More Sun Science

This week I had the chance to fly up to Auckland to present a workshop called “Sun Smart”.  The basic premise of this workshop is to rebalance the often very one-sided information that is presented to the public regarding health and sun exposure, taking an evidence-based approach.  The final message being that sensible sun exposure, without burning, is an important aspect to our overall physical health.  Sensible sun exposure, for a corporate population, means getting out in the noon sun sans sunscreen, with the sleeves rolled up and the skirts hiked.

In reviewing the evidence that we use to support this workshop, I thought I would throw some rather interesting quotes into a post, hard on the heels of my recent sun exposure and circadian rhythms post.  The public health messages, in this country at least, that revolve around this topic, are typically of the “stay out of the sun, it causes cancer” -type of message.  But there is a lack of fidelity to this message of fear.  It would seem, when going through the evidence, that yes – sunburns and total ultraviolet radiation exposure are key factors in the development of skin cancer.  But then “skin cancer” isn’t a single pathology.  We have skin cancers that can be locally disfiguring, but have minimal risk of metastizing and becoming fatal – and these are by far and away the predominant forms of skin cancer seen (examples being basal cell carcinoma [BCC] and squamous cell carcinoma [SCC]).  And we have cutaneous malignant melanoma [CMM] – the least common, but having the unfortunate distinction of being the type of cancer that can spread and become fatal.  All have slightly different signatures when it comes to their initiation and propagation, but all get lumped together in the “awareness” campaigns.

The two main types of ultraviolet radiation we are exposed to are UVA and UVB.  Each of these has the capacity, in the right context, to initiate a skin cancer – be it BCC, SCC, or CMM.  But of these, it would appear that one UVR type has the capacity to be protective against the deadliest of these cancers.  Let’s take a closer look.  I pull heavily on one main paper, published in Medical Hypothesis, as it offers both a good evolution-based theory and multiple lines of recent evidence to support the theories put forward. From…

Increased UVA exposures and decreased cutaneous Vitamin D3 levels may be responsible for the increasing incidence of melanoma

This passage sets the scene for us…

We agree that intense, intermittent overexposure to solar UVR and sunburns initiate melanoma [CMM]. Here we now propose that indoor solar UVA exposures, which cause mutations and depletes vitamin D3 in the skin, and inadequately maintained amounts of cutaneous vitamin D3 can promote CMM.

In the early 20th century, people went against evolution by going indoors during the day to work, which drastically decreased their daily amount of cutaneous vitamin D3 and, along with it, their blood levels. With the addition of larger buildings and sky scrapers, people created an unnatural UV barrier when windows were developed and used in abundance. The UV barrier created by window glass divided UVB from UVA, so that the vitamin D making UVB was excluded from our indoor working environment; only the vitamin D-breaking and DNA-mutating UVA was included. Because this unnatural UV environment existed for decades in buildings and cars, CMM began to steadily increase about 20–30 years later in the mid-1930s.

Prior to finding this paper, I was always of the opinion that it was those individuals who spent the most time outdoors who were most at risk of developing any of the skin cancers.  Later, I refined my thinking to believe, particularly with regard to CMM, that many of the cancer statistics were being made up by those who spent a large proportion of their time indoors during the year, only to head outdoors and soak up very large doses of UVR in a very short space of time, with limited defences to handle that exposure.  Perhaps I was partly right…

Outdoor workers can get three to nine times as much erythemally weighted solar UVR exposure as indoor workers… Paradoxically, although outdoor workers get much higher outdoor solar UV doses than indoor workers get, only the indoor workers’ incidence of cutaneous malignant melanoma (CMM) has been increasing at a steady exponential rate since before 1940 (World Health Organization, WHO, and Connecticut cancer registry). Likewise, the calculated lifetime risk for getting CMM follows the same pattern. In fact, outdoor workers have a lower incidence of CMM compared to indoor workers. Thus, unlike squamous cell carcinoma (SCC), some factor(s) other than cumulative UVR exposures plays a role in CMM.

