Vitamin D and Global Health

Despite Malaysia’s year-round sunny climate, vitamin D deficiency is surprisingly common among Malaysians. However, we hypothesise that vitamin D levels among coastal populations are above average. Thus, we aim to investigate vitamin D levels and correlate them with the potential contributing factors from three selected coastal villages in Johor, Melaka, and Negeri Sembilan. Convenient sampling was employed to recruit 120 Malay male and female participants, and dried blood spots (DBS) were obtained to measure 25 (OH) vitamin D3 levels via immunoassay. Participants also completed two questionnaires: the Sun Exposure and Protection Index (SEPI) and a validated food frequency questionnaire for Malaysians. The participant pool comprised 35.20% males and 64.80% females who completed all questionnaires and underwent DBS sampling. Our analysis revealed a significant difference (p < 0.05) based on skin tones, impacting various facets of the SEPI, including sunscreen usage, protective clothing utilisation, and the adoption of protective headwear. Furthermore, gender emerged as another pivotal factor, demonstrating significant distinctions in these SEPI components. Nevertheless, there is a weak correlation between SEPI scores and vitamin D levels. Subsequent regression analysis did produce statistically significant results (p = 0.018), yet the associated low R² value indicated a weak correlation between dietary vitamin D intake that impacts vitamin D levels. In conclusion, our preliminary findings indicate that sun exposure and dietary factors are not the sole determinants of 25-OH vitamin D3 levels. However, we require more samples from various coastal locations for a definitive justification. Full article

Background: Increasing evidence points at an important physiological role of the timekeeping system, known as the circadian clock (CC), regulating not only our sleep–awake rhythm but additionally many other cellular processes in peripheral tissues. It was shown in various cell types that environmental stressors, including ultraviolet B radiation (UV-B), modulate the expression of genes that regulate the CC (CCGs) and that these CCGs modulate susceptibility for UV-B-induced cellular damage. It was the aim of this pilot study to gain further insights into the CCs’ putative role for UV-B-induced photocarcinogenesis of skin cancer. Methods: Applying RT-PCR, we analyzed the expression of two core CCGs (brain and muscle ARNT-like 1 (Bmal1) and Period-2 (Per2)) over several time points (0–60 h) in HaCaT cells with and without 1,25-dihydroxyvitamin D (D₃) and/or UV-B and conducted a cosinor analysis to evaluate the effects of those conditions on the circadian rhythm and an extended mixed-effects linear modeling to account for both fixed effects of experimental conditions and random inter-individual variability. Next, we investigated the expression of these two genes in keratinocytes representing different stages of skin photocarcinogenesis, comparing normal (Normal Human Epidermal Keratinocytes—NHEK; p53 wild type), precancerous (HaCaT keratinocytes; mutated p53 status), and malignant (Squamous Cell Carcinoma SCL-1; p53 null status) keratinocytes after 12 h under the same conditions. Results: We demonstrated that in HaCaT cells, Bmal1 showed a robust circadian rhythm, while the evidence for Per2 was limited. Overall expression of both genes, but especially for Bmal1, was increased following UV-B treatment, while Per2 showed a suppressed overall expression following D₃. Both UVB and 1,25(OH)₂D₃ suggested a significant phase shift for Bmal1 (p < 0.05 for the acrophase), while no specific effect on the amplitude could be evidenced. Differential effects on the expression of BMAL1 and Per2 were found when we compared different treatment modalities (UV-B and/or D₃) or cell types (NHEK, HaCaT, and SCL-1 cells). Conclusions: Comparing epidermal keratinocytes representing different stages of skin photocarcinogenesis, we provide further evidence for an independently operating timekeeping system in human skin, which is regulated by UV-B and disturbed during skin photocarcinogenesis. Our finding that this pattern of circadian rhythm was differentially altered by treatment with UV-B, as compared with treatment with D₃, does not support the hypothesis that the expression of these CCGs may be regulated via UV-B-induced synthesis of vitamin D but might be introducing a novel photoprotective property of vitamin D through the circadian clock. Full article