Maximizing the wrong variable
The suffix is doing a lot of work. Tanmaxxing borrows its grammar from the optimization subcultures that gave us looksmaxxing and gymmaxxing, and it applies the same logic to melanin: pick a measurable output, push it as far as it will go, treat anyone advising moderation as a coward. The output here is pigment. The method is a stack — a UV-index app to find peak intensity, an oil or accelerator with little or no SPF, a tanning bed on cloudy weeks, and in one corner of the subculture, a nasal spray containing an unapproved peptide.
The trend reached mainstream coverage over the past two months. Dermatology outlets flagged it in mid-June, national television and syndicated press picked it up in early July, and the industry trade press was writing about how sun-care brands should respond by the end of the month. Named tanning-optimization apps circulated alongside it. "Tan lines" content on TikTok is reported in the hundreds of millions of views.
What makes this worth a review rather than an eye-roll is that the underlying beliefs are measurable, and they have been measured. The American Academy of Dermatology's 2026 Practice Safe Sun Survey, fielded by Versta Research from January 19 to February 2, 2026 among 1,132 U.S. adults with a margin of error of roughly three percentage points, found that 52% of American adults believe at least one tanning myth.1 Specifically: 29% think tanning is safe as long as you don't burn, and 19% believe a base tan prevents sunburn or reduces cancer risk. Sixty-four percent of adults aged 18 to 29 report encountering sunscreen misinformation online, and more than 16 million U.S. adults say they reduced or stopped using sunscreen because of claims they saw there.1
That is the actual story. Not that young people like being tan — people have liked being tan since Coco Chanel got off a boat in 1923 — but that a specific set of factual claims is circulating, those claims are checkable, and they have already changed behavior at population scale.
Sources: Surgeon General's Call to Action (2014); Gerami et al., Science Advances (2025); AAD Practice Safe Sun Survey (2026).1,2,8
What a tan is actually worth
Start with the load-bearing claim, because if it falls, most of the structure goes with it. The base tan is supposed to be a down payment: suffer a little now, buy protection later.
The number is SPF 3. That figure comes from the 2014 Surgeon General's Call to Action to Prevent Skin Cancer, which states that a UVB-induced tan "provides minimal sun protection, equivalent to an SPF of about 3," and warns that belief in a base tan "may lead to a false sense of security and inadequate use of sun protection."2 For orientation: SPF 3 blocks roughly two-thirds of erythemal UVB. The lowest SPF the FDA permits a product to advertise as sun protection is 15.
But the more interesting finding is the one that separates kinds of tan. In a 2011 study in Pigment Cell & Melanoma Research with the admirably blunt title "The deceptive nature of UVA tanning versus the modest protective effects of UVB tanning on human skin," Miyamura and colleagues compared skin tanned under UVB-containing versus UVA-dominant protocols.3 Visually, the tans looked similar. Biochemically, they were not remotely the same thing.
Design. Human skin exposed to UVB-containing versus UVA-dominant tanning protocols, with subsequent measurement of melanin content, photoprotection against a challenge dose, and DNA damage markers.3
Results: Only UVB-induced tanning raised melanin content and conferred measurable protection against UV-induced DNA damage. UVA tanning darkened skin through photo-oxidation and redistribution of existing melanin. The authors concluded that UVA tanning "contributes essentially no photoprotection, although all types of UV-induced tanning result in DNA and cellular damage."
Limitation: Mechanistic study in a modest number of subjects; it establishes the biology, not a population-level effect estimate.
Hold onto that, because it detonates under the tanning bed specifically. Commercial sunlamps are UVA-dominant. So the machine sold as the efficient way to build a base tan produces the visually convincing tan that protects you least, while delivering the DNA damage in full. You are paying by the session for the cosmetic signal of protection stripped of the protection.
The general point is the one I keep coming back to in this newsletter: a tan is not a coating your skin applies. It is a wound response. Melanogenesis is downstream of UV-induced DNA damage; the pigment is what your keratinocytes and melanocytes do after the photons have already broken something. There is no mechanism by which the visible result arrives without the injury that caused it, because the injury is the signal.
The tan is not protection your skin built. It is the receipt for damage your skin already absorbed.
Dr. Maren ColeGroup 1, and what single-cell sequencing added
In June 2009, a twenty-scientist working group convened by the International Agency for Research on Cancer reclassified UV-emitting tanning devices from Group 2A, "probably carcinogenic to humans," to Group 1, "carcinogenic to humans" — the same tier as tobacco and asbestos.4 The working group's own meta-analysis found melanoma risk elevated by roughly 75% when device use began before age 30, and cited consistent case-control evidence for ocular melanoma as well.