So it might seem, with regard to CMM at least, that some of the given public health messages telling us to stay out of the sun, might just be adding to our overall melanoma risk.  But by what mechanism?

Outdoor exposures include UVB (290–320 nm) radiation, so that previtamin D3 and thermal conversion to vitamin D3 can occur in the skin. Vitamin D3 can then be converted to its most hormonally active form, 1a,25-dihydroxvitamin D3 or calcitriol, which kills melanoma cells and SCC in vitro and reduces tumor growth in vivo. Calcitriol is not only formed by enzymes in the kidneys and liver but also by enzymes in melanoma cells and keratinocytes. Calcitriol can control or eliminate melanoma cells by binding to the vitamin D3 receptor (VDR) on the nuclear membrane signaling for either growth inhibition or cell death via apoptosis, while it protects normal melanocytes from apoptosis. Calcitriol can exhibit these effects on a variety of cancer cells possessing a functional VDR: melanoma, leukemia, breast, prostate, colon, and other cancers as well.

Furthermore;

Moreover, UVB makes the precursor of vitamin D3, previtamin D3, while UVA (321–400 nm) can only break down vitamin D3 and can do so in human serum while bound to the vitamin D binding protein [34]. Because 35–50% of the incident UVA radiation can penetrate to the dermal layer of the skin [35], UVA cannot only possibly break down the vitamin D3 in the skin but also the vitamin D circulating through the capillaries. Thus, indoor workers may be at a higher risk for getting melanoma because they make little vitamin D3 locally in the skin during their workweek and UVA window exposures can break down any vitamin D3 just formed in the skin or circulating through the capillaries.

The ideal then, it would seem, would be to obtain UVR exposures where there is a good balance between UVA and UVB wavelengths.  As UVA strikes the Earth’s surface with good power right throughout the day, and UVB at the Earth’s surface is maximal across the solar noon period (roughly 10/11am – 3/4pm at my latitude here in the Southern Hemisphere [41 deg S], assuming a clear day in Spring-Summer), the ratio between UVA & UVB is at its lowest over this period and thus presents the best time to be outside, maximising vitamin D production whilst minimising CMM risk.

Indeed, other authors have also modelled this time as being the optimum exposure period…

At what time should one go out in the sun?

To get an optimal vitamin D supplement from the sun at a minimal risk of getting cutaneous malignant melanoma (CMM), the best time of sun exposure is noon. Thus, common health recommendations given by authorities in many countries, that sun exposure should be avoided for three to five hours around noon and postponed to the afternoon, may be wrong and may even promote CMM. The reasons for this are (1) The action spectrum for CMM is likely to be centered at longer wavelengths (UVA, ultraviolet A, 320-400 nm) than that of vitamin D generation (UVB, ultraviolet B, 280-320 nm). (2) Scattering of solar radiation on clear days is caused by small scattering elements, Rayleigh dominated and increases with decreasing wavelengths. A larger fraction of UVA than of UVB comes directly and unscattered from the sun. (3) The human body can be more realistically represented by a vertical cylinder than by a horizontal, planar surface, as done in almost all calculations in the literature. With the cylinder model, high UVA fluence rates last about twice as long after noon as high UVB fluence rates do. In view of this, short, nonerythemogenic exposures around noon should be recommended rather than longer nonerythemogenic exposures in the afternoon.This would give a maximal yield of vitamin D at a minimal CMM risk.

If we were to add this to the data from my previous post, suggesting that a key protein produced by the body to repair UVR-induced damage shows greater activity throughout the earlier part of the day (and shows a circadian rhythm for its activity), then we have a strong case for getting outside in the sun (unprotected) throughout the morning and perhaps into the early afternoon, with maximal health benefit at minimal melanoma risk.  Perhaps a bit more user-friendly than the blanket ban on sun exposure that seems to be the perception of the common sun exposure message.

