Sunlight and the circadian rhythms in your skin

SUNLIGHT entrains circadian rhythms.  It gives us vitamin D and melanin; it can give us a sunburn, but some evidence suggests that it does NOT cause skin cancer.

“lifetime sun exposure appeared to be associated with a lower risk of malignant melanoma” (Kennedy et al., 2003)

Anecdotally (or so I’ve heard), skin cancer frequently develops in places not regularly exposed to sunlight.  If true, this flies in the face of the dogma which goes something like this (Tl;dr): ultraviolet light from the sun penetrates into the nuclei of skin cells and damages DNA; if the right [wrong] genes are altered/mutated and the mutated cells proliferate, it can develop into a tumor (gross oversimplification).

So, what might explain the discord?

LIGHT entrains the circadian clock; this includes regulating cell cycle genes.  Aberrant cell cycling may lead to out-of-control proliferation in the wrong context, aka cancer.  Interestingly, some evidence suggests that part of the circadian regulation of cell cycle genes includes turning down proliferation when exposure to UV light is expected to be high (daytime); so DNA repair machinery has more time to fix any cell cycle genes that are mutated by UV light before the cell proliferates (Geyfman and Andersen, 2009) = lower chance of creating and propagating a potentially cancerous skin cell.

Another thing is that DNA repair mechanisms in the skin are upregulated, in circadian fashion, during the day (perhaps directly via bona fide clock genes).

Running for time: circadian rhythms and melanoma (Markova-Car et al., 2014) 

Sunblock = less potentially damaging UV?  Sunblock prevents sunburn, but does it reduce skin cancer?  Studies are mixed on this; however, skin cells NEED to proliferate… perhaps doing so at night (as would occur with proper circadian signaling) is the simple solution.

Are some melanomas caused by artificial light? (Kvaskoff and Weinstein, 2010)

The incidence rate of cutaneous melanoma has been increasing faster than that of any other cancer in white-skinned populations over the past decades. The main risk factors for melanoma (i.e. exposure to sunlight, naevus count, phototype, and family history of melanoma) may not wholly explain the epidemiological trends observed for this cancer. The light-at-night theory postulates that increasing use of artificial light-at-night may contribute to the increasing breast cancer incidence through suppressed secretion of melatonin (a hormone produced in the dark and inhibited by light, which regulates circadian rhythms). Here, we postulate that this theory may also apply to melanoma and that it may explain a part of this cancer burden. Consistent with our hypothesis is evidence from experimental studies suggesting a lightening effect of melatonin on frog skin and mammal hair during seasonal changes, its antioxidant and anti-carcinogenic effects in skin melanocytes, as well as the expression of melatonin receptors in melanocytes. Also, epidemiological data suggest lower melatonin concentrations in melanoma patients compared with controls; a potential therapeutic effect of melatonin in patients with metastatic disease; a higher prevalence of melanoma in pilots and aircrews, with increased risks with higher time zones travelled; and increased melanoma risks in office workers exposed to fluorescent lighting. Moreover, melanoma incidence and seasonal patterns are consistent with a reduction of melatonin secretion with intensity of exposure to light, although it remains difficult to distinguish the effect of melatonin disruption from that of sun exposure on the basis of ecological studies. Finally, the reported associations between hormonal factors and melanoma are consistent with melatonin inhibition increasing the risk of melanoma by increasing circulating oestrogen levels. Despite the existing suggestive evidence, the light-at-night hypothesis has never been directly tested for melanoma. Very few studies examined the potential associations between melanoma risk and shift work or melatonin concentrations, and we found no studies reporting on the relationship between melanoma and number of sleeping hours, use of melatonin supplements, blindness, night-time city light levels, bedroom light levels, or clock genes polymorphisms. Therefore, since several observations support our hypothesis and very little research has been undertaken on this subject, we strongly encourage analytic epidemiological studies to test the light-at-night theory for melanoma causation.

All of this suggests to me: get unadulterated sunlight during the day; and there’s not a whole lot of UV in devices like iPads and smart phones, but there IS a lot of circadian rhythm-disrupting blue light which may shift the proliferation of skin cells such that less is occurring at night and more during the day.  So it’s not the UV per se, but rather a circadian mismatch.

Some of this is speculation, and is assuming that at least part of the circadian regulation of skin cell cycle genes is mediated centrally via SCN, but it could also explain the discord regarding sunblock and skin cancer… also, it’s important to keep in mind that circadian biology is a fully integrated system (it controls just about everything).

Nix the sunblock and avoid artificial light (as much as possible); enjoy natural sunlight (as much as possible)… and break your fast in the morning (to entrain peripheral with central clocks).

Premature skin aging (wrinkles, sun spots, etc) is probably a real phenomenon due to excess skin tanning and sun bathing, so don’t do that… but don’t avoid regular exposure to sunlight.

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