The epidemiology has been re-run several times since, and it keeps landing in the same place.
Design. Systematic review and meta-analysis of observational studies on sunbed use and cutaneous melanoma, with a Western European focus.5
Results: Ever-use of sunbeds, summary RR 1.20 (95% CI 1.08–1.34). First use before age 35, RR 1.59 (95% CI 1.36–1.85). A dose-response of roughly 1.8% additional melanoma risk per extra tanning session per year.
Correction — and cite this one carefully: The originally published before-age-35 figure was RR 1.87 (1.41–2.48). A data file corruption was identified and corrected in BMJ 2012;345:e8503, revising it down to 1.59. Secondary sources still quote 1.87 constantly. The corrected number is the right one, and it is still an elevated risk.
Design. Systematic review and meta-analysis of indoor tanning and non-melanoma skin cancer across PubMed, Embase and Web of Science.6
Results: Squamous cell carcinoma, ever versus never, RR 1.67 (95% CI 1.29–2.17). Basal cell carcinoma, RR 1.29 (95% CI 1.08–1.53). For first use before age 25, the BCC estimate was 1.40 (1.29–1.52); the SCC estimate of 2.02 had a confidence interval crossing 1, so treat it as directional only. The authors estimated a U.S. population attributable fraction of 8.2% of SCC and 3.7% of BCC — on the order of 170,000 cases a year.
Limitation: Observational input studies with self-reported exposure; recall bias runs in both directions and the pooled estimates are modest in size.
A larger 2021 systematic review in Cancers, searching the literature through July 2021 and pooling 54 studies, reported sunbed exposure at RR 1.17 (95% CI 1.05–1.31) and sunlamp exposure at RR 1.31 (95% CI 1.04–1.64), again with dose-response by frequency and by earlier age at first exposure.7
Those relative risks are real but unglamorous, and the tanmaxxing rebuttal writes itself: 1.2 is nothing, epidemiology is confounded, everyone who tans also goes outside. Which is why the most consequential paper on this topic is eight months old and does not depend on questionnaires at all.
Design. Two arms. First, medical records of roughly 3,000 tanning bed users compared with 3,000 age-matched controls with no indoor tanning history. Second, single-cell DNA sequencing of 182 individual melanocytes drawn from 11 long-term indoor tanners, 9 matched never-tanners and 6 cadaver donors.8
Results: Melanoma was diagnosed in 5.1% of tanning bed users versus 2.1% of non-users; after adjustment for age, sex, sunburn history and family history, an adjusted 2.85-fold increase. Users were more likely to develop melanoma at sun-shielded sites such as the lower back and buttocks, and to have multiple primary melanomas. Genomically, tanners' melanocytes carried roughly twice the mutation burden, and — the finding that matters — the excess was most pronounced at body sites that receive comparatively little natural sun. Tanners in their thirties and forties carried more mutations than general-population individuals in their seventies and eighties.
Limitation: The genomic arm rests on 26 donors. The records arm is retrospective, so surveillance bias is live — people who tan may also get screened more. Funding included NIH, the Department of Defense Melanoma Research Program, the Melanoma Research Alliance and the LEO Foundation, whose associated company sells dermatology drugs. Treat 2.85 as a high-exposure clinic estimate, not the population effect size; the meta-analyses remain the population number.
The reason the genomic arm is the important one: it explains the anatomy. Natural sun exposure damages the skin you expose, which for most people is a face, a neck and two forearms. A tanning bed irradiates you like a rotisserie. The single-cell data shows a whole-body mutational field, including in skin that sunlight has essentially never reached — which is precisely why the melanomas in that cohort turned up on lower backs and buttocks. The bed is not a more efficient sun. It is a different exposure with a different anatomy of injury.
A 27,000-storefront industry, and one regulatory reversal
The trend did not arrive in a policy vacuum. In 2015, the FDA proposed a rule barring anyone under 18 from commercial tanning beds and requiring adult users to sign a risk acknowledgment. It sat unfinalized for a decade. In March 2026 the agency formally withdrew it, in a notice signed by HHS Secretary Robert F. Kennedy Jr.9 The withdrawal notice records more than 8,100 comments, from trade associations arguing personal choice and small-business compliance burden, and from medical and cancer-advocacy organizations arguing the other way. An FDA spokesperson noted that withdrawing the restrictions "does not mean that exposure to UV radiation does not cause skin cancer."
