Vitamin Sun — One Source, Two Sides of the Ledger

What you'll learn

What reaches you from the sun, and what the atmosphere removes on the way down

The sunlight benefits that arrive through your eyes rather than your skin

What vitamin D supplementation does and doesn't do — and why that's a narrower finding than either side claims

Why latitude, season and skin pigmentation make universal exposure advice impossible

What the randomized sunscreen evidence shows, what regulators changed in June 2026, and whether two viral sun claims survive scrutiny

How SmartBar applies the deficiency framework

SmartBar's educational framework begins with two organizing terms, and applies them wherever the body has inputs and burdens — starting with what we can verify in food: ingredient composition, level of processing, and nutritional data. Deficiency means something the body needs and isn't getting. Toxicity means a burden the body must process and clear — not a poison.

Sunlight is one source arriving on both sides of that ledger at once — the same source that helps set your body clock is classified as a human carcinogen. Few inputs we cover put the two that close together, and this page is about where the line falls. It's educational rather than medical advice — if you have a history of skin cancer, a family history of melanoma, photosensitivity, or take photosensitising medication, your line is different and belongs to your clinician.

What actually arrives

The sun radiates across an enormous range of wavelengths, including high-energy radiation that would make the surface of this planet uninhabitable. Almost none of it gets to you. The atmosphere blocks it long before it arrives, and within the ultraviolet range specifically, oxygen and ozone remove essentially all solar UVC and most UVB.[1]

What survives is a filtered mixture dominated by visible and infrared radiation, with ultraviolet making up only a small fraction. Within that ultraviolet fraction, about 95% is UVA and 5% is UVB.[1]

Those two do different work. UVB — the small fraction — converts a cholesterol precursor in skin into vitamin D. UVA penetrates deeper and makes no vitamin D at all.

Neither band is biologically clean. UVB is strongly sunburning and damages DNA directly; UVA penetrates further and contributes through oxidative damage, photoaging and cancer risk. The atmosphere isn't protecting you from the bad half and delivering the good half. It's delivering a filtered dose of something that does real work in both directions.

The part that arrives through your eyes

Here is the most established non-vitamin-D benefit of daylight, and it involves no bare skin whatsoever.

Bright light reaching the retina sets the timing of your circadian clock. When researchers compared a week of ordinary indoor living against a week camping under natural light alone, the indoor week was associated with less daytime light, more light after sunset, and a delayed circadian clock. Campers received roughly four times more daytime light.[2] A follow-up found that even a single weekend outdoors shifted timing measurably.[3]

Laboratory work illustrates the steep dose-response: under the conditions tested, roughly 550 lux produced a near-maximal circadian phase shift, around 100 lux about half that, and 50 lux or less very little.[2] The exact response also depends on timing, spectrum, duration and recent light history. Typical indoor lighting sits near the bottom of that range, and even an overcast outdoor environment is commonly far brighter.

This connects straight to our Sleep page: light is the primary signal your body clock uses, and daylight after waking is the cheapest circadian intervention available.

An emerging metabolic finding points the same way. In a 2026 randomized crossover study, 13 adults with type 2 diabetes spent four and a half working days under natural daylight through windows and a separate period under constant artificial office lighting. Under daylight they spent more time within the normal glucose range, shifted toward greater fat oxidation, and showed an advance in skeletal-muscle clock timing.[20] The sample was tiny and the intervention brief — this is an early physiological signal, not evidence that office daylight treats diabetes. But it strengthens the case that daytime light is a biological input rather than merely something that helps you see.

Children have a second reason to be outside. School-based randomized trials have repeatedly reduced the onset of myopia by adding outdoor time. Roughly 80 minutes of outdoor recess cut one-year myopia incidence from 17.65% to 8.41%; adding 40 minutes a day over three years produced a 23% relative reduction; and a cluster-randomized trial across 24 schools and 6,295 children reduced two-year incidence by 11–16%.[4] The effect tracked with duration and light intensity, and was clearest in children not yet myopic — better at preventing myopia than reversing it.

Both findings are about outdoor light exposure, not deliberate ultraviolet exposure. You can obtain them through ordinary outdoor light without deliberately exposing bare skin — and myopia-prevention benefits have been observed with time spent in shaded outdoor environments. Neither requires a tan, or looking anywhere near the sun.

Vitamin D: what UVB does, and what a capsule doesn't reproduce

UVB genuinely makes vitamin D in your skin, and vitamin D genuinely matters — it's central to bone and mineral metabolism, it's one of the micronutrients worth tracking, and correcting a real inadequacy is worth doing.

