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Sunlight Exposure and Cardiovascular Risk Factors

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Sunlight Exposure and Cardiovascular Risk Factors

Discussion


This analysis adds to the limited previous research addressing the relationship between sunlight and vascular health. Higher myocardial infarction, stroke, and adverse vascular risk factor rates have been reported in farther northern latitudes, but it is not clear whether this is due to environmental, social, or other factors. There is also some evidence of higher myocardial infarction and stroke rates during the winter although other research contradicts this. While lower temperatures have been shown to be associated with high blood pressures, there may also be seasonal variations in lipid levels that are independent of temperature. Sunlight exposure is another seasonal factor, and might affect vascular risk factors through vitamin D metabolism, which is increasingly found to be related to various chronic diseases. There is indication that vitamin D insufficiency may increase vascular event risk and adversely impact various vascular risk factors. For most people, vitamin D status is primarily determined by sunlight exposure. Blood serum 25(OH)D levels are usually used to determine vitamin D status and can fluctuate with differential exposure to light and dietary intake.

This study is the third using REGARDS data merged with NASA meteorological data that demonstrated a possible link between sunlight and health. The results of this study suggest that lower long-term sunlight exposure has an association with lower HDL levels, after accounting for confounders. Since this association was found in both exploratory and confirmatory models, it is not likely that this finding is due to chance. However, the magnitude of this association is small, since those in the lowest, compared to the highest quartile of insolation exposure had only about 2 mg/dL lower HDL levels compared to those with higher sunlight exposures. In addition, while observational studies have shown that higher HDL levels are associated with lower cardiovascular risk, interventional studies have not been consistent and are ongoing, so the clinical significance of this association is unknown. Sunlight also had significant univariate relationships with SBP in both exploratory and confirmatory models, but this association did not remain significant after confounder adjustment in the confirmatory models. In addition, the associations with SBP were also small, with adjusted effect sizes less than 3 mmHg. We also found that the association between insolation and SBP may be stronger among blacks than whites, but this interaction was also not significant in adjusted confirmatory models. We determined that this was due to the inclusion of temperatures in the model. Previous research in REGARDS and other studies have found lower temperatures to be related to higher blood pressures. It is not clear why the inclusion of temperature would eliminate the significant association between insolation and SBP in the exploratory, but not confirmatory analyses. Collinearity may be an issue, with higher maximum temperatures correlated with higher insolation levels. These results agree with our previous analyses which suggest that decreased sunlight exposure is related to increased stroke incidence and increased likelihood of cognitive impairment and decline, although given the effect sizes it is unlikely that the traditional risk factors explored fully mediate these associations.

There is little other research examining sunlight and vascular risk, but a recent Hong Kong study found that temperature and air pressure, but not solar radiation, were significantly associated with stroke. Our current and previous research differs from this study in many ways, including temporality (exposure within days of outcome, rather than one year exposure in this analysis), location (a small tropical area rather than a wide range of mostly temperate areas), and that our study did not include air pressure. Since 25(OH)D3 has a biological half-life of several weeks, it would be plausible that our longer term sunlight exposure would have a larger effect on vitamin D levels, and thus on vascular risk. And while we did not include air pressure in our models, we did account for temperature, as this is the primary meteorological variable that has been shown to have associations with vascular risk.

Exposure misclassification exists as a possible source of bias. This could happen if during the time period of an exposure measurement a participant spent a large amount of time in a climate different from that indicated by the outdoor exposures linked to his or her residence. In addition to exposure misclassification, it is possible that our findings are confounded by spatial autocorrelation, although that is not likely since adding region to the model did not attenuate the relationship. Another potential limitation is that there may be confounders for which we have not accounted, such as air pollution. While we did not correct for variables such as cloudiness and altitude, insolation measures represent the sunlight energy received on the ground, so the effects of such variables do not need to be included.

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