Abstract

Light, whether natural or artificial, has a profound impact on our lives: it plays a crucial role in regulating our circadian rhythm and all related natural biorhythms, has a strong influence on our mood, our sleep quality and well-being and influences our cardiovascular system.
The electromagnetic spectrum emitted by the sun contains three components of optical radiation: ultraviolet (UV), visible and infrared. Detrimental effects of UV radiation are well known to the general population: increased incidence of skin cancer, photo-aging and induction or exacerbation of photosensitive dermatoses. However, UVA, but not UVB, leads to release of nitric oxide (NO), 1 decreasing blood pressure and, therefore, from a cardiovascular point of view, may be responsible for potential benefit.
Epidemiological data support the hypothesis that sunlight exposition might reduce blood pressure and heart disease. Population studies showed that blood pressure values correlate inversely with latitude and seasonality. 2 A similar correlation was found with atherosclerosis, for which high blood pressure is an important risk factor. Specifically, daylight exposure was found to be inversely associated with blood pressure and this effect was independent of other factors such as, for example, air temperature. 3
Of course, as usually happens with epidemiologic studies, not all data are pointing in the same direction: the REGARDS Study 4 did not find any association between sunlight exposure and blood pressure in a large population including 17,773 Black and White participants with age > 45 years.
Nevertheless, studying the effect of exposure to daylight on humans is an interesting area of research.
Experimental exposure of human skin to UVA physiologically leads to a fall in blood pressure and rise in heart rate, independently of induced skin temperature change.5,6 Mechanisms such as increase in vitamin D and NO were suggested to be at least in part responsible for this effect of sunshine/UVA exposure. Measurements of serum vitamin D levels (as 25-hydroxyvitamin D) show that populations with higher vitamin D levels are less likely to have hypertension, cardiovascular or cerebrovascular disease. Unfortunately, there is no evidence that vitamin D supplements can reduce blood pressure or the incidence or arterial hypertension. 7
In contrast, convincing evidence supports the role of the UV light-induced increase in NO: exposure to artificial sources of UV radiation was associated with release of NO stores in human skin, leading to vasodilation and a lowering of blood pressure. 5
Indeed, human skin contains photolabile NO derivates such as nitrite and S-nitrosothiols, which upon UVA radiation decompose and exert NO-specific biological responses such as increased local blood flow or reduced blood pressure.
In humans, the UVA-induced decrease in blood pressure was paralleled by increased forearm blood flow, increased flow-mediated vasodilatation of the brachial artery and decreased forearm vascular resistance. 6
Forearm venous plethysmography experiments showed that UVA has a direct vasodilatory effect on the human arterial vasculature mediated by increased NO level. The first hypothesis was that this could be due to increase in NO production by NO synthase (NOS). Infusion of L-N-monomethyl arginine, an antagonist of NOS, into the brachial artery failed to blunt the vasodilatation induced by UVA, suggesting that UVA-induced NO release is NOS independent and supporting the UVA-radiation induced photolysis of cutaneous stores of NO. 5
Even taking into consideration this positive effect, chronic exposition to UVA is not something we would recommend to a broad population in order to prevent cardiovascular disease.
In looking for a method which allows avoidance of the injurious effects of UVA radiation without giving up the positive effect, the mechanism and biological relevance of blue-light (420–453 nm)-induced non-enzymatic NO generation from photolabile NO derivates in human skin in vitro and in vivo were evaluated. Indeed, visible blue light was shown to induce non-enzymatic NO release from cutaneous photolabile NO derivates, similar to UV light but without inducing DNA strand breaks. 8
The use of monochromatic blue light (420–453 nm) was therefore proposed as an alternative to UV with the same positive cardiovascular effect but no carcinogenic potential.
Following these preliminary data Stern and co-authors investigated the effect of whole body exposure to visible blue light on blood pressure and endothelial function in healthy males. 9 This very interesting, hypothesis-generating, cross-over study was conducted in 14 male volunteers, age 30–60 years, and showed that whole body exposure to visible blue light over 30 min induced an acute reduction of blood pressure and arterial stiffness (as measured by assessing pulse wave velocity) and improved endothelial function (as measured by flow mediated dilatation of the brachial artery) while exposure to control light (filter foil covering the volunteers) did not show any vascular effect. These positive effects were paralleled by increased circulating NO species and nitroso compounds and similar to the ones induced by daily sunlight exposure.
Poor blood pressure control is still an important issue all over Europe: the EUROASPIRE IV survey 10 shows that large proportions of patients at high cardiovascular risk have uncontrolled hypertension. Indeed less than half (42.8%) of the patients on blood pressure lowering medication reached the target of < 140/90 mmHg (<140/80 mmHg in people with self-reported diabetes). This percentage is higher if we consider patients with isolated systolic hypertension.
Blue visible light seems to be an easy and quick option for modulating blood pressure: as this effect is particularly evident on systolic blood pressure it could be useful in an older population to reduced poly-pharmacy and increase blood pressure control.
However, bearing in mind ‘there is no light without shadow’, the short-term effect of blue light exposure needs to be confirmed in a broader health population including older subjects and women, as well as in people with arterial hypertension or cardiovascular disease. Moreover, the long-term effects need to be carefully evaluated.
Footnotes
Declaration of conflicting interests
The author declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding
The author received no financial support for the research, authorship, and/or publication of this article.