What's been tested, and what failed, is a narrower and more specific hypothesis: that giving extra vitamin D to generally healthy, largely vitamin-D-replete populations would reproduce the broad health associations attributed to sunlight.

VITAL randomized 25,871 US adults to 2,000 IU daily or placebo for a median 5.3 years. Neither primary endpoint was met — invasive cancer HR 0.96, major cardiovascular events HR 0.97, all-cause mortality HR 0.99.[5] The Finnish Vitamin D Trial found no significant differences across five years at 1,600 or 3,200 IU, in a population with a baseline mean 25(OH)D of 75 nmol/L — that is, already replete.[6]

There is one persistent narrower signal: VITAL found reduced cancer mortality — not incidence — reaching significance when the first year or two of follow-up were excluded.[5]

So the honest split. Vitamin D's established role is maintaining adequacy and supporting bone and mineral metabolism, including in people with clinical indications — 2024 Endocrine Society guidance identifies groups — including pregnancy, adults 75 and older, children and adolescents, and adults with high-risk prediabetes — that may benefit from empiric supplementation, while advising generally healthy adults under 75 against routine doses beyond established dietary reference intakes, and against routine testing.[19] What the large trials do not support is using extra vitamin D as a general cancer or cardiovascular prevention drug in people who already have enough.

That distinction matters because it's usually collapsed in both directions. The trials didn't fail vitamin D. They failed the idea that giving extra vitamin D to already-replete people reproduces all the broad health associations attributed to sunlight.

Neither one replaces the other

This page has spent several sections explaining what a capsule cannot reproduce. The reverse is equally true and gets said far less often: for many people, sunlight alone is not a reliable route to vitamin D sufficiency.

The structural reason is already in this page. Skin exposed to cloudless winter sunlight in Boston produced no measurable previtamin D3 from November through February, and in Edmonton the window ran October through March.[7] Where the sun does not climb high enough, no amount of time outdoors changes the chemistry.

A real-world illustration comes from people you would expect to be the exception. Among 409 Polish elite athletes, 80% of those training outdoors and 84% of those training indoors fell below the study's prespecified 30 ng/mL threshold in winter. Even in summer, 42% of the outdoor athletes remained below that threshold.[21]

That threshold is not a universally established modern definition of sufficiency, and this page has already noted that outcome-specific blood thresholds remain unsettled.[19] The useful finding survives regardless of where the cutoff is placed: extensive outdoor training did not guarantee a high 25(OH)D concentration, even in summer.

So the two do different jobs. Supplementation can provide vitamin D when sunlight is insufficient or unreliable, and can correct inadequacy where supplementation is clinically indicated. Sunlight is associated with effects that supplementation has not reproduced in trials, including the circadian and ocular benefits described earlier, which have nothing to do with vitamin D at all.

The protocol for a randomised trial designed specifically to compare the two strategies states the unresolved question plainly: the optimal approach, sun, supplement or both, remains unclear, as does whether sunlight carries benefits beyond initiating vitamin D synthesis.[22]

The mistake to avoid runs in both directions. Taking a capsule is not a reason to stay indoors, because the capsule addresses one output of sunlight and not the others. And getting outdoors is not by itself an assurance of vitamin D sufficiency, because geography and skin type may make that impossible for part of the year.

Latitude, season and skin change the answer

Generic sun advice assumes one recommendation fits everyone. Two variables make that impossible.

Where and when. At many mid- and high-latitude locations, winter brings a period when solar UVB is simply too weak for meaningful cutaneous vitamin D production — the sun never climbs high enough, and standing outside longer doesn't help. In the classic experiments, skin exposed to cloudless winter sunlight in Boston (42°N) produced no previtamin D3 from November through February, and in Edmonton (52°N) that window ran October through March.[7]

Who. Melanin absorbs UVB. In one location-specific model, reaching about 1,000 IU with a quarter of the body exposed took roughly five minutes for the lightest skin type and about twenty-five for the darkest.[8]

That gap is the most practically useful thing on this page, and it's almost always missing. Much generic clock-time advice has historically been derived from or framed around lighter skin. Someone with deeply pigmented skin may synthesise substantially less vitamin D over the same clock time — though the relationship between clock time, vitamin D production, burning and cancer risk isn't identical across skin types, and skin colour isn't the same variable as self-identified race.

The mechanism still being investigated

If sunlight is associated with outcomes that a vitamin D capsule doesn't reproduce, there are two live explanations, and honesty requires holding both.

