Sunlight Advice Should Weigh Total Mortality, Not Skin Cancer Alone

Rowan Jacobsen says the standard advice on sun exposure no longer reflects the science as he understands it. The familiar public-health message has become, in his description, increasingly categorical: stay out of the sun in summer and winter, regardless of circumstances; use sunscreen even if you will be indoors all day; treat unprotected skin exposure as a risk to be eliminated.

Jacobsen does not deny the risk that gave rise to that advice. He agrees that sun exposure raises the risk of skin cancer. His claim is that the risk has been treated as if it were the whole health question, rather than one part of a broader tradeoff. “The sun is a killer,” Russ Roberts says as a summary of the received wisdom. Jacobsen’s answer is that the same sentence omits what he thinks the past few decades of research have made harder to ignore: moderate sun exposure may improve health in both direct and indirect ways.

The strongest version of Jacobsen’s argument, as he presents it, is not mainly about mood or comfort, though both enter the discussion. It is about mortality. Skin cancer matters, he says, but it is not a major cause of death compared with cardiovascular disease, cancer overall, diabetes, infectious disease, and other large disease categories. In the United States, he says, about 10,000 people a year die from skin cancer. Cardiovascular disease is closer to a million deaths, and cancer overall is around 600,000. If sunlight slightly raises the risk of skin cancer but slightly lowers the risk of cardiovascular disease, the relevant public-health question changes.

The mechanism Jacobsen emphasizes most strongly is nitric oxide. He credits Richard Weller, a dermatologist in Scotland, as the first person he saw pose the tradeoff question directly. Weller’s research showed, in Jacobsen’s account, that when sunlight hits skin, it produces nitric oxide. Nitric oxide is a vasodilator: it allows blood vessels to expand, lowers blood pressure, and is used in heart medications. Jacobsen notes that Viagra is based on nitric oxide’s ability to increase blood flow. In Weller’s experiments, as Jacobsen describes them, exposing volunteers’ arms to the equivalent of roughly 20 to 25 minutes of summer sunlight produced nitric oxide in the skin, raised nitric oxide in the blood, and lowered blood pressure by about five or six points. Jacobsen says a reduction of that magnitude, if generalized, could reduce worldwide deaths from heart disease by something like a million people.

Roberts pushes for caution. A plausible mechanism does not settle the magnitude. Observational data still require controls for income, geography, diet, genetics, and other confounders. Richer people may travel more, get more sun, and have better health for reasons unrelated to sunlight. Jacobsen accepts the limits of observational evidence but thinks the tradeoff deserves attention precisely because skin cancer is a relatively small cause of death compared with cardiovascular disease.

The most direct evidence Jacobsen cites for this mortality tradeoff is a recent preprint from Weller’s group using the UK Biobank. The UK Biobank contains detailed health data on about 500,000 volunteers, initially ages 40 to 69, tracked for roughly 20 years. Weller’s group, in Jacobsen’s description, used location data, satellite estimates of light exposure, and self-reported sun-seeking habits to relate sun exposure to disease incidence and mortality. Jacobsen says their final study population was about 420,000 people.

Of those 420,000 people, Jacobsen says about 45,000 had died over the study period. Cardiovascular disease and cancer accounted for most deaths. Only 440 had died of melanoma, and only 60 had died of other skin cancers. According to his account of the preprint, people with a lot of sun exposure were about 20% more likely to die of melanoma than those with little sun exposure, while those with a whole lot of sun were no more likely to die of melanoma. The excess melanoma deaths amounted to fewer than 100 people over 20 years in the study population. Meanwhile, he says, higher-sun groups were less likely to die from cardiovascular disease or cancer.

The ratio Jacobsen cites from Weller’s preprint is 75 to 1: for every extra melanoma death associated with more light, roughly 75 deaths from larger disease categories were avoided.

Roberts’s response is the skeptical one a reader should retain. To have high confidence, one would need to examine the study’s controls and the biological plausibility of the effect size. The finding is not a license to ignore skin cancer. But it is provocative evidence for Jacobsen’s central claim: skin-cancer avoidance alone is the wrong denominator. The relevant question is total health and mortality.