The salon trade body welcomed the withdrawal and pointed to existing parental-consent practices. The American Academy of Dermatology, which had lobbied for the rule, did not. Underneath the argument sits an industry of roughly 27,000 U.S. tanning businesses generating about $1.9 billion in annual revenue — a sector that has been consolidating for years and now has both a federal deregulation and a viral aesthetic movement working in its favor in the same twelve months. Tan accelerators and bronzing oils add roughly another billion dollars in global category revenue.
I want to be careful here, because The Corneum critiques claims rather than people, and "an industry benefits" is not an argument that a claim is false. It is, however, the reason to check the claims rather than assume they emerged spontaneously. Sunlamps remain Class II medical devices carrying a boxed warning against use by minors. What the FDA does not regulate is the UVA-to-UVB ratio a given bed emits — which, given the Miyamura finding, is the single specification that determines whether the tan you buy carries any protective value at all.
Four claims, checked
Tanmaxxing's second engine is not enthusiasm for tanning. It is distrust of sunscreen. Four claims do nearly all the work, and they deserve to be taken one at a time rather than waved off, because two of them started from real findings.
Claim one: sunscreen filters get into your blood. True, and the FDA is the one who demonstrated it. In a 2019 randomized trial published in JAMA, 24 healthy adults applied sunscreen at 2 mg/cm² to 75% of body surface area, four times daily, for four days — the agency's "maximal use" condition.10 Geometric mean peak plasma oxybenzone reached 209.6 ng/mL for one spray formulation. A 2020 follow-up extended the finding to six filters including homosalate, octisalate and octinoxate, all of which exceeded 0.5 ng/mL after a single day-one application.11
Here is the part the viral version omits. 0.5 ng/mL is not a toxicity threshold. It is an FDA regulatory trigger: the plasma concentration above which the agency requires a sponsor to conduct nonclinical toxicology work, including carcinogenicity and reproductive studies. Crossing it means "we lack the data," not "we found harm." The FDA said explicitly at the time that the results were not a reason to stop using sunscreen. It is also worth noting that the maximal-use protocol is roughly four to eight times heavier than real-world behavior, since application studies consistently find people using 25% to 50% of the labeled dose.
Claim two: oxybenzone is an endocrine disruptor. The rodent studies behind this fed oxybenzone orally at doses that bear no relationship to topical use. A 2011 research letter in Archives of Dermatology ran the arithmetic: an average U.S. woman would need to apply sunscreen daily for up to 277 years to reach the systemic exposure per unit body mass given to immature rats in those experiments.12 In fairness — and this is the nuance the calculation's fans usually skip — that letter predates the Matta absorption data, which showed real plasma levels higher than anyone had assumed. The honest statement in 2026 is that the rodent-to-human dose gap is still enormous, and that "no harm has been measured in humans" is a more accurate sentence than "safety has been proven."
Claim three: sunscreen is contaminated with benzene. Some of it was. In May 2021 an independent laboratory detected benzene in 27% of 294 sunscreen batches tested, prompting recalls of several major brands. The contamination traced to raw materials and propellants rather than to the UV filters themselves. When the FDA ran its own testing and published results in March 2025, more than 90% of the 95 products tested showed undetectable or extremely low benzene, with six elevated products voluntarily recalled. The correct conclusion is that a manufacturing problem was found and largely fixed — an argument for buying well-made sunscreen, not for buying none.
Claim four: sunscreen causes vitamin D deficiency. A systematic review conducted to MOOSE standards and published in the British Journal of Dermatology in 2019 examined this directly.13 Experimental studies confirm a theoretical mechanism — filters do block the UVB that drives cutaneous synthesis — but field trials and observational data indicate the real-world risk is low, and in several studies sunscreen users had higher vitamin D levels, plausibly because people who wear sunscreen spend more time outdoors. And there is a second problem with this argument, which is that it assumes the conclusion. VITAL, a randomized trial of 2,000 IU daily vitamin D3 in roughly 25,871 adults over five years, found no reduction in cancer incidence or major cardiovascular events.14 If repleting vitamin D does not deliver the outcomes, "I need UV for my vitamin D" cannot carry the weight being placed on it. You can take the pill. The pill doesn't do much.
Against that, the affirmative case for sunscreen has something the skeptics rarely acknowledge exists: randomized trials, from the same Australian community cohort.