Obtaining sun exposure during a period of optimal UVA:UVB and during a time when the skin’s own defences are at their peak, is understandable.  But how does this translate to a higher CMM risk for indoor workers?  They are, after all, indoors and out of the sun, presumably with a low total UVR exposure…

Indoor workers go to and from work five days a week, usually before 9 a.m. and after 4 p.m., respectively, when the solar UVB is negligible, so that indoor workers hardly make any vitamin D3 commuting during the workweek and work year. Meanwhile, people can be exposed to UVA passing through the windows of their cars, which can break down vitamin D3. While at work, many indoor workers are exposed to some UVA through their office windows and to minor amounts of UVA and UVB from fluorescent lights, but they usually get little or no short-term (5–15 min) moderate UVB exposure during the peak hours (11 a.m.–3 p.m.) of their workdays and, most people do not go outside at all.

In the northern regions of the world (above 37degN) [would include the equivalent southern latitudes - Auckland is 36degS. Ed], a vitamin D3 ‘‘winter” occurs from at least November–February [May-August in NZ. Ed], when the dose-rate of UVB is too low to make any previtamin D3 even if an office worker goes outside during peak hours. Meanwhile, the UVA entering through their windows can cause DNA damage and mutations that accumulate during the week. On the weekend, indoor workers can go outside and make vitamin D3 (although not in the winter above 37degN), weather permitting, but they either do not or cannot go out every weekend during peak UVB hours. Worse yet, indoor UVA exposures can break down vitamin D3 formed in the skin from outdoor UVB exposures. In fact, after only 3h of winter sunlight exposure near 42degN (primarily UVA) [the equivalent of Christchurch in the south. Ed] only 26% of the initial amount of vitamin D remained in human serum, neither the vitamin D binding protein nor other serum components can prevent its photodegradation. On the other hand, outdoor workers get little UVA alone exposures from windows, but do get some UVB exposure during the ‘peak’ vitamin D making hours of their work day (11 a.m.–3 p.m.).

The supporting evidence for this hypothesis;

  1. UVB exposure alone cannot explain the increasing incidence of CMM because outdoor workers get much more UVB than indoor workers, yet indoor workers have a higher incidence of CMM.
  2. The blood levels of vitamin D in outdoor workers (gardeners), who get about five times the solar dose that indoor workers get are about twice as high as indoor workers.
  3. The prediagnostic levels of vitamin D serum levels in melanoma patients were significantly lower than controls.
  4. UVB-absorbing sunscreens are associated with a significant increased risk of melanoma in humans; they promote the growth of melanoma in mice, while they suppress cutaneous vitamin D3 formation.
  5. An all-year-tan is protective against melanoma, and outdoor workers, who get three to nine times the erythemally effective UV dose that indoor workers get have a significantly lower incidence of melanoma.
  6. Outdoor activities in childhood decrease the incidence of melanoma (excluding sunburns) and there is no ‘‘critical period,” such as childhood, where intense exposures contribute more towards the induction of melanoma. In fact, some studies found that sunburns throughout life are an important risk factor for melanoma, while low-level solar UV exposures are protective.
  7. Melanoma patients who receive regular sun exposures live longer than those who do not, while those with polymorphisms in their VDR receptors have a poor prognosis.
  8. UVA not only promotes skin tumor growth in mice after initiation by artificial sunlight, but also causes twice as many tumors to form.
  9. UVA increases melanomas in a mouse model after initiation by UVB.
  10. Calcitriol [Active vitamin D] decreases stage II (promotional phase) carcinogenesis in vivo, while it does not significantly affect stage I carcinogenesis (initiation phase). Thus, lack of cutaneous calcitriol/vitamin D3 as well as increased UVA exposures may promote CMM in humans.

The authors point to data that people can receive considerable UVA exposures from sitting near windows;

…if a person sits 3 m or less from a double-pane window on the sunlit east or west side of a building for about 4 h, they can get about 90 kJ/m2 of UVA in one day. An entire work year (5 days/wk for 48 wk) of this exposure could give a UVA dose around 21,700 kJ/m2.

Of course, one can argue that all of this is merely hypothesis.  Can it explain all aspects of the increasing melanoma incidence?