The analogy Jacobsen uses is orthopedic advice about exercise. If orthopedists looked only at knee injuries, they could warn people not to run and perhaps not even to walk much. The warning would be grounded in a real fact: movement can increase the chance of knee injury. But it would be bad public-health advice if it ignored the wider effects of exercise. Jacobsen thinks something similar happened with sunlight. Dermatology and skin-cancer prevention focused on one category of harm while research in other fields, in his reading, was pointing toward possible benefits from sunlight in areas such as cardiovascular function, mood, vitamin D biology, and other health systems.

Roberts frames the tension as a mature tradeoff rather than a reversal of the old slogan. The sun is not simply “bad for you”; it may be good for you in meaningful ways. It also has costs. Thoughtful people, in his view, should know both sides. Jacobsen accepts that summary, while also emphasizing that he is not trying to offer a “slam dunk” case or medical advice. His ambition is to bring research that has been scattered across specialties into the general discussion.

That distinction matters because the claim can sound, as Roberts says, “rah-rah” or contrarian for its own sake. Jacobsen’s response is that his own skepticism was part of the project. He was drawn in not by one small study, but by decades of work in multiple fields. Individual scientists would publish findings suggesting that sun exposure might be beneficial in a particular domain, but those papers did not necessarily change the broader public message. No one, Jacobsen says, had made it their job to synthesize the work into a general account.

Rowan Jacobsen divides skin cancer into three major categories. Squamous cell carcinoma and basal cell carcinoma account for about 98% of skin-cancer cases. Melanoma accounts for about 2%. The distinction is central to his argument because melanoma is the form associated with significant mortality, while basal and squamous cell cancers are common in older people and usually need to be removed but rarely become invasive.

Before World War II, Jacobsen says, skin cancer was not high on doctors’ radar. It was associated with sailors, who received heavy sun exposure and often had poor diets, and sometimes with farmers. After World War II, reported numbers rose sharply. Some of that rise can be explained by demographics: as infectious disease and cardiovascular mortality declined, more people lived long enough to develop cancers of various kinds. Age adjustment reduces part of the apparent increase.

But Jacobsen says age alone cannot explain the explosion in diagnosed skin cancer. The conventional explanation was that people must have become dramatically more irresponsible about sun exposure. Doctors had shown in laboratory work that enough UV radiation could produce skin cancer in mice, so they attributed the human increase to excess sunlight.

Russ Roberts questions the plausibility of that explanation. Over the twentieth century, he notes, Americans moved indoors. Farming fell from 40% of the workforce in 1900 to 3% by the end of the century. Office work expanded. Professional exposure among sailors became less common. Leisure tanning may have increased, he concedes, but occupational sun exposure declined. Jacobsen says good long-run data on adult outdoor time are limited. For children, however, the available studies show a gradual decline in time outdoors, from several hours per day in earlier decades to less than an hour per day now.

The diagnostic issue is, for Jacobsen, crucial. His “fun fact” is that the best predictor of whether someone will be diagnosed with skin cancer in the United States is not sun exposure but how many dermatologists are in the person’s county, along with the county’s age profile. More looking produces more finding. That can be beneficial if dangerous cancers are caught earlier. But it can also create the impression of an epidemic if diagnostic intensity changes faster than underlying disease.

Melanoma illustrates the problem. Jacobsen says the research community generally agrees that overdiagnosis is occurring, though there is debate about how much it matters. Until melanoma becomes invasive, he says, doctors do not have a solid way to know which early lesions will become dangerous. If a lesion might be melanoma, patients generally want it removed. That pushes practice toward caution.

He describes a study in which slides of lesions evaluated 20 years earlier were shown again to dermatologists, including some of the same dermatologists who had seen them the first time. Twenty years earlier, 11 of the lesions had been judged melanomas. On re-evaluation, the same slides produced 18 melanoma judgments. Jacobsen’s point is not that caution is foolish, but that diagnostic thresholds have shifted. If the definition of melanoma becomes more inclusive, incidence will rise even if mortality does not.