The first is confounding. People who get more sun are also more likely to be outdoors, active, less housebound, and differently situated in ways observational studies struggle to remove.

The second is that sunlight does something else. In 24 healthy volunteers, UVA irradiation of skin lowered blood pressure, with circulating nitrate falling and nitrite rising — consistent with sunlight mobilising stored nitric oxide from skin. The effect was independent of vitamin D, independent of nitric oxide synthase, and not explained by warming.[9]

That mechanism has been proposed as one possible contributor to seasonal and geographical blood-pressure patterns that vitamin D alone may not explain.

Three boundaries. The study had 24 participants. The effect was acute and temporary. And the dose was two standard erythemal doses — an exposure sufficient to redden skin, and not one to imitate. The experiment establishes a mechanism under controlled conditions; it does not establish that seeking comparable UVA improves long-term cardiovascular outcomes.

The Swedish cohort we cite on our Lifestyle page reported lower mortality among women describing more active sun-exposure habits — observational, female, high-latitude, and not to be read causally.[10]

The other side of the ledger

IARC classifies solar ultraviolet radiation — and ultraviolet-emitting tanning devices — as Group 1: carcinogenic to humans.[11] That's the agency's highest confidence tier. For calibration, the night-shift-work classification on our Sleep page is Group 2A, probably carcinogenic. Same scale, and UV sits above it.

UV is the principal cause of basal cell carcinoma, squamous cell carcinoma and melanoma.[11] The patterns differ: cumulative lifetime exposure matters particularly for squamous cell carcinoma, while intermittent intense exposure and sunburn are especially relevant to melanoma.

Which is why "I didn't burn" is not a clean bill of health. Burning is unambiguous evidence the dose was excessive — but damage begins before skin visibly reddens, and a tan is itself a response to UV-induced DNA damage rather than proof the exposure was harmless.

Tanning devices are not a workaround. Users' median annual exposure has been estimated at 20–30 times the dose that reddens skin, and modern units emit predominantly UVA — the band that produces no vitamin D at all.[1] The WHO position is blunt: artificial tanning should never be considered a route to vitamin D sufficiency.[12]

What the sunscreen evidence actually shows

Sunscreen is argued about in two directions online, and the randomized evidence supports neither extreme.

In Nambour, Queensland, 1,621 adults were randomized to daily versus discretionary sunscreen. Daily use reduced squamous cell carcinoma (rate ratio 0.61, 95% CI 0.46–0.81). Basal cell carcinoma was not significantly reduced.[13]

Ten years after the trial ended: 11 melanomas in the daily group versus 22 in the discretionary group — hazard ratio 0.50, 95% CI 0.24–1.02, P = .051.[14]

Read that carefully, because it's routinely reported as "sunscreen halves melanoma risk." The point estimate is a halving. It was a secondary endpoint, and it did not cross conventional significance.

On the absorption question. FDA studies found several organic UV filters enter the bloodstream above the threshold that triggers requests for further safety data.[15] That finding does not demonstrate harm — it identifies missing data. Zinc oxide and titanium dioxide hold the longest-standing safety dossier among legacy US filters. And on 9 June 2026 the FDA added bemotrizinol to the OTC sunscreen monograph at up to 6% — the first new active ingredient since the late 1990s — a photostable broad-spectrum filter with low skin absorption, effective from 9 August 2026.[16]

That last point matters beyond regulatory trivia. Mineral filters leave a white cast, which is a documented reason people with deeper skin tones skip sunscreen. A cosmetically elegant, low-absorption, broad-spectrum option may help address a real adherence gap — for the same readers who already need longer exposure for vitamin D.

And the framing that beats all of it: WHO's guidance is that protection is best achieved through shade and clothing, with sunscreen for the skin clothing can't cover — and that sunscreen should not be used to extend time in the sun.[12]

A note on the K2 pairing

Since we've discussed vitamin D, the claim usually attached to it: that D requires K2 to direct calcium toward bone rather than arteries.

The mechanism is plausible. The randomized evidence is inconsistent and has not established the pairing as necessary. In the largest relevant trial, two years of MK-7 plus vitamin D did not slow the primary endpoint of aortic valve calcification, and no conclusive reduction in coronary calcification was established. The pooled evidence is genuinely split, and split within a single review as well as between reviews. A 2023 meta-analysis of 14 randomized trials found, from the four of them that could be combined on coronary artery calcification, a small but statistically significant slowing of its progression, while eight other trials in the same review reported no appreciable benefit on other arterial or valve calcification and its authors described vitamin K's role as remaining controversial. A separate review confined to chronic kidney disease found no significant change in calcification scores at all. Both sets of authors concluded that better-designed trials are needed before efficacy is established.[17]

So we won't give you a K2 dose, and the reason isn't caution about medical advice — it's that the trials which would justify a number haven't produced consistent results. Vitamin K has a better signal on bone than on arteries.

