Data Insight - Is insufficient sunlight exposure an under-recognised risk factor for CVD?
Categories: Data Insights, Data Insights: ADR Scotland
15 June 2026
Is insufficient sunlight exposure an under-recognised risk factor for cardiovascular disease mortality in Scotland? An analysis of the Scottish Historical Population Platform (1880-1973).
Summary
Cardiovascular disease (CVD) risk rises in winter and is higher further from the equator, a pattern long attributed to, for example, cold temperatures. Recent evidence suggests that sunlight itself plays a role, acting on cardiovascular health independently of temperature1 and through short-term mechanisms distinct from vitamin D. For example, dermal ultraviolet exposure releases nitric oxide from skin stores within minutes and that can days,2 promoting vasodilation3 and suppressing inflammation.4 Red and near-infrared light, meanwhile, have been demonstrated to stimulate mitochondrial ATP production5 and suppress inflammation.6 Yet the short-term effects of insufficient sunlight exposure have been understudied.
Figure 1. Plausible protective mechanisms of short-term sunlight exposure and cardiovascular disease mortality.
We analysed ~1.67 million Cardiovascular disease (CVD) deaths in Scotland between 1880 and 1973, and found that low sunlight was linked to more CVD deaths than cold and heat combined. These findings identify an underrecognised contributor to winter cardiovascular mortality, with implications for public health messaging and National Health Service (NHS) winter planning.
What we did?
We used the Scottish Historical Population Platform, a newly digitised database of vital events records for the entire Scottish population from 1855 to 1973, the first of its kind in the UK. From it, we aggregated CVD deaths to create a daily time-series between 1880 and 1973 and linked the data with daily temperature and sunlight conditions.
The analysis used a time-stratified design that compares death counts and weather conditions on the same day-of-week within the same month and year (for example, every Tuesday in February 1910). Because the population at risk is stable within such a narrow time window, time-invariant confounders (e.g., age structure, smoking prevalence, healthcare access, etc.) are accounted for by design. We then estimated non-linear exposure-response relationships using conditional Poisson regression with distributed lag non-linear models, allowing effects to play out over different timescales: one day for heat and sunlight (which act quickly) and five days for cold (which has a more delayed effect). Sunlight was adjusted for in the temperature models and temperature in the sunlight models, since these are the main time-varying confounders of each other.
What remains is the short-term independent effects of temperature and sunlight on the risk of dying from CVD. We ran the analysis separately by sex and across three historical periods (1880–1909, 1910–1939, 1940–1973) to see how the relationships shifted as demographics, cities, main causes of illness and climate shifted in Scotland.
What we found?
Across the full window, the three exposures were independently associated with higher CVD mortality:
- Low sunlight: 8.3% of CVD deaths attributable
- Cold: 6.0% of CVD deaths attributable
- Heat: 0.68% of CVD deaths attributable
Insufficient sunlight accounted for the greatest attributable burden of CVD deaths across the whole period, larger than cold and heat combined. The relationships were nonlinear: risk rose steeply at the extremes, particularly during the darkest days of the Scottish winter and levelled off in the sunnier seasons.
Source: Scottish Historical Population Platform
Figure 2. Daily relative risk of cardiovascular mortality as a function of solar radiation (MJ/m²/day) across three historical periods (1880–1909, 1910–1939, 1940–1973) and by sex, adjusted for temperature. In all periods, low sunlight was associated with elevated CVD mortality in a non-linear pattern, with the highest risk on the darkest days. Analyses compare relatively small changes on the same days of the week within the same month, and combines these comparisons into a single exposure-response curve.
The patterns shifted over the historical study period. Heat-related deaths fell 2.4-fold between the late 19th century and the mid-20th, which may reflect better housing, less intensive chores and working conditions or medical advances in treating heat stroke and CVD. Cold-related risk, by contrast, declined only modestly over the same period.
Sex differences also emerged after 1900. Men bore more of the cold-related risk, while women bore more of the heat- and low-sunlight-related risk after the turn of the century. These patterns may reflect differences in occupation, indoor time, and social isolation. For example, women tend to outlive their male partners, leaving older widows particularly vulnerable during heat extremes.
Why it matters?
Insufficient sunlight exposure appears to be an underrecognised but important risk factor for CVD health. Scottish winters are characterised by short, dark days, and much of it spent indoors in the modern era. This study suggests that the loss of the physiological signals of sunlight during dark periods has a substantial effect on CVD mortality risk.
Our study points to a vitamin D-independent mechanism, such as nitric oxide release or red/near infrared light induced photobioimmodulation. Ultraviolet-B rays are not strong enough to sufficiently penetrate the skin to synthesise vitamin D in Scottish winters and this process is longer-term, as opposed to the short-term (day-to-day) protective effect we see of sunlight exposure.
This study suggests that low sunlight exposure should be considered in temperature, climate and health studies, as some of the risk of cold reported in previous studies may be explained by insufficient sunlight. With climate change heat-related mortality could rise without intervention and the effects of changing sunlight exposure remains uncertain.
Interventions that increase safe, low-dose sunlight exposure, particularly in winter, could reduce CVD mortality. The National Health Service could plan for increased CVD admissions during prolonged periods of low sunlight, as it already does for cold snaps and heatwaves. Public health messaging could encourage populations to seek outdoor light exposure during winter daylight hours, even on overcast days, and to ensure that prescribed cardiovascular medications are taken consistently through the darker periods, when risk is higher.
Acknowledgments
This work was supported by Health Data Research UK (grant ID: EDIN1), which is funded by the UK Medical Research Council, Engineering and Physical Sciences Research Council, Economic and Social Research Council, Department of Health and Social Care (England), Chief Scientist Office of the Scottish Government Health and Social Care Directorates, Health and Social Care Research and Development Division (Welsh Government), Public Health Agency (Northern Ireland), British Heart Foundation and the Wellcome Trust. This work was supported in part by UKRI's Securing Better Health, Ageing and Wellbeing strategic theme.
The SHiPP data was accessed through the SHiPP programme, part of ADR Scotland, funded by Economic and Social Research Council (ESRC) through the award to ADR UK. The Grant Ref is: UKRI3324.
We would also like to thank the contribution and support of National Records of Scotland & EPCC.
ACS was also supported by a Fonds de recherche du Québec – Santé Postdoctoral Award (FRQS; https://doi.org/10.69777/353073)
References
1Mackay, Daniel F., et al. "UVA and seasonal patterning of 56 370 myocardial infarctions across Scotland, 2000–2011." Journal of the American Heart Association 8.23 (2019): e012551.
2Hazell, G., Khazova, M., Cohen, H., Felton, S., & Raj, K. (2022). Post-exposure persistence of nitric oxide upregulation in skin cells irradiated by UV-A. Scientific reports, 12(1), 9465.
3Liu, Donald, et al. "UVA irradiation of human skin vasodilates arterial vasculature and lowers blood pressure independently of nitric oxide synthase." Journal of Investigative Dermatology 134.7 (2014): 1839-1846.
4Mao, K., Chen, S., Chen, M., Ma, Y., Wang, Y., Huang, B., ... & Sun, B. (2013). Nitric oxide suppresses NLRP3 inflammasome activation and protects against LPS-induced septic shock. Cell research, 23(2), 201-212.
5Dompe, Claudia, et al. "Photobiomodulation—underlying mechanism and clinical applications." Journal of clinical medicine 9.6 (2020): 1724.
6Hamblin, Michael R. "Mechanisms and applications of the anti-inflammatory effects of photobiomodulation." AIMS biophysics 4.3 (2017): 337.
