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Vitamin E or beta-carotene supplementation had no effect on skin sensitivity to UVR. Although vitamin E supplements significantly reduced the skin malondialdehyde concentration, neither supplement affected other measures of UVR-induced oxidative stress in human skin, which suggested no photoprotection of supplementation.

Purpose To determine serum 25(OH)D and 1,25(OH)2D relationship with hepatitis B vaccination (study 1). Then, to investigate the effects on hepatitis B vaccination of achieving vitamin D sufficiency (serum 25(OH)D ≥ 50 nmol/L) by a unique comparison of simulated sunlight and oral vitamin D3 supplementation in wintertime (study 2). Methods Study 1 involved 447 adults. In study 2, 3 days after the initial hepatitis B vaccination, 119 men received either placebo, simulated sunlight (1.3 × standard-erythema dose, 3 × /week for 4 weeks and then 1 × /week for 8 weeks) or oral vitamin D3 (1000 IU/day for 4 weeks and 400 IU/day for 8 weeks). We measured hepatitis B vaccination efficacy as percentage of responders with anti-hepatitis B surface antigen immunoglobulin G ≥ 10 mIU/mL. Results In study 1, vaccine response was poorer in persons with low vitamin D status (25(OH)D ≤ 40 vs 41–71 nmol/L mean difference [95% confidence interval] − 15% [− 26, − 3%]; 1,25(OH)2D ≤ 120 vs ≥ 157 pmol/L − 12% [− 24%, − 1%]). Vaccine response was also poorer in winter than summer (− 18% [− 31%, − 3%]), when serum 25(OH)D and 1,25(OH)2D were at seasonal nadirs, and 81% of persons had serum 25(OH)D < 50 nmol/L. In study 2, vitamin D supplementation strategies were similarly effective in achieving vitamin D sufficiency from the winter vitamin D nadir in almost all (~ 95%); however, the supplementation beginning 3 days after the initial vaccination did not effect the vaccine response (vitamin D vs placebo 4% [− 21%, 14%]). Conclusion Low vitamin D status at initial vaccination was associated with poorer hepatitis B vaccine response (study 1); however, vitamin D supplementation commencing 3 days after vaccination (study 2) did not influence the vaccination response. Clinical trial registry number Study 1 NCT02416895; https://clinicaltrials.gov/ct2/show/study/NCT02416895; Study 2 NCT03132103; https://clinicaltrials.gov/ct2/show/NCT03132103.

Dietary omega‐3 polyunsaturated fatty acids (ω‐3 PUFA) reduce sunburn, an acute inflammatory response, in humans, We assessed whether this may be mediated by reduced ultraviolet‐B (UV‐B) induction of proinflammatory mediators tumor necrosis factor‐α (TNF‐α), interleukin (IL)‐1β, IL‐6, IL‐8 and prostaglandin (PG)E2 in healthy skin. In a double‐blind, randomized study, 28 humans received 4 g daily of 95% ethyl esters of eicosapentaenoic acid (EPA) or oleic acid (OA) orally for 3 months. Skin biopsies and suction blister fluid were taken from unexposed and UV‐B‐exposed skin and examined for mediator expression immunohistochemically and quantitatively by immunoassay; plasma levels were also assayed. The subjects taking EPA, but not OA, showed a significant rise in their minimal erythemal dose (MED) (data reported elsewhere). Before supplementation, irradiation with 3X MED UV‐B increased blister fluid TNF‐α, IL‐6, IL‐8 and PGE2 at 16 h (all P < 0.001). No significant change occurred in baseline or UV‐B‐induced skin levels of cytokines after either supplement, whereas UV‐B induction of PGE2 was abolished after EPA but not OA. Immunohistochemical expression of the cytokines at baseline and after UV‐B was unaltered by EPA and OA; circulating cytokine and PGE2 levels were also unchanged. Hence, in healthy skin in vivo, there was no evidence that reduction of the sunburn response by EPA is mediated by the proinflammatory cytokines examined; abrogation of UV‐B‐generated PGE2, may play a role.