The underlying biochemistry is real rather than invented: matrix Gla protein, an inhibitor of vascular calcification, requires vitamin K as a cofactor to become active, and circulates in an inactive form when vitamin K is insufficient. What remains unsettled is whether supplementing K2 alongside D3 changes clinical outcomes. We take that apart properly in our dedicated vitamin D3 and K2 article, including where the mechanism is solid, where the trials disagree, and who is selling the certainty.

Two things the internet says

Sungazing. There's a published case report of a young woman who developed bilateral solar retinopathy with a permanent central scotoma in one eye, visible on retinal imaging months later, after taking up the practice from a viral trend.[18]

Two details matter more than mockery. Retinal injury can occur without pain or immediate warning, so nothing stops you while it happens. And the usual defence — that sunrise and sunset are safe because the sun looks dim — is the dangerous part: reduced brightness invites people to stare far longer.

Seed oils and sunburn. The claim circulating is not a modest one about fatty acid balance; it's that removing seed oils lets you tolerate more sun. Human trials directly testing seed-oil removal against measured UV sensitivity are lacking. Mechanistic plausibility and rodent work don't establish that people can safely absorb more ultraviolet after changing cooking fats — and the strongest versions of the claim are frequently published by companies selling the alternative fat.

Key Takeaways

The atmosphere is why sunlight is survivable. UVC and most UVB never arrive; of what does, about 95% is UVA and 5% UVB — and only UVB makes vitamin D.

Some of sunlight's best-established non-vitamin-D benefits reach you through your eyes. Daylight sets circadian timing, and outdoor time reduces myopia onset in children. Neither requires exposed skin.

Vitamin D matters; extra vitamin D isn't a prevention drug. Large trials found no reduction in cancer incidence or major cardiovascular events in generally healthy, largely vitamin-D-replete populations.

Latitude, season and skin pigmentation materially change vitamin D production. In one location-specific model, estimated exposure time varied about five-fold between the lightest and darkest Fitzpatrick skin types — and many mid- and high-latitude locations have a genuine "vitamin D winter."

UV is a Group 1 carcinogen, and burning isn't the threshold. Damage begins before skin reddens; use the UV Index instead.

Sunscreen has real randomized benefit, clearest for squamous cell carcinoma, with a suggestive but imprecise melanoma signal — and shade and clothing outrank it.

How to think about sun in thirty seconds

Use the UV Index, not a fixed number of minutes. Latitude, season, altitude, cloud and reflection all change UV intensity. Below UVI 2, protection generally isn't needed; at 3 and above, it is.
Separate daylight from UV exposure. Getting outside after waking helps anchor the daytime side of your light-dark cycle — and in children, outdoor time helps reduce myopia onset — without deliberately exposing large areas of skin.
Don't use sunburn as the safety threshold. Burning means you went well past it. Damage starts earlier.
Protect with shade, clothing and sunglasses first, sunscreen on what's left uncovered — and not as permission to stay out longer.
Use vitamin D for vitamin D. Correct a genuine inadequacy or a clinical indication. Don't expect a capsule to reproduce everything associated with being outdoors.

What SmartBar does with this

SmartBar scores food, and sunlight never passes a barcode scanner. That's the boundary, and we'd rather state it than imply otherwise.

Where the two meet is the supplement aisle. Vitamin D is among the most-sold supplements in the world, and the distance between what the bottle implies and what the trials support is exactly the gap our front-of-package article is about — a real nutrient, a real function, and a marketing story that outran the evidence. We track vitamin D as a micronutrient because adequacy matters. That's a different claim from prevention, and the difference is the whole point.

The rest of this page is the part no product covers. Sunlight may be the clearest input in our framework that gives and costs at the same time, through the same source, in the same hour. Most decisions are easier than that. This one asks you to hold two true things at once.

This article is educational and is not medical advice. Sun exposure decisions are genuinely individual: a personal or family history of skin cancer, immunosuppression, photosensitising medication, autoimmune conditions such as lupus, pregnancy, very fair or very dark skin, and age all change the calculation. Discuss yours with a qualified clinician rather than adjusting exposure based on anything you read online, including here. Any new, changing, or asymmetric skin lesion warrants professional assessment.