And mortality, he says, has been flat decade after decade while melanoma incidence has risen steeply. Roberts adds an important caveat: flat mortality could reflect better treatment and earlier detection preventing what would otherwise have been more deaths. Jacobsen’s narrower point remains that rising incidence alone is not straightforward evidence that sunlight has made human health worse. It may partly show that medicine has become better, more vigilant, and more willing to remove ambiguous lesions.

Rowan Jacobsen gives sunscreen an awkward place in the story, while repeatedly stopping short of a simple causal claim against it. Its use expanded dramatically during the same decades in which skin-cancer incidence rose. He says sunscreen sales and skin-cancer rates track each other “spectacularly well,” and epidemiological studies often find more sunscreen use correlated with more skin cancer.

He does not treat that as proof that sunscreen causes cancer. Russ Roberts immediately raises the standard reverse-causation problem: people with paler skin, higher baseline risk, and more time in the sun are more likely to use sunscreen. Jacobsen agrees. But he still thinks the historical record shows sunscreen has not reduced skin-cancer incidence as much as the public was led to expect. SPF values rose, adoption rose, sun avoidance rose, and skin-cancer cases did not turn around.

The technical details matter. SPF means sun protection factor. It measures how much longer a person can remain in the sun before burning compared with no sunscreen. If someone would burn in 10 minutes with no protection, SPF 20 implies they could spend 200 minutes before the same burn. SPF 50 implies 50 times as long. Jacobsen says the FDA originally did not want the sunscreen industry to use numbers like SPF 50 because, in his view of the history, no one should be staying in the sun that long.

SPF is also a measure of protection against UVB, the part of ultraviolet light that causes sunburn. But ultraviolet light is divided into UVA and UVB, and they affect the body differently. Early sunscreens blocked UVB because UVB was understood to cause sunburn and could directly damage DNA. UVA was thought less dangerous. Those early products were not really conceived as health products, Jacobsen says, but as tanning aids: they prevented burning so people could stay outside longer and become more bronzed.

That became a problem once researchers realized that UVA was also contributing to skin cancer, indirectly and perhaps more importantly than had been recognized. A sunscreen that blocked UVB but allowed UVA through could suppress the warning signal of sunburn while permitting much longer exposure to UVA. Jacobsen says that may have made early sunscreens “possibly worse than nothing” because they let users feel protected while receiving large amounts of UVA.

Modern broad-spectrum sunscreens are different. Jacobsen says the observational studies fit that timeline: studies from the 1970s often showed no benefit or a negative association; by the 1980s and 1990s the results looked more like a wash; more recent studies look better for sunscreen. He thinks current sunscreens can be a useful part of a sun strategy and that no sunscreen should be allowed on the market unless it blocks both UVA and UVB. He also says sunscreens available in Europe, Asia, and Israel are much better than those allowed in the United States, which he describes as a generation behind, and that better products appear likely to reach the U.S. market starting next year.

The point is not that sunscreen is useless. It is that sunscreen did not simply remove the sun-risk tradeoff. It may have changed behavior, changed exposure patterns, and, in its early forms, blocked one part of ultraviolet radiation while leaving another significant part unblocked.

Vitamin D is the most familiar argument for sunlight, and it is also where Rowan Jacobsen thinks the story became misleading. Observational data beginning in the 1980s made vitamin D look extraordinarily important. Low vitamin D levels were associated, he says, with higher rates of cancer, cardiovascular disease, autoimmune disease, Alzheimer’s and other dementias, diabetes, and many other conditions. Mechanistic studies also made vitamin D seem plausible as a causal agent: it helped bone mineralization, affected cell behavior, and appeared to have protective effects in laboratory settings.

Because the natural way to make vitamin D is sunlight on skin, the finding created a dilemma. By the 1980s, doctors were already deeply concerned about skin cancer. Rather than tell people to expose their skin to sunlight, they recommended supplements. Vitamin D became, Jacobsen says, probably the most prescribed supplement in the world.