Any hypothesis concerning the increasing incidence of melanoma must explain the documented observations such as intense intermittent exposures and sunburns (weekend and vacation), incidence over time, and distribution over body surface. It must also explain the following epidemiologic observations: sun (or other) exposure; latitude; prevalence in upper pay scale and white-collar occupations and higher incidence in indoor workers (especially office workers) compared to outdoor workers.

Our hypothesis appears to explain all the observations to date. Overexposures and especially sunburns from UVB exposures initiate melanoma, while UVA exposures and inadequate levels of vitamin D3 in the skin may promote it.

The authors background to many of these factors makes for interesting reading.  Of the cultural changes in the early 20th century;

…nothing culturally important that occurred after the first noted increase in the incidence of CMM should have been blamed for its increase because anything that could have been responsible had to occur about 10–30 years before, rather than after, the first documented increase. The major thrust of the industrial revolution began about 30 years before the increase in CMM, when both windows, along with high-rise, steel-reinforced office buildings, cars, and gasoline containing volatile lead (tetraethyl lead), which is a co-carcinogen with UVC (200–290 nm), became abundant. However, if volatile lead were responsible, then outdoor workers would have a higher incidence of melanoma than indoor workers of the same socio-economic status because they would have been exposed to it all day; but the opposite is true.
Sunlamps, sunscreens, cultural changes (clothes and outdoor activities), as well as fluorescent light exposures have all been blamed for the increasing incidence of melanoma, but they all occurred after 1936 when the first increase in CMM in the US was documented in Connecticut.

What of the influence of sunbedding?  Perhaps, for those indoor workers who can’t get outside during the day, or are faced with a seasonal “UVB winter”, sunbedding represents an option?

…the new high-pressure, UVA-emitting sunlamps may now be contributing toward increasing the incidence of melanoma in the population of indoor tanners who use them and UVB-absorbing sunscreens may have increased the incidence among beach goers.

As UV lamps tend to have higher ratios of UVA to UVB, and are potentially used outside of our “circadian window”, it would seem that they represent more of a health risk than a benefit.

The authors state that the industrial revolution gave us two critical events that pertain to the increasing incidence of melanoma – increased numbers of people working indoors, making less vitamin D in their skin, and more windows becoming available, exposing people to the mutagenic and vitamin D-depleting effects of UVA.  But haven’t windows been around longer than just the last 100 years?

Windows were around for hundreds of years prior to the industrial revolution; however, they were smaller in size, contained smaller panes of glass, and few people could afford them. The industrial revolution and some technical advances made large window panes easy to mass-produce and readily distribute, so that everyone could afford to have them in abundance. In addition, high-rise office buildings, needing many large window panes, became increasingly popular around the mid 1910s, about 20 years prior to the first observed increase in the incidence of CMM. The time-line for the industrial revolution fits the CMM observations, unlike the introduction of fluorescent lights in the mid-1940s or any other events that occurred after the mid-1930s. Thus, the industrial revolution caused many workers to stay indoors during the day reducing their cutaneous vitamin D3 levels and, the UVA entering their offices caused photodegradation of vitamin D3 and mutations to the DNA of their skin cells.

There is also an important behavioural component that goes hand in hand with this information, and for us here in New Zealand, we are coming into the time of year where we are likely to see this behaviour – summer holidays.  This represents a period where we go from potentially having had minimal UVR exposure on our body to having very high doses of it within a very compressed period of time.

UVB initiates CMM when normal people are overexposed and this usually happens when they have minimal clothing on, exposing most of their body to intense sunlight. They wear clothes at work covering these body sites, so that when and if, they do go outside they cannot make vitamin D3 locally in the covered skin that was previously exposed. In addition, due to its longer wavelengths, UVA penetrates clothing much better than UVB [86] and clothing prevents the formation of previtamin D3. People tend to remove their suit jackets at work in their offices allowing UVA to penetrate through their shirts, decreasing vitamin D3 and increasing mutations in the trunk skin, thus increasing the occurrence of CMM on their trunks, especially in men. Furthermore, unlike men, women can wear skirts and dresses to work allowing their legs to get more UVA exposure, even through stockings, thus increasing the occurrence of CMM on their legs.