Keep exploring: Vitamin D3 and K2 · Lifestyle · Sleep · Nutrition · Front-of-package claims

Medical Disclaimer: Read our full Medical Disclaimer

References

IARC Monographs Vol 100D, "Solar and Ultraviolet Radiation," and NTP 15th Report on Carcinogens, "Ultraviolet-Radiation-Related Exposures" (NCBI Bookshelf NBK304366; NBK590946). (UV spans 100–400 nm: UVA 315–400, UVB 280–315, UVC 100–280. Terrestrial UV from midday sun is approximately 95% UVA and 5% UVB; UVC and most UVB are removed by stratospheric ozone, molecular oxygen and water vapour. Tanning appliance users' median annual dose estimated at 20–30 times the minimal erythemal dose; modern units emit predominantly UVA.)
Wright, K.P. Jr, McHill, A.W., Birks, B.R., Griffin, B.R., Rusterholz, T., Chinoy, E.D. (2013). "Entrainment of the human circadian clock to the natural light-dark cycle." Current Biology 23(16):1554–1558. PMCID: PMC4020279. (Electrical lighting and indoor environments associated with reduced daytime light, increased post-sunset light, and delayed circadian timing versus a week camping under natural light; campers received ~4× more daytime light. Laboratory phase-shifting comparison cited within: ~550 lux near-saturating, 100 lux about half-maximal, ≤50 lux minimal. Small sample of physically active volunteers; camping alters far more than light exposure alone.)
Stothard, E.R., McHill, A.W., Depner, C.M., et al. (2017). "Circadian Entrainment to the Natural Light-Dark Cycle across Seasons and the Weekend." Current Biology 27(4):508–513. PMID: 28162893. (Winter study n=5; separate weekend summer study. Measurable circadian shift after a single weekend outdoors. Very small samples.)
Outdoor time and myopia onset — randomized evidence. Wu, P.C., Tsai, C.L., Wu, H.L., et al. (2013), Ophthalmology 120:1080–1085 (~80 min outdoor recess; 1-year incidence 8.41% vs 17.65%); He, M., et al. (40 min/day added over 3 years; 30.4% vs 39.5%, ~23% relative reduction); Wu, P.C., et al. (2018), "Myopia Prevention and Outdoor Light Intensity in a School-Based Cluster Randomized Trial," Ophthalmology 125(8):1239–1250, PMID 29371008 (693 grade-1 children; 14.47% vs 17.40%, OR 0.65, 95% CI 0.42–1.01, p=0.05); "Time Outdoors in Reducing Myopia: A School-Based Cluster Randomized Trial with Objective Monitoring of Outdoor Time and Light Intensity" (2022), Ophthalmology, PMID 35779695, NCT02980445 (6,295 children, 24 schools, Shanghai; adjusted 2-year incidence reduced 16% [IRR 0.84, 0.72–0.99] and 11% [IRR 0.89, 0.79–0.99]; effect related to duration and light intensity, clearest in non-myopic children). Meta-analysis: Acta Ophthalmologica (2025), DOI 10.1111/aos.17478 (15 studies, 16,597 participants; GRADE and AMSTAR-2 assessed). Evidence is stronger for preventing onset than for slowing established myopia.
Manson, J.E., Cook, N.R., Lee, I.-M., et al. (2019). "Vitamin D Supplements and Prevention of Cancer and Cardiovascular Disease." New England Journal of Medicine 380(1):33–44. DOI: 10.1056/NEJMoa1809944. PMID: 30415629. NCT01169259. (n=25,871, 2,000 IU/day, median 5.3 years, including 5,106 African American participants. Invasive cancer HR 0.96 [0.88–1.06]; major CVD HR 0.97 [0.85–1.12]; all-cause mortality HR 0.99 [0.87–1.12]. Cancer mortality HR 0.83 [0.67–1.02], reaching significance excluding the first year [0.79] or two [0.75]. A largely vitamin-D-replete population — the trial tested supplementation on top of adequacy, not treatment of deficiency.)
Virtanen, J.K., Nurmi, T., Aro, A., et al. (2022). "Vitamin D supplementation and prevention of cardiovascular disease and cancer in the Finnish Vitamin D Trial." American Journal of Clinical Nutrition 115(5):1300–1310. PMCID: PMC9071497. (n=2,495, 5 years, placebo vs 1,600 vs 3,200 IU/day; no significant differences. Baseline mean 25(OH)D 75 nmol/L.)
Webb, A.R., Kline, L., Holick, M.F. (1988). "Influence of season and latitude on the cutaneous synthesis of vitamin D3." Journal of Clinical Endocrinology & Metabolism 67(2):373–378. PMID: 2839537. (No previtamin D3 production in Boston, 42.2°N, November–February; Edmonton, 52°N, October–March. Model and in vitro exposure rather than serum outcomes in living subjects.)
UV index-based model for predicting synthesis of (pre-)vitamin D3 (2024). Scientific Reports 14. DOI: 10.1038/s41598-024-54188-5. PMID: 38347060. (Estimated time for 1,000 IU at 25% body surface area: ~5.05 min for Fitzpatrick Type I to ~25.25 min for Type VI. Simulation study, location-specific — the five-fold ratio is the transferable finding, not the exact minutes.)
