Why did evolution fail to protect humans against sun?

Question

Experts recommend that people apply sunscreen every two hours throughout the year, even in winter.

Especially phototypes I - III are supposed to be most vulnerable to harmful UV radiation, so especially these phototypes should take care to keep applying sunscreen and to use at least SPF 50. This, at least, is what European health agencies tell us.

Native to Europe are phototypes I - III. This means that these phototypes evolved in these precise conditions. Isn't evolution suppose to lead to best adaptations to the precise conditions native to the area an organism evolved in?

So, by this line of argument, phototypes I - III should be well-adapted to the levels of Sun radiation present in Europe. They should not have to use sunscreen there. When traveling to areas that are significantly higher in Sun radiation, such as equatorial areas, they may have to start using sunscreen - but not in areas they are native to.

Yet European agencies keep telling us that especially phototypes I - III should use sunscreen while in Europe.

Where is the error in my thinking?

Answer 1

Skin cancer typically results from a lifetime of sun exposure, and is usually seen in older individuals. 90% of new melanoma cases are diagnosed in people over 45. Nearly 95% of melanoma deaths are observed in people over 45. Simply put, humans' currently level of adaptation to the sun is "good enough" - the vast majority of people do not have their reproductive fitness affected in any way by how they handle sun exposure. There is little selective pressure that would result in someone with better sun adaptation being more likely to pass on their genes. Evolution won't typically operate on traits that are only meaningful after reproductive age, as "selective pressure" refers to selection for reproduction specifically.

https://seer.cancer.gov/statfacts/html/melan.html

Answer 2

_{I find your question to be fine for this site, and you've provided the asked for sources, so it's fair to give you an answer.}

Where is the error in my thinking?

The error is in thinking that evolution is somehow directed towards the greater good. It's not. It's the result of random mutations.

Evolution doesn't make us perfect for the environment in which we evolved. We will never be perfect in any way, let alone every way. You're only addressing the risks of UV light, but people can come up with any number of imaginable "deficiencies" in humans that make us "imperfectly evolved".

That we're imperfect in no way means evolution has failed us somehow. Evolution doesn't occur to select for perfection. Evolution doesn't happen for any "reason" at all, in that it's not directed by a goal; evolution simply happens because DNA is mutable. If a mutation is harmless or beneficial in an environment, it will be passed on and likely persist. If it's harmful, depending on the degree to which it's detrimental, it will not be passed on. Sometimes in an particular environment, a mutation is both (e.g. sickle cell trait.)

If we're "good enough" overall to reproduce, if we're able to survive and pass on our genetic material, then that's what's going to happen, regardless of our perceived imperfections.

Also, somewhat aside to your question are the benefits of UV light to humans. We know that UVB allows us to synthesize Vitamin D, which is critical for survival. There are other possible benefits to UV light as well. It might well happen that we'll discover more concrete benefits.

The question which has been linked to as a duplicate discusses evolution in more detail (and more helpfully). This is only a fairly quick answer.

Answer 3

Besides the arguments already mentioned in the previous answers, the human body has developed numerous ways to protect itself from the harmful effects of sunlight and ultraviolet (UV) radiation.

• Melanin Production:

  Melanin is the main pigment in the skin that absorbs UV radiation to keep it from damaging its structure. So, if the skin is exposed to UV rays, it is going to make more of this pigment, making the skin darker, or tanned, which is a way of a protective response to the deeper layers of the skin from getting damaged. This process helps absorb and dissipate UV radiation, reducing the risk of DNA damage that can lead to skin cancer.

• Epidermal Thickening:

  Another defense mechanism is the thickening of the outermost skin layers (epidermis) in response to UV exposure. This thickening serves to attenuate UV penetration to deeper skin layers, thus providing an additional barrier against potential damage.

• DNA Repair Mechanisms:

  The human skin protects its genetic material from being damaged by DNA repair. These mechanisms are the body's way of dealing with and repairing UV-induced damage by the sun. This includes repair mechanisms like the photolyase repair mechanism, which specifically repairs pyrimidine dimers of the DNA which are generated by UV exposure.

• Inflammatory Response:

  The acute response to excessive UV exposure is sunburn. This reaction is part of the body's inflammatory response, which serves to alert the immune system to potential damage and initiate repair processes.

