vitamin D production.

• Supports skin barrier formation through keratinocyte differentiation
• Enhances innate antimicrobial defence (cathelicidin production)
• Modulates inflammatory immune responses relevant to acne, eczema, psoriasis
• Supports wound healing
• Correcting deficiency may improve atopic dermatitis severity

Maintenance dose: 1,000–2,000 IU (25–50mcg) vitamin D3 daily for most adults. This maintains adequate levels in the absence of significant sun exposure.

Correcting deficiency: 4,000–5,000 IU daily for 8–12 weeks, then retest. Doses above 4,000 IU/day should ideally be guided by blood test results (25-hydroxyvitamin D).

Target serum level: 30–50 ng/mL (75–125 nmol/L) is the generally accepted adequate range. Below 20 ng/mL is deficient; 20–30 ng/mL is insufficient.

Timing: Take with your largest fat-containing meal of the day. Vitamin D is fat-soluble and absorption increases significantly when taken with dietary fat.

Co-factor: Vitamin K2. Vitamin D increases calcium absorption. Vitamin K2 (MK-7, 100–200mcg daily) directs calcium to bones rather than soft tissues. This pairing is commonly recommended when supplementing vitamin D at higher doses long-term.

Preferred: Vitamin D3 (cholecalciferol). D3 is more effective at raising and maintaining serum 25(OH)D levels than vitamin D2 (ergocalciferol).

Vegan option: Lichen-derived vitamin D3 is available. Vitamin D2 from fungi is an alternative but less potent per unit.

Format: Softgels in oil or liquid drops are preferred over tablets for fat-soluble vitamins. Oil-based formats may improve absorption, particularly when not taken with a fatty meal.

The sunscreen paradox: If you wear SPF 30+ daily (which you should for skin health), you are almost certainly reducing your vitamin D synthesis substantially. Oral supplementation resolves this without compromising UV protection. This is one of the clearest cases where a supplement directly compensates for a skin-health practice.

Vitamin D and topical retinoids: Both promote keratinocyte differentiation but through different receptors (VDR and RAR/RXR respectively). Adequate vitamin D status may support the cellular processes that retinoids depend on. No negative interactions.

Vitamin D and barrier repair protocols: When repairing a compromised barrier, adequate vitamin D supports the keratinocyte differentiation required to rebuild the epidermal barrier. If your barrier is damaged and you are vitamin D-deficient, correction may accelerate repair alongside topical ceramide-based approaches.

Calcipotriol (topical vitamin D analogue): This is a prescription topical used for psoriasis. Oral vitamin D supplementation and topical calcipotriol work through related but distinct mechanisms. If you are prescribed calcipotriol, inform your doctor about oral vitamin D supplementation to avoid excessive calcium absorption.

• Assuming adequate sun exposure provides enough vitamin D if you wear sunscreen daily
• Not getting baseline blood levels tested before supplementing
• Using vitamin D2 instead of D3
• Taking vitamin D without fat (dramatically reduces absorption)
• Mega-dosing without monitoring (weekly 50,000 IU protocols without medical supervision)
• Not pairing with vitamin K2 when using higher doses long-term

Lim et al. (2016): Meta-analysis of 14 studies found significantly lower serum vitamin D levels in acne patients compared to healthy controls. Correlation between deficiency severity and acne severity was observed. (Journal of Cosmetic Dermatology)

Hata et al. (2008): Vitamin D supplementation (4,000 IU/day for 21 days) increased cathelicidin expression in atopic dermatitis patients, enhancing antimicrobial skin defence. (Journal of Allergy and Clinical Immunology)

Mattozzi et al. (2020): Review of vitamin D’s role in skin barrier function, concluding that deficiency impairs epidermal differentiation and barrier integrity, and that supplementation may improve barrier-related skin conditions. (Nutrients)