Jacobsen’s account is that the randomized trials then disappointed the broader hopes placed on supplementation. He describes large, rigorous, long-term clinical trials in which one group received vitamin D pills and another received placebo. In his reading of that evidence, unless participants were extremely vitamin D deficient, raising blood levels through supplementation did not help with the broad range of conditions vitamin D had been expected to improve. He also says editors of the New England Journal of Medicine have published editorials urging doctors to stop routinely prescribing vitamin D pills because, in that view, they are not helping.

Russ Roberts’s own experience captures the practical confusion. His doctors have told him he is vitamin D deficient and recommended pills. He has resisted the assumption that raising a blood marker by supplementation is equivalent to getting the benefits associated with naturally higher vitamin D from sun exposure. He wonders whether a pill that improves the test score delivers the same outcomes as sunlight-induced vitamin D: stronger bones or lower risk of other conditions. Jacobsen describes supplementation as starting to look like “cheating on the test.” It raises the measured level without necessarily producing the desired health effect.

That creates a conundrum in Jacobsen’s telling. People who naturally have high vitamin D levels tend to have lower rates of many diseases. People who artificially raise vitamin D through pills do not seem, in the trials he describes, to gain the same broad protection. His interpretation is that vitamin D may often be a marker for sun exposure rather than the full mechanism by which sun exposure benefits health. It may be “along for the ride.” If so, sunlight could be doing other things that matter, and vitamin D blood levels may be a proxy for those processes.

Age complicates the practical question. Roberts notes that, at 71, he can spend more time in the Israeli sun and raise his vitamin D score, but his body no longer produces vitamin D as efficiently as it did when he was younger. Morning sun may not be intense enough; midday sun may be inconvenient or risky. Jacobsen says that by around age 70, people produce only about half as much vitamin D from the same amount of sunlight as they did in their 30s. But if vitamin D is not the only mechanism, older adults may still receive other benefits from sunlight even if their vitamin D production is reduced.

The current suspicion of sunlight is historically recent in Rowan Jacobsen’s account. In the late nineteenth and early twentieth centuries, physicians in Europe and the United States treated sunlight as a therapeutic tool. The movement was called heliotherapy, and it reached a peak in the early 1900s.

Much of it began with tuberculosis. Jacobsen says tuberculosis was responsible for roughly one in four deaths in Europe in the late 1800s. A Faroe Islands doctor named Finsen discovered that concentrated sunlight could kill cutaneous tuberculosis, the form that infects the skin and can consume flesh. This was before antibiotics, when both pulmonary and cutaneous tuberculosis were far more threatening than they are now in many places.

At roughly the same time, doctors were recognizing that rickets, a disease that had become common among children in industrial cities, was caused by lack of sunlight. Children in tenements were no longer receiving the sunlight that farm life had provided. Without adequate vitamin D, their bones did not mineralize properly, producing bowed legs and deformed skulls. Sunlight hitting skin was found to produce vitamin D, and vitamin D cured rickets.

Those successes changed the medical imagination. Two major diseases of the era, tuberculosis and rickets, could be treated by sunlight. Clinics appeared. Patients went to Swiss Alpine sanitariums not only for fresh air, Jacobsen says, but for the quality of the light. Doctors then began asking what else light might cure. Public-health experts in the 1920s and 1930s increasingly embraced light exposure as a general health principle. Schools were redesigned to increase children’s exposure. Jacobsen describes photographs from Switzerland showing children in boxer shorts sitting at desks in the snow, with instructors dressed similarly, taking lessons outdoors for the sake of light.

He thinks the movement eventually went too far. But he also thinks its existence matters because it shows that the “sun is poison” frame is not timeless medical wisdom. Earlier physicians saw clinical effects from light exposure that were not imaginary, even if they overextended the lesson. The reversal began when evidence emerged in the 1930s and 1940s that heavy light exposure might also be causing skin cancer. From there, the frame began to flip: sunlight moved from medicine to menace.

Russ Roberts introduces a less formal but important intuition: humans evolved under the sun. It would be strange, he says, if a constant feature of human life for hundreds of thousands of years were only a killer and not also a source of health. Humans are relatively hairless, not furry, which itself would be odd if sunlight on skin were simply bad. The first warm sun after winter feels, to Roberts, as if it reaches the bones and lifts the spirits. That is not proof, he says, but it is a deeply human experience.

