Sunlight and Heart Disease; Why Infrared Light May Matter More than Vitamin D

The practice of “heliotherapy” or the use of light (generally sunlight) to produce health benefits dates back as far as Hippocrates, who is said to have recommended sunlight exposure for medical purposes. Since this time it has been established that wavelengths of light contained in sunshine can have notable effects on human health. Ultraviolet light stimulates the production of vitamin D in the skin. Visible light (especially blue light), when it reaches the eyes, suppresses the synthesis of the hormone melatonin. Finally, infrared light also appears to have notable biological effects which will be discussed later.

A number of studies have observed an apparent relationship between factors affecting sun exposure in populations and coronary heart disease mortality. For example, a given area is exposed to more sunlight the closer the it is to the equator, so latitude is a variable which can affect a population’s level of sunshine exposure. A number of ecological studies have reported an increase in coronary heart disease mortality in populations as latitude increases1-6.

Season changes the amount of sunlight an area’s population is exposed to throughout the year, with summer representing the period of greatest sunlight and winter the period of least sunlight. A number of studies on populations throughout the world (in both the northern and southern hemispheres) have reported coronary heart disease mortality is higher in the winter than the summer7-15.

Altitude can also affects sunlight exposure, as sunlight intensity is greater at higher altitudes. It has been frequently observed that people living at higher altitudes have a lower mortality from coronary heart disease16-20.

A limited number of studies have examined actual levels of sunlight on rates of coronary heart disease. These studies, performed in the United Kingdom, have observed a reduction in coronary heart disease risk with greater sunlight exposure21-23.

Finally, serum levels vitamin D, an indirect marker of sunlight exposure, have frequently been associated with a lower risk of coronary heart disease mortality24-28. Understandably, this has resulted in many proposing that sunlight exposure may protect against coronary heart disease mortality due to its ability to stimulate vitamin D production. Further support for this hypothesis comes from randomized experiments where vitamin D supplementation seems to reduce risk factors for atherosclerosis and cardiovascular disease, such as blood pressure32 and inflammation markers29-31. However, long term clinical trials on vitamin D supplementation have provided almost no support for the hypothesis that vitamin D protects against coronary heart disease33,34

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Furthermore, genetic evidence64 (which helps minimize confounding) looking at variations in the enzymes which activate vitamin D (increasing active vitamin D levels in the body) show no effect of lower vitamin D on cardiovascular disease risk:

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Effect of genetically lowered vitamin D levels (induced by 4 different enzyme SNPs) on coronary artery disease.

In 1996 a paper entitled “Sunlight and Heart Disease”, published in the Quarterly Journal of Medicine investigated the relationship between sunlight exposure and coronary heart disease mortality rates5. Similar to other studies a reduction in death from coronary heart disease with greater sunlight exposure was observed (in the United Kingdom specifically). The investigators also observed that cholesterol levels varied both by season and by latitude, both suggesting greater sunlight exposure lowers cholesterol levels (see graph below). This is not the only time such observation has been made; a number of studies have reported that cholesterol levels are higher in the winter35 and at higher latitudes36.

There is little experimental evidence on sunlight and cholesterol levels, although one trial performed in Russia in 1966 reported that sunbathing reduced cholesterol levels in patients with coronary atherosclerosis37. A trial on psoriasis patients in Norway reported a 7% reduction in LDL cholesterol’s after 15 days of treatment, but this effect did not quite reach statistical significance (p=0.074)38.

Because LDL cholesterol (i.e. its oxidation in the sub-endothelial space) appears to be involved in atherosclerosis39, the ability of sunlight to reduce LDL could represent a potential mechanism involved in the seemingly protective role of sunlight on CHD.

The authors of “Sunlight and Heart Disease” speculated that cholesterol levels may be lowered by sunlight due to the action of vitamin D or the process of it’s synthesis. However, randomized clinical trials have reported quite consistently that oral vitamin D supplementation does not lower LDL cholesterol levels40,41. Furthermore, studies appear to show exposure to ultraviolet light alone also does not lower cholesterol either42-46. Thus, it would seem another explanation must be required to explain the potentially hypocholesterolemic effect of sunlight. One potential candidate for the effect may infrared light.

Infrared light appears have some significant biological effects. Perhaps most notably, it appears to stimulate mitochondrial enzymes46,48 and in doing so, increase levels of ATP47,48, the main energy unit of the cell. Experiments in which human50-53 or animal subjects54 are exposed to infrared light have generally reported a reduction in cholesterol levels. Furthermore, infrared light also appears to reduce inflammation55-59. In one experiment the inflammation markers TNF-a and IL-6 were dramatically lower after exposure to infrared light59. Because inflammation appears to play role in coronary heart disease60-62 this represents another mechanism by which infrared light (from sunlight) may protect against CHD. Finally, an experiment on rabbits found a reduction in atherosclerosis from infrared light exposure54.

However, it should not be concluded that infrared light represents the only component of sunlight which can help prevent CHD. Ultraviolet light may have cardioprotective effects independently of vitamin D (i.e. UV light increases nitric oxide signaling63). It is also feasible that the effect of visible light in sunshine on melatonin secretion and circadian rhythm regulation could also exert effects on CHD risk. Therefore, the ultimate contribution of infrared light to the seemingly protective role of sun exposure, while seemingly important, remains unclear.

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