Liu, D., Fernandez, B.O., Hamilton, A., Lang, N.N., Gallagher, J.M.C., Newby, D.E., Feelisch, M., Weller, R.B. (2014). "UVA Irradiation of Human Skin Vasodilates Arterial Vasculature and Lowers Blood Pressure Independently of Nitric Oxide Synthase." Journal of Investigative Dermatology 134(7):1839–1846. DOI: 10.1038/jid.2014.27. PMID: 24445737. (n=24; two standard erythemal doses of UVA — an erythemogenic dose. Hypothesis-generating; does not establish long-term outcome benefit from seeking comparable exposure.)
Lindqvist, P.G., Epstein, E., Nielsen, K., Landin-Olsson, M., Ingvar, C., Olsson, H. (2016). "Avoidance of sun exposure as a risk factor for major causes of death." Journal of Internal Medicine 280(4):375–387. DOI: 10.1111/joim.12496. PMID: 26992108. (Observational; high-latitude female cohort. Shared with the Lifestyle page and scoped identically there.)
IARC (2009/2012). Solar radiation and ultraviolet-emitting tanning devices classified Group 1, carcinogenic to humans. See also European Code Against Cancer 4th Edition, "Ultraviolet radiation and cancer," Cancer Epidemiology (2015), DOI: 10.1016/j.canep.2014.12.014.
World Health Organization, "Ultraviolet radiation" fact sheet, and "Radiation: the ultraviolet (UV) index" (WHO Q&A). (Protection best achieved through shade and clothing rather than sunscreen; sunscreen for areas clothing cannot cover; sunscreens should not be used to extend time spent in the sun; wraparound sunglasses blocking 99–100% UVA and UVB; artificial tanning should never be considered an option for achieving vitamin D sufficiency. Particular care advised at UV Index 3 or above; below UVI 2, risk is limited even for very fair skin and protective measures are not normally needed.)
Green, A., Williams, G., Neale, R., et al. (1999). "Daily sunscreen application and betacarotene supplementation in prevention of basal-cell and squamous-cell carcinomas of the skin: a randomised controlled trial." The Lancet 354(9180):723–729. DOI: 10.1016/S0140-6736(98)12168-2. PMID: 10475183. (n=1,621, Nambour, Queensland. SCC rate ratio 0.61 [0.46–0.81]; BCC not significantly reduced. Eight-year follow-up, van der Pols et al. 2006, reported sustained ~35% lower SCC incidence.)
Green, A.C., Williams, G.M., Logan, V., Strutton, G.M. (2011). "Reduced melanoma after regular sunscreen use: randomized trial follow-up." Journal of Clinical Oncology 29(3):257–263. DOI: 10.1200/JCO.2010.28.7078. PMID: 21135266. (11 vs 22 melanomas; HR 0.50, 95% CI 0.24–1.02, P = .051 — a secondary endpoint that did not cross conventional significance, frequently reported as though it had.)
Matta, M.K., Florian, J., Zusterzeel, R., et al. (2020). JAMA 323(3):256–267. DOI: 10.1001/jama.2019.20747; and Matta et al. (2019), JAMA 321(21):2082–2091. DOI: 10.1001/jama.2019.5586. (Organic UV filters absorbed above the FDA's 0.5 ng/mL threshold for further safety assessment. Absorption identifies missing data; it does not establish harm. Shared with the Lifestyle page.)
U.S. Food and Drug Administration, Final Administrative Order OTC000039, issued 9 June 2026, adding bemotrizinol (bis-ethylhexyloxyphenol methoxyphenyl triazine) to OTC Monograph M020 at concentrations up to 6% for adults and children 6 months and older; effective 9 August 2026. (First new active ingredient added to the US OTC sunscreen monograph since the late 1990s, and the first via the CARES Act administrative order pathway. FDA review found broad-spectrum UVA/UVB protection, low percutaneous absorption and infrequent irritation; determined GRASE. Long used in the EU and elsewhere at up to 10%.)
Vitamin K2 with vitamin D — vascular outcomes. Diederichsen, A.C.P., Lindholt, J.S., Möller, S., Øvrehus, K.A., Auscher, S., Lambrechtsen, J., Hosbond, S.E., Alan, D.H., Urbonaviciene, G., Becker, S.W., Fredgart, M.H., Hasific, S., Folkestad, L., Gerke, O., Rasmussen, L.M., Møller, J.E., Mickley, H., Dahl, J.S. (2022). "Vitamin K2 and D in Patients With Aortic Valve Calcification: A Randomized Double-Blinded Clinical Trial" (AVADEC). Circulation 145(18):1387–1397. DOI: 10.1161/CIRCULATIONAHA.121.057008. PMID: 35465686. ClinicalTrials.gov NCT03243890. (Community-dwelling Danish men aged 65–74 with aortic valve calcification score ≥300 AU. 365 men were randomized to MK-7 720 µg plus vitamin