Design. Community-based randomized trial in Nambour, Queensland, 1992–1996. 903 adults under 55 randomized to daily versus discretionary sunscreen, factorially crossed with 30 mg beta-carotene versus placebo. Photoaging graded from silicone casts of the back of the hand by assessors blinded to allocation.15
Results: The daily-sunscreen group showed no detectable increase in skin aging over 4.5 years, and 24% less photoaging than the discretionary group — odds ratio 0.76 (95% CI 0.59–0.98). Beta-carotene did nothing.
Limitation: Open-label for participants; the comparator was discretionary use rather than none, which biases toward the null — the true daily-versus-nothing effect is probably larger. Single latitude, predominantly fair-skinned population, hand microtopography as a surrogate for facial aging.
Design. The full Nambour cohort of 1,621 residents aged 25–75, randomized in 1992 to daily versus discretionary sunscreen on head and arms, followed to 2006 through questionnaires, pathology laboratories and the cancer registry.16
Results: Ten years after the trial ended, 11 new primary melanomas in the daily group versus 22 in the discretionary group, HR 0.50 (95% CI 0.24–1.02, P = .051). For invasive melanoma specifically, 3 versus 11, HR 0.27 (95% CI 0.08–0.97).
Limitation — and I am not going to soften this: The overall melanoma result does not cross conventional significance. The significant invasive-disease finding rests on 14 total events. This is the only randomized evidence in existence that sunscreen reduces melanoma, and it is thin. It also tested routine daily use in a subtropical town, not vacation behavior.
The tanmaxxing crowd's single best line is "sunscreen has never been shown in a randomized trial to prevent melanoma." The accurate reply is that it has, once, barely, with 33 events — and that the invasive-melanoma arm reached significance. That is a more persuasive sentence than an overclaim, and it has the additional virtue of being true.
Melanotan II is not Scenesse
The most dangerous corner of this trend is also the smallest. Melanotan II, sold in nasal sprays and injection vials at roughly £18 to £30 a bottle through social channels that nominally ban it, is a synthetic melanocortin agonist that stimulates eumelanin production. It is not approved for any use by the FDA. UK regulators have called it dangerous for the better part of a decade, and selling medicinal products containing it there is illegal — though a genuine loophole persists, in that nasal sprays marketed as cosmetics fall outside both the medicines remit and cosmetics regulation, receiving less scrutiny than an ordinary drugstore moisturizer. Australia's TGA has issued repeated consumer alerts.
The documented harms include a 2025 case report of oral mucosal malignant melanoma in a 22-year-old woman who had used melanotan II nasal spray for tanning17; a published case of rhabdomyolysis and renal dysfunction in a man who injected 6 mg of internet-purchased material; a case of low-flow priapism requiring cavernosal aspiration and intracavernosal phenylephrine; and multiple reports of eruptive and atypical nevi following melanotan use. That last one deserves emphasis, because it is quietly the worst: the drug changes the number, color and morphology of moles, which are exactly the features dermatologists screen on. It makes melanoma harder to find while plausibly making it more likely.
The confusion that makes this spread is a naming problem. Afamelanotide — melanotan I, brand name Scenesse — is a real, FDA-approved drug, cleared in October 2019 to increase pain-free light exposure in adults with erythropoietic protoporphyria, a rare inherited disorder in which light exposure is genuinely agonizing. It is a 16 mg subcutaneous implant placed by a trained clinician every two months. Three things follow. It is approved for a rare disease, under supervision, with a benefit-risk ratio that holds only in that population. Melanotan II is a different, less receptor-selective peptide, which is why it causes priapism and nausea, and it is unapproved everywhere. And "melanotan-1" purchased online is not Scenesse — it is compounded or research-grade material of unverified identity, purity and potency.
Unapproved and unregulated
Melanotan II has no marketing authorization in the US, UK, EU or Australia. Material bought online has no verified identity, purity or dose. Nasal "cosmetic" framing evades both medicines and cosmetics oversight.
It camouflages the thing you're screening for
Eruptive atypical nevi and darkening of existing moles are repeatedly reported after melanotan use — degrading the exact clinical signals used to catch melanoma early.
Systemic effects beyond skin
Documented cases include rhabdomyolysis with renal dysfunction and low-flow priapism requiring emergency intervention. These are melanocortin receptor effects, not contaminant effects.
The name collision
Afamelanotide (Scenesse) is approved for erythropoietic protoporphyria and administered as a clinician-placed implant. It is not what is being sold in nasal sprays, and the shared prefix is doing marketing work.
The good argument, and its exact boundaries
There is a serious case on the other side, and pretending otherwise is how you lose an audience that has already decided dermatology is not being straight with them.