Rowan Jacobsen thinks the evolutionary point is more than sentiment, though not a substitute for evidence. Because many sunlight-benefit claims come from observational studies, they are vulnerable to confounding. Scientists can try to control for obvious factors, but Roberts calls the practice an “intellectual cesspool,” and Jacobsen calls it a “dark art.” Randomized clinical trials assigning some people to high sun exposure and others to low exposure for years are unlikely, he says, because they would be considered unethical given skin-cancer concerns. The same limitation applies in reverse: the evidence that sunlight causes skin cancer also relies heavily on observational inference rather than long-term randomized trials telling people to “fry themselves.”

In that kind of uncertainty, Jacobsen argues, evolutionary norms deserve weight. Human beings spent most of their history with far more daylight exposure than modern indoor life provides. The radical intervention may not be sunlight; it may be near-total indoor living. In his formulation, humans have spent their first hundreds of thousands of years getting something like 12 hours of daylight a day, while the shift to predominantly indoor life occurred mainly over the past century.

That does not mean ancient exposure levels are automatically optimal now. People live longer, work differently, travel to different latitudes, and use products that change exposure patterns. But Jacobsen thinks the burden of suspicion should not fall only on sunlight. It should also fall on the new condition of spending most of life indoors and treating incidental sun as contamination.

There is also a psychological dimension. Jacobsen says learning the science and becoming more comfortable with the sun improved his daily life. Fear had been operating in the background. Realizing that the fear might be overblown did not remove the need for caution, but it changed his experience of ordinary outdoor life. For Roberts, that is part of the book’s appeal: not a denial of danger, but a recovery of the idea that the sun can be “something of a friend.”

Rowan Jacobsen’s practical advice has two firm poles: do not aim for zero sun exposure, and do not burn.

He says the evidence, as he reads it, points away from zero sun exposure as a healthy target. It is also clear to him, and every scientist he spoke with agreed, that burning is bad. A sunburn means skin cells have been damaged beyond recovery; they are “committing suicide,” as he puts it, to avoid becoming cancerous, and that process is not perfectly successful. His own rule is to stay well short of burning because burns can sneak up even when one is trying to avoid them.

What remains individualized is the amount and timing. Jacobsen favors something closer to the advice doctors gave in the 1950s and 1960s: do not get sunburned at the beach, do not become overexposed, but do not worry about small amounts of incidental sun during ordinary life. He thinks a little daily exposure is probably healthy.

Skin tone is the first variable. People with darker skin can tolerate much more sun exposure than people with lighter skin. People with the lightest skin, often including red hair and reddish freckles, are especially susceptible to melanoma and need to be careful. Jacobsen argues that public recommendations are often written as if everyone were in that highest-risk group. The assumption has been that everyone else can follow the same strict advice without harm. His view is that this assumption is now questionable, especially for people with darker skin tones who may be poorly served by applying ultra-cautious sun avoidance to themselves.

The other variables are practical: location, latitude, season, time of day, age, clothing, and habit. Roberts’s own attempt to raise vitamin D through Israeli sunlight illustrates the difficulty. Morning sun may be pleasant but less effective for vitamin D production; midday sun may be biologically stronger but harder to fit into life and riskier for burning; older skin produces less vitamin D; exposed body area matters. There is no single rule that can cover a fair-skinned child in a high-UV environment, a darker-skinned adult in winter, and an older person trying to correct vitamin D deficiency.

Jacobsen also urges readers not to outsource the entire question to his book. He encourages people to look at the underlying research. Large language models can help locate studies, he says, though he warns not to trust AI summaries uncritically. Use them to find the sources, then read the sources directly.

The central practical shift is not from “avoid sun” to “seek as much sun as possible.” It is from prohibition to calibration. In Jacobsen’s account, sunlight raises skin-cancer risk, especially with burns and in susceptible people. But he believes the evidence also points to benefits or plausible benefits in domains such as cardiovascular function, mood, vitamin D-related biology, sleep, and other systems that supplements and indoor life may not replicate. His argument is that public advice should reflect that tradeoff rather than treating skin cancer as the only relevant endpoint.