The occurrence of melanoma decreases on body sites chronically exposed to the sun…

When people go outside, their hands and face can get exposed to UVB and make vitamin D3 locally in that skin. If a melanoma cell forms on the hands or face, the vitamin D3 produced from outdoor UVB exposure can cause it to be growth inhibited or to die via apoptosis. The melanoma cells in those skin areas can take up the newly formed vitamin D3 and convert it to calcitriol before the person has a chance to go back inside and possibly destroy it from UVA window exposure.

In contrast, if a person goes outdoors during workdays, they will not make vitamin D3 on body sites covered by clothing: so, any melanoma cells formed by sunburns from previous exposures in those areas can survive and multiply. Vitamin D or 25-hydroxyvitamin D is present in the blood and circulates throughout the body, so that it can enter skin that was not exposed to UVB. However, the circulating concentration may not provide enough vitamin D3 or calcitriol to cause growth arrest or cell death of the melanoma cells.

It would also seem that the incidence of CMM is not dependent on cumulative UVR exposure…

Scientists examined the relationship between total accumulated sun exposure and the incidence of melanoma from 1969 to 1990. Only two out of 14 scientific studies found a significant positive association between outdoor solar UVR exposure and the incidence of melanoma. Seven of 14 (50%) case-controlled studies found no association at all and, quite remarkably, five studies found a negative correlation. Furthermore, outdoor workers get more solar exposure than indoor workers get, but have a lower incidence of CMM. Thus, intense overexposure to solar radiation can initiate CMM, but unlike SCC [squamous cell carcinoma], CMM is not dependent on cumulative UV exposure. In fact, continuous, rather than intermittent, exposure may reduce the risk for getting CMM, as demonstrated by the lower incidence in outdoor workers.

Here is one of the studies finding a negative correlation between lifetime sun exposure and melanoma…

The Infuence of Painful Sunburns and Lifetime Sun Exposure on the Risk of Actinic Keratoses, Seborrheic Warts, Melanocytic Nevi, Atypical Nevi, and Skin Cancer

…lifetime sun exposure appeared to be associated with a lower risk of malignant melanoma

So to wrap up, based on the evidence presented here, it makes sense to me that one might try to get a balance between the amount of UVA they might be exposed to whilst working indoors by ensuring that they keep vitamin D levels replete – preferably via progressive unprotected UVB exposure over the solar noon period.  One might also want to minimise the periods of time where they go from virtually no UVB exposure to obtaining very large UVB & UVA exposures over very large areas of skin.  Build a slow tan, and pay attention to what internal resources (supplied via your nutrition), your body might require in order to combat the inevitable damage that UVR can do.

18 thoughts on “More Sun Science

  1. Good to see this addressed in NZ. My mum works at a primary school where all the children have to wear hats to protect them from the sun. 80% of the pupils are Pacific Islanders, the rest are Maori. Do Maori and PI have skin cancer issues?

  2. Good stuff. I hope that in a future post you will provide practical D3 supplementation strategies and the rationales behind them for those of us who live at more polar than equatorial latitudes.

    1. Vitamin D supplementation strategies become a very individual and contextual affair. I have written on this in the past however, and certainly, there is plenty of information on this topic on the web. Start at the Vitamin D Council website.

  3. A very important and well-written post highlighting a very important article – Thanks Jamie! I would add a couple of things to the discussion: total cholesterol levels appear to be strongly associated with sun-related vitamin D status, and skin-production of vitamin D from sun exposure does NOT seem to be associated with skin pigmentation:

    http://bit.ly/gc8kxO

    The last bit, related to skin pigmentation, is controversial yet definitely worth exploring. It does seem to be an evolutionarily sound idea; one that Darwin himself appears to have championed (see under comments below the post linked above for more on this).

  4. Hi Jamie. Great post. I wondered if there is any connection between diet (vegetable oil consumption) and sunburn, and between sunburn and skin cancer. I have heard of anecdotal evidence that once processed vegetable oils are removed from the diet the skin is less likely to burn. Do you know if this is true and is there any research to back it?