The Melanoma in Southern Sweden cohort followed 29,518 women recruited between 1990 and 1992, aged 25 to 64 at baseline, for twenty years. In a competing-risk analysis published in the Journal of Internal Medicine in 2016, women with active sun exposure habits had lower cardiovascular and non-cancer mortality than sun avoiders, and the life expectancy of sun avoiders was reduced by 0.6 to 2.1 years relative to the highest-exposure group.18 The authors' headline framing was that nonsmoking sun-avoiders had life expectancy comparable to smokers in the highest sun exposure group.
There is a plausible non-vitamin-D mechanism, too. Richard Weller's group has shown that UVA irradiation of human skin mobilizes cutaneous nitrite stores, releasing nitric oxide, producing vasodilation and lowering blood pressure — independently of nitric oxide synthase and independently of vitamin D.19 Roughly twenty minutes of sun lowers blood pressure for hours. Given that cardiovascular disease kills vastly more people than melanoma does, the arithmetic is not something to wave away. And VITAL's null result actually strengthens this line of argument rather than weakening it: if the pill doesn't work, something other than vitamin D is doing the work.
So here is what that literature supports. Do not be a hermit. Go outside daily. Get morning light, which is genuinely well-supported for circadian entrainment and mood. Treat "avoid all sun always" as itself an unexamined health claim, because it is one, and because dermatology has a documented habit of optimizing a single organ.
And here is what it does not support, on four counts. It is observational, in a population where sun-seeking correlates with wealth, mobility, physical activity and not being too ill to leave the house; reverse causation is not adjustable away. It is Swedish, from a high-latitude country with long dark winters — the same research question asked in Queensland, by the Nambour investigators, returned the opposite answer. It is about a dose of roughly twenty minutes of ambient daylight, not hours at peak UV index under oil, and nothing in this literature tests or endorses deliberate erythema. And it says nothing whatsoever about tanning beds, a Group 1 carcinogen in a cabinet emitting up to fifteen times the UV irradiance of midday sun, which the Miyamura data tells us delivers the damage without even the modest photoprotective consolation prize.
The rhetorical move at the center of tanmaxxing is the slide from "get light" to "get tan." Those are different interventions. The circadian and mood benefits of light are driven substantially by visible-spectrum intensity through melanopsin-containing retinal cells — not by the ultraviolet fraction that mutates melanocytes. You can have the entire steelman without the pigment.
Dr. Cole's assessment
I reserve Marketing Hype for cases where claims dramatically exceed the evidence, and I hand it out sparingly. This one earns it, and not because the data are thin — because they are unusually thick and point the other way.
Two independent BMJ meta-analyses, a 54-study replication, an IARC Group 1 classification standing since 2009, two randomized trials from the same Australian cohort, and now single-cell genomics showing whole-body mutational fields in tanning bed users that exceed what natural sunlight produces. Designs that rarely agree with each other agree here.
The specific claims fail individually, too. The base tan is worth about SPF 3, and functionally nothing if it came from a UVA-dominant bed. The absorption scare misreads an FDA regulatory trigger as a toxicity threshold. The oxybenzone rodent data is off by something like 277 years of human-equivalent exposure. The vitamin D argument was closed by a systematic review and then closed again by VITAL, where supplementation delivered nothing.
What keeps this from being merely wrong and makes it hype is the attached economy: a $1.9 billion salon sector that just won a decade-long federal deregulation fight, a billion-dollar accelerator category, and an unapproved peptide moving through influencer content at £18 a bottle. When claims are this checkable and this profitable simultaneously, the label writes itself.
One honest asymmetry, stated plainly. The case for daily broad-spectrum sunscreen as an anti-photoaging measure is Strong Evidence. The case that sunscreen prevents melanoma specifically is only Promising — one trial, 33 events, a primary endpoint at P = .051. I would rather say that than overclaim, because the people reading this are already, correctly, suspicious of anyone who won't.
A tan is your skin logging DNA damage, and it buys you about SPF 3 — effectively zero if it came from a UVA-dominant tanning bed, which the WHO classifies alongside asbestos and which single-cell sequencing just showed mutates melanocytes across nearly your whole body, including skin the sun has never touched. Go outside; the steelman is about daylight, not pigment.
- 1. American Academy of Dermatology. Practice Safe Sun Survey. Fielded by Versta Research, January 19–February 2, 2026; n = 1,132 U.S. adults; margin of error ±3 percentage points. Released May 1, 2026.