Answer 4

The best natural sun protection is melanin. But melanin makes it harder for the skin to produce vitamin D. In places with lots of UV radiation black skin is an evolutionary advantage, and the weaker vitamin D absorption is no big problem because there is so much UV radiation.

Now if you live in northern areas, your sun protection isn’t as good as it could be, but lots of melanin would reduce vitamin d absorption too much, because there isn’t enough UV radiation around. So there is a balancing act: Better sun protection would hurt your health in different ways.

Also careless sun exposure was very much a thing say 1980 to 2000. Many people have wised up to the dangers and will avoid roasting themselves on the beach. So hopefully cases of cancer etc. will go down in the future. And health agencies are much more risk averse nowadays, and to some degree they have to because people get older and more survive to an age where skin cancer actually hits them.

Answer 5

There are some excellent answers already referencing melanin. I used to live in the Solomon Islands, and noticed that the people from the West of the islands, and also in the East of PNG were much darker than the neighbours: in fact they were among the darkest people I ever encountered anywhere in the world. I found this article useful: The Case of Melanin in Melanesia. It includes a map showing ultra violet levels, and it is quite clear that the high UV levels are correlated with the regions where skins are very dark.

I recall Tim Flannery writing (alas, the book was lost during a move) that there are reefs in that area of the Western Solomons with an abundance of seafood, but that the optimum time for harvesting was also the peak for UV, hence greater selection pressure for melanin...

Answer 6

To add to other answers, there have been behavioral changes in many societies with paler skin phototypes that have increased the risk of skin cancer. Laying on a beach or in a park to get a suntan is an activity that's only become common in recent decades, for centuries Europeans avoided working outside around the midday sun during summer (such as sleeping in the shade) and when working outside wore clothing that covered up most of the skin along with wide brimmed hats or other head covering (have a look at typical medieval peasant dress). That was enough to mitigate most of the risk of skin cancer, but not in more equatorial countries.

Answer 7

Because cancer wasn't likely to be one's cause of death. Look at this comparison between 1900 and 2022:

Cancer used to be the cause of 5% of human deaths. Nowadays its at 24% thanks to us conquering diseases like tuberculosis and influenza. Similar data is available for the UK in the 1850s:

Cancers were relatively rare. While the Victorians did not possess sophisticated diagnostic or screening technology, they were as able to diagnose late stage cancer as we are today; but this was an uncommon finding. In that period, cancer carried none of the stigma that it has recently acquired, and was diagnosed without bias. For example, in 1869 the Physician to Charing Cross Hospital describes lung cancer as ‘… one of the rarer forms of a rare disease. You may probably pass the rest of your students life without seeing another example of it.’

Evolution can't solve every problem all at once. Cancer was simply too far down the list of causes of mortality for it to enact sufficient evolutionary pressure. We also have evidence from the Tasmanian Devil population showing that immunity to certain types of cancers can evolve very quickly if necessary:

Devil facial tumour disease (DFTD) is an aggressive non-viral clonally transmissible cancer which affects Tasmanian devils, a marsupial native to the Australian island of Tasmania. The cancer manifests itself as lumps of soft and ulcerating tissue around the mouth, which may invade surrounding organs and metastasise to other parts of the body. Severe genetic abnormalities exist in cancer cells—for example, DFT2 cells are tetraploid, containing twice as much genetic material as normal cells. DFTD is most often spread by bites, when teeth come into contact with cancer cells; less important pathways of transmission are ingesting of infected carcasses and sharing of food. Adult Tasmanian devils who are otherwise the fittest are most susceptible to the disease. DFTD is estimated to have first developed in 1986.

...

In 2016, devils are endangered as the localised populations were shown to have declined by 90 per cent and an overall species decline of more than 80 per cent in less than 20 years, with some models predicting extinction. Despite this, devil populations persist in disease-stricken areas. The devils have, in a way, fought back the extinction by developing the gene that is immune to face tumors. The genes have already existed in the Tasmanian devil as part of their immune system. They increased in frequency due to natural selection. That is, the individuals with particular forms of these genes (alleles) survived and reproduced disproportionately to those that lacked the specific variants when disease was present.