    1. Hi Mel

      Have a look within the comments section of my previous post on sun exposure and circadian rhythms. Someone was kind enough to post some information on this very topic there.

  5. Excellent post. Thank you for posting this.

    According to my (very limited) research, the ratio of UVA to UVB from the sun is roughly 95% to 5%. Does that sound accurate? I have started tanning indoors on beds that are reportedly 96% UVA to 94% UVB. Do you have an opinion on the benefit vs. risk in this situation?

    Outdoor exposure isn’t currently an option, and when faced with oral supplementation vs a tanning bed, I felt the tanning bed was the best available option.

    Thanks,
    Mike

    1. Hi Mike

      As far as I’ve read, of the total UVA energy striking Earth, 95% hits the Earth’s surface. For UVB, this is 5%. I don’t know enough about UVR to know what this translates to in terms of an actual ratio. However, as UVB striking the ground increases throughout the day, then the ratio between UVA and UVB narrows.

      I do question the need to maintain sky-high vitamin D levels throughout the year. Even people who are ancestral to equatorial regions will have a nadir in their vitamin D levels corresponding to the likes of monsoon season. In my mind, it makes more sense to ensure that vitamin D levels are replete over the summer months and to go through a natural seasonal transition rather than to send a signal to your system that it is year around summer by sun-bedding.

      By exposing skin to even low levels of UVB early in the season, ensuring you have all the necessary precursors there for robust production and metabolism (see Ned’s link above), and that you aren’t rapidly depleting what you are making (via a high grain fibre intake, being in an inflammatory state, destroying vitamin D with high UVA exposure), and trying to maximise the final amounts of UVB late in the summer/early autumn, I think one can get through the winter without having their vitamin D levels tank on them. There is a big difference, heading into winter, with a serum vitamin D over 200nmol/L, as opposed to heading into the same period already vitamin D deficient.

      Lastly, showing health benefits of vitamin D supplementation over winter in a vitamin D deficient population, with all the usual inflammatory ailments, is somewhat different to those with low levels of inflammation and who have maximised vitamin D levels over summer. I think we need to be cautious in applying the enthusiasm for vitamin D replenishment throughout the year (be it via supplementation or sunbedding) when you are living in an entirely different context from the general population.

  6. Well done Jamie, I’m pleased that you are raising this issue here in NZ, a country along with Australia, whose people are often vilified by the skin cancer brigade. Who peddle, the overly simplistic cover up message without wanting/being able to relate that message to a wider context of health.

    Now that I am entering my second Paleo summer, I have noticed marked changes in how my skin/body responds to the sun. I don’t recall noticing this in summer 2010/11, probably too soon. I was born a “mild” ginga, and while age has given me the salt and pepper look, I retain the basic characteristics – easy burn and peel. Despite all the messages, I would inevitably start the summer with a peel.

    Having recently completed a couple of century rides with my Wellington (non-tan) arms out and ivory coloured elbow pits tipped up to the sun, I now have a good tan on them. The first ride I did come away with some pink in there, but no peel!

    Not being one to do things with a cautious approach, over the last couple of weekends I have been out painting in just shorts, full sun. While my back did have some exposure previously, it wasn’t tanned, yet already it has tanned up.

    I didn’t expect such a marked response. And I can only put it down to the change in diet/lifestyle.

    I read a recent post on the importance, not only of Vit D, but most importantly the balance between D, A and K2 – each a fat soluble vitamin. (Dont recall the source) My takeaway from that post was the significance of all 3 in the response of the skin to sunlight.

  7. Lots to think about! I’ve recently been apartment hunting, and was turned off by the minimal windows in an otherwise very nice apartment… maybe I need to reconsider!

    I started noticing a number of years back that melanomas were frequently in areas rarely seen by the sun… Makes the whole ‘sun is evil’ argument seem kind of weird. Also- I think it’s fascinating that melanoma cells can convert D3! Very, very cool!

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