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Cardiovascular disease outcomes in relation to 25-hydroxyvitamin D and its seasonal variation: Results from the
Viktor Oskarsson1, Veikko Salomaa2, Pekka Jousilahti2
1Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden.
Insights
This study found no evidence that seasonal vitamin D (25[OH]D) level changes drive cardiovascular disease (CVD) increases. However, higher vitamin D levels were consistently linked to lower CVD incidence and mortality.
Area of Science:
- Cardiology
- Endocrinology
- Public Health
Background:
- Hypovitaminosis D (vitamin D deficiency) has been hypothesized to contribute to the winter increase in cardiovascular disease (CVD).
- This hypothesis has been infrequently tested, necessitating further investigation into the relationship between vitamin D levels and CVD seasonality.
Purpose of the Study:
- To investigate the association between CVD incidence and mortality with seasonal variations in 25-hydroxyvitamin D (25[OH]D) levels.
- To examine the relationship between individual 25[OH]D concentrations and CVD risk.
Main Methods:
- Utilized harmonized 25(OH)D data from the Biomarkers for Cardiovascular Risk Assessment in Europe (BiomarCaRE) project (n=79,570).
- Employed Poisson regression to analyze CVD incidence and mortality rates across two-month categories based on 25(OH)D seasonality.
- Applied Cox regression to assess hazard ratios for CVD incidence and mortality across quarters of baseline 25(OH)D concentrations.
Main Results:
- No significant association was found between seasonal 25(OH)D troughs and increased CVD incidence.
- CVD mortality was slightly higher during 25(OH)D trough months, but this did not meet statistical significance compared to other periods.
- Higher concentrations of 25(OH)D were inversely associated with both CVD incidence (HR: 0.82) and CVD mortality (HR: 0.64).
Conclusions:
- The study does not support the hypothesis that short-term seasonal reductions in 25(OH)D drive increases in CVD.
- Consistent with other observational studies, higher 25(OH)D concentrations show an inverse relationship with CVD risk.
Background:
It has been hypothesized but seldom tested that the winter excess in cardiovascular disease (CVD) is related to hypovitaminosis D. The present study examined the association between CVD and (i) seasonality of 25-hydroxyvitamin D (25[OH]D) and (ii) individual 25(OH)D concentrations.
Methods And Findings:
Harmonized 25(OH)D data were obtained from the Biomarkers for Cardiovascular Risk Assessment in Europe (BiomarCaRE) project, including 79,570 participants examined between 1984 and 2010. One 25(OH)D measurement was available per participant. Primary endpoints were CVD incidence (coronary heart disease or stroke; n = 6006) and CVD mortality (n = 2985). To study (i), Poisson regression-derived rate ratios were compared according to two-month categories, ordered by baseline 25(OH)D concentrations. To study (ii), Cox regression-derived hazard ratios were compared according to quarters of baseline 25(OH)D concentrations. With respect to (i), despite a median 25(OH)D concentration ratio of 1:1.79, the trough months of 25(OH)D in March and April had a similar CVD incidence as the peak months of 25(OH)D in August and September (rate ratio: 1.07, 95% CI: 0.98-1.17). CVD mortality was slightly higher in the trough months compared to the peak months (rate ratio: 1.27, 95% CI: 1.12-1.44) but not compared to the other months (despite median 25[OH]D concentration ratios up to 1:1.62; p ≥ 0.077). The CVD mortality peak in January preceded the 25(OH)D trough, not adhering to the temporality criterion of Bradford Hill. With respect to (ii), compared to the lowest quarter, the highest quarter of 25(OH)D was associated with lower CVD incidence (hazard ratio: 0.82, 95% CI: 0.76-0.89) and CVD mortality (hazard ratio: 0.64, 95% CI: 0.57-0.72).
Conclusion:
The present study does not support the hypothesis that seasonal increases in CVD are driven by short-term reductions in 25(OH)D. As in most observational studies, higher 25(OH)D concentrations were inversely associated with CVD.
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