- 2. U.S. Department of Health and Human Services, Office of the Surgeon General. The Surgeon General's Call to Action to Prevent Skin Cancer. Washington, DC, 2014.
- 3. Miyamura Y, et al. The deceptive nature of UVA tanning versus the modest protective effects of UVB tanning on human skin. Pigment Cell & Melanoma Research. 2011;24(1):136–147.
- 4. El Ghissassi F, Baan R, Straif K, et al. A review of human carcinogens—Part D: radiation. The Lancet Oncology. 2009;10(8):751–752. (IARC Working Group; UV-emitting tanning devices reclassified to Group 1.)
- 5. Boniol M, Autier P, Boyle P, Gandini S. Cutaneous melanoma attributable to sunbed use: systematic review and meta-analysis. BMJ. 2012;345:e4757. Correction: BMJ. 2012;345:e8503.
- 6. Wehner MR, Shive ML, Chren MM, Han J, Qureshi AA, Linos E. Indoor tanning and non-melanoma skin cancer: systematic review and meta-analysis. BMJ. 2012;345:e5909.
- 7. Indoor tanning and the risk of overall and early-onset melanoma and non-melanoma skin cancer: systematic review and meta-analysis. Cancers. 2021;13(23):5940.
- 8. Gerami P, et al. Molecular effects of indoor tanning. Science Advances. 2025;11:eady4878. Published December 12, 2025. (Northwestern Medicine / UCSF. Funding: NIH R01 CA265786 and AR080626; DoD Melanoma Research Program ME210014; Melanoma Research Alliance; LEO Foundation; P30CA082103.)
- 9. U.S. Food and Drug Administration. Withdrawal of proposed rule, General and Plastic Surgery Devices: Restrictions on Sunlamp Products. March 2026.
- 10. Matta MK, et al. Effect of sunscreen application under maximal use conditions on plasma concentration of sunscreen active ingredients: a randomized clinical trial. JAMA. 2019;321(21):2082–2091. (NCT03582215; n = 24 randomized, 23 completed.)
- 11. Matta MK, et al. Effect of sunscreen application on plasma concentration of sunscreen active ingredients: a randomized clinical trial. JAMA. 2020;323(3):256–267.
- 12. Wang SQ, Burnett ME, Lim HW. Safety of oxybenzone: putting numbers into perspective. Archives of Dermatology. 2011;147(7):865–866. See also Burnett ME, Wang SQ. Current sunscreen controversies: a critical review. Photodermatology, Photoimmunology & Photomedicine. 2011;27(2):58–67.
- 13. Neale RE, Khan SR, Lucas RM, Waterhouse M, Whiteman DC, Olsen CM. The effect of sunscreen on vitamin D: a review. British Journal of Dermatology. 2019;181(5):907–915.
- 14. Manson JE, et al. Vitamin D supplements and prevention of cancer and cardiovascular disease (VITAL). New England Journal of Medicine. 2019;380(1):33–44. (n ≈ 25,871; 2,000 IU/day; median 5.3 years.)
- 15. Hughes MCB, Williams GM, Baker P, Green AC. Sunscreen and prevention of skin aging: a randomized trial. Annals of Internal Medicine. 2013;158(11):781–790.
- 16. Green AC, Williams GM, Logan V, Strutton GM. Reduced melanoma after regular sunscreen use: randomized trial follow-up. Journal of Clinical Oncology. 2011;29(3):257–263.
- 17. Melanotan II nasal spray: a possible risk factor for oral mucosal malignant melanoma? International Journal of Oral and Maxillofacial Surgery. 2025. PMID 40210573.
- 18. Lindqvist PG, Epstein E, Nielsen K, Landin-Olsson M, Ingvar C, Olsson H. Avoidance of sun exposure as a risk factor for major causes of death: a competing risk analysis of the Melanoma in Southern Sweden cohort. Journal of Internal Medicine. 2016;280(4):375–387.
- 19. Weller RB and colleagues. UVA irradiation of human skin vasodilates arterial vasculature and lowers blood pressure independently of nitric oxide synthase. Journal of Investigative Dermatology. 2014. See also: Does incident solar ultraviolet radiation lower blood pressure? Journal of the American Heart Association. 2020;9:e013837.
- 20. Gordon JRS, Brieva JC. Images in clinical medicine: unilateral dermatoheliosis. New England Journal of Medicine. 2012;366:e25. (Single case; cited illustratively only.)
- 21. U.S. Food and Drug Administration. SCENESSE (afamelanotide) implant — approval for erythropoietic protoporphyria, October 8, 2019.