D3 25 µg daily or placebo for 24 months. The primary analysis did not establish a significant reduction in aortic valve calcification progression, and the authors state in published correspondence that the trial found no significant difference after two years. A prespecified secondary coronary analysis — reported in JACC: Advances (2023), DOI 10.1016/j.jacadv.2023.100643 — included 304 participants without ischaemic heart disease and found a numerically smaller increase in coronary calcification with supplementation, but the between-group difference was not statistically significant. Correction record: v5 and v6 stated that 389 men were randomized and that 365 reflected an analysed subset. That was wrong. The primary Circulation report gives 365 as the randomized population; the figure of 389 comes from the trial's own secondary analysis in JACC: Advances. The discrepancy is between two publications by the same investigators, not between a paper and a summary of it. Corrected at v7 after checking the primary report. The same correction was applied to the D3/K2 article in the same pass.) Systematic reviews, both openly accessible and reaching different headline conclusions: Li, T., Wang, Y., Tu, W-P. (2023). "Vitamin K supplementation and vascular calcification: a systematic review and meta-analysis of randomized controlled trials." Frontiers in Nutrition 10:1115069. DOI: 10.3389/fnut.2023.1115069. PMID: 37252246. PMCID: PMC10218696 (14 RCTs, 1,842 participants enrolled and 1,533 analysed overall. Five trials measured change in coronary artery calcification; one was excluded for reporting results in an incompatible form, leaving four trials and 424 participants in the pooled CAC analysis, which found a statistically significant slowing of progression, MD −17.37, 95% CI −34.18 to −0.56, p = 0.04, I² = 34%. Separately, seven trials and 578 participants showed a significant reduction in dephospho-uncarboxylated matrix Gla protein, MD −243.31, p = 0.0001, I² = 71%, and six trials and 547 participants showed no significant difference in adverse events. The same review records that eight other trials measuring major arterial or valve calcification reported no appreciable benefit, and its authors state that vitamin K's role in CAC seems to remain controversial. The included trials varied substantially in vitamin K form, dose, population, disease state and imaging endpoint, and the authors conclude that more rigorously designed RCTs are required to verify benefit. The authors declare no commercial or financial conflict of interest.) Contrast, in chronic kidney disease specifically: "Effects of vitamin K supplementation on vascular calcification in chronic kidney disease: A systematic review and meta-analysis of randomized controlled trials," Frontiers in Nutrition, DOI: 10.3389/fnut.2022.1001826 (ten RCTs, 733 patients; serum biomarkers decreased and vascular elasticity improved mildly, but no significant change in calcification scores derived from radiological examination; the authors conclude there is not yet solid evidence for a protective effect in CKD. Note that the review reports only ten trials because it is restricted to CKD, and that half the included studies were judged low risk of bias.) Correction record: the v5 note described only the eight trials in this review that found no appreciable benefit, and the authors' remark that the role remains controversial, both of which the paper does say. It omitted the review's headline pooled CAC result entirely, which made an equivocal review read as a null one. Corrected at v6 after reading the full paper. An initial account of this error, written before the full text was retrieved, attributed the v5 wording to the CKD review; that account was itself wrong and is recorded here rather than removed. Bone: Knapen, M.H.J., Drummen, N.E., Smit, E., Vermeer, C., Theuwissen, E. (2013). "Three-year low-dose menaquinone-7 supplementation helps decrease bone loss in healthy postmenopausal women." Osteoporosis International 24(9):2499–2507. DOI: 10.1007/s00198-013-2325-6. PMID: 23525894 (244 healthy postmenopausal women, MK-7 180 µg/day or placebo for three years; slowed decline at some skeletal sites. Does not establish that vitamin D supplementation universally requires K2.) Cited here only to note that the popular D3-plus-K2 pairing is not established by current trial evidence; the topic belongs to a dedicated article.
Schroeder, A., Zimmerman, A., Fogt, N. (2024). "Case Report: Solar Retinopathy Secondary to the Viral TikTok Trend '#SunGazing.'" Clinical Insights in Eyecare 2(4). DOI: 10.66574/001c.123720. (A single case report — cited as demonstration that the injury occurs, not as an incidence estimate.)
Demay, M.B., Pittas, A.G., Bikle, D.D., et al. (2024). "Vitamin D for the Prevention of Disease: An Endocrine Society Clinical Practice Guideline." Journal of Clinical Endocrinology & Metabolism 109(8):1907–1947. (Advises against routine supplementation beyond dietary reference intakes and against routine 25(OH)D testing in generally healthy adults younger than 75, while identifying selected populations — including pregnancy, adults 75 and older, children and adolescents, and adults with high-risk prediabetes — that may benefit from empiric supplementation. Also notes that outcome-specific blood thresholds have not been firmly established.)
Harmsen, J.-F., Habets, I., Biancolin, A.D., et al. (2026). "Natural daylight during office hours improves glucose control and whole-body substrate metabolism." Cell Metabolism 38(1):65–81.e10. DOI: 10.1016/j.cmet.2025.11.006. PMID: 41418772. (Randomized crossover in 13 adults with type 2 diabetes comparing 4.5 days of natural daylight through windows against constant artificial office lighting; daylight increased time in normal glucose range, shifted substrate use toward fat oxidation, and advanced muscle-cell circadian timing. Very small and short — hypothesis-generating, not outcome evidence. Published 6 January 2026.)
Krzywanski, J., Mikulski, T., Krysztofiak, H., Mlynczak, M., Gaczynska, E., Ziemba, A. (2016). "Seasonal Vitamin D Status in Polish Elite Athletes in Relation to Sun Exposure and Oral Supplementation." PLOS ONE 11(10):e0164395. DOI: 10.1371/journal.pone.0164395. PMID: 27732653. PMCID: PMC5061377. Published 12 October 2016; open access. (409 Polish elite athletes, serum 25(OH)D measured 2010–2014. Inadequate status in winter in 80% of outdoor-training and 84% of indoor-training athletes; in summer, 42% and 83% respectively. Oral supplementation increased concentrations by 45%; training at low latitude in winter increased them by 85%. Observational cohort of a young athletic population at high latitude, so the proportions are specific to that setting; the transferable finding is that outdoor activity alone did not secure sufficiency. The authors' own conclusion is that adequate vitamin D status can be achieved by both increased sun exposure and oral supplementation, and that athletes should routinely assess their status rather than assume either route is sufficient.)
Hartley, M., Hoare, S., Lithander, F.E., et al. (2015). "Comparing the effects of sun exposure and vitamin D supplementation on vitamin D insufficiency, and immune and cardio-metabolic function: the Sun Exposure and Vitamin D Supplementation (SEDS) Study." BMC Public Health 15:115. DOI: 10.1186/s12889-015-1461-7. PMCID: PMC4391331. Published trial protocol, not results. Australia New Zealand Clinical Trials Registry ACTRN12613000290796. (Multi-centre randomised controlled trial of two vitamin D doses and placebo alongside two patterns of sun exposure, in adults aged 18–64 with baseline 25(OH)D of 40–60 nmol/L. Cited for the authors' own framing that the optimal strategy — sun exposure, supplementation, or both — remains unclear, and that whether sun exposure carries benefits beyond initiating vitamin D synthesis is unresolved. This is a protocol paper, cited for the stated research question rather than for results.)

Sourcing note: this article cites IARC monographs, national toxicology assessments, WHO guidance, randomized controlled trials and peer-reviewed modelling studies with DOI/PMID where available. Sample sizes, study designs, and the distinction between primary and secondary endpoints are stated in the reference notes rather than left implicit — particularly where a widely repeated claim rests on a result that did not reach significance, or on a population already replete in the nutrient being tested. Where a mechanism is promoted mainly by parties selling a product, that is stated in the body rather than omitted. Cross-link targets (#) resolve once the site structure is live. Reading time is measured, not asserted: body words excluding the reference list and the metadata header, counted at 225 words per minute and rounded to the nearest minute.