Does the Sun Increase Testosterone?

Sun exposure is linked to higher testosterone levels in men, but the relationship is indirect, modest, and far more tangled than the viral “sunlight boosts T” claims suggest. Multiple pathways connect sunlight to the hormonal system: vitamin D synthesis, UVB effects on skin signaling, bright-light exposure through the eyes, and even simply spending time outdoors. Yet when researchers have tried to isolate any single pathway and replicate the effect with supplements or light boxes, the testosterone boost mostly vanishes. The honest picture is that sunlight is probably part of a larger hormonal equation, not a lever you can pull on its own.

What the Seasonal Testosterone Data Shows

If sunlight straightforwardly raised testosterone, you would expect men’s levels to peak in summer and bottom out in winter. The reality is messier. A large study of men in Tromsø, Norway (above the Arctic Circle, where daylight hours swing dramatically across the year) found that total testosterone actually followed a bimodal pattern: a small peak in February, a dip in June, and a more prominent peak in October and November. Free testosterone peaked in December and hit its lowest point in August. In other words, the months with the most daylight and warmth had the lowest testosterone levels, not the highest.¹

That pattern does not replicate everywhere. A study drawing on two large institutional databases in Pittsburgh and Miami found no statistically significant seasonal variation in testosterone for either overall cohorts or when men were broken down by age group.² Meanwhile, an Austrian study found both vitamin D and testosterone peaked together in late summer, with the lowest values in March.³ The seasonal data, taken together, is genuinely contradictory. Geography, latitude, cultural habits around outdoor activity, and body composition all seem to shape whether a seasonal testosterone rhythm shows up at all, and in which direction.

The Vitamin D Connection

The most commonly cited mechanism linking sun to testosterone is vitamin D, which your skin synthesizes when UVB radiation hits it. Cross-sectional studies consistently find that men with higher vitamin D levels also tend to have higher testosterone. In a European study of over 2,000 men, vitamin D was positively associated with both total and free testosterone, and the relationship was linear up to a point: it rose steadily at lower vitamin D levels but plateaued once 25(OH)D reached roughly 75 to 85 nmol/L.⁴ A separate Austrian cross-sectional study found the same pattern, with men who had sufficient vitamin D (above 30 µg/L) showing significantly higher testosterone and free androgen index compared to deficient men.³

A systematic review pulled together various study designs on this question. A Mendelian randomization analysis of over 4,000 Chinese men found that genetically lower vitamin D predicted lower testosterone, suggesting a causal direction. A Dutch cross-sectional study similarly found men with vitamin D levels below 25 nmol/L had lower total and bioavailable testosterone.⁵

So the observational picture looks solid. But here is where it falls apart.

Why Vitamin D Supplements Do Not Replicate the Effect

If low vitamin D caused low testosterone, raising vitamin D through supplementation should raise testosterone. Multiple randomized controlled trials have tested this, and the results are uniformly disappointing. A trial of healthy men given vitamin D supplements found no significant effect on total testosterone.⁶ Another trial specifically targeted middle-aged men with low testosterone and gave them vitamin D; again, no significant treatment effect on testosterone levels.⁷ A third trial in young healthy men tested vitamin D and calcium supplementation for six months and found no significant effect on serum testosterone.⁸

This disconnect matters. The fact that vitamin D and testosterone track together in population data, yet raising vitamin D with a pill doesn’t raise testosterone, strongly suggests that vitamin D is a marker rather than a cause. Men who have more vitamin D tend to be the same men who spend more time outdoors, exercise more, carry less body fat, and get more sunlight through pathways that have nothing to do with the vitamin itself. The correlation is real. The causal arrow from vitamin D to testosterone appears weak, and supplementation does not seem to be a shortcut.

The UVB Skin-Brain-Gonad Pathway

While the vitamin D story has disappointed, a different biological pathway has emerged from animal research that is genuinely intriguing. In 2021, researchers published a study showing that UVB exposure (the same type of light your skin uses to make vitamin D) activated a signaling cascade in mice that went from the skin to the brain to the reproductive system. Exposure to UVB increased sex-steroid hormone levels and changed sexual behavior. In female mice, the effect included larger ovaries and increased expression of a key reproductive hormone. The mechanism ran through a protein called p53 in skin cells: when p53 in epidermal cells was specifically knocked out, the hormonal effects of UVB disappeared entirely.⁹

This “skin-brain-gonad axis” represents a fundamentally different mechanism from the vitamin D story. The idea is that UVB hitting your skin triggers a hormonal signal that reaches the brain’s hypothalamic-pituitary axis, which then influences the gonads. It is a plausible explanation for why sunlight correlates with hormonal changes in ways that a vitamin D capsule cannot replicate: the pill bypasses the skin entirely, and it is the skin’s UV response that may be doing the heavy lifting.¹⁰

The major caveat: this has been demonstrated in mice, not yet confirmed in humans at the hormonal level. Mouse models of UV exposure are useful but do not always translate. The research is provocative and biologically coherent, but it would be premature to treat it as settled science for human testosterone.

Bright Light Through the Eyes

A separate line of research focuses not on UV hitting the skin but on visible light entering the eyes. A cross-sectional analysis of over 2,200 men from the U.S. National Health and Nutrition Examination Survey found that bright-light exposure was significantly associated with higher testosterone, with an increase of roughly 15 ng/dL per additional ten minutes of bright-light exposure per day. Afternoon light showed the strongest association. The effect was most pronounced in men who otherwise had limited baseline light exposure.¹¹

However, when light therapy has been tested as an intervention, the results have been underwhelming. A systematic appraisal of alternative therapies in men’s health found that light therapy produced non-significant changes in hormone levels, though improvements in sexual satisfaction were noted.¹² This echoes the vitamin D supplementation story: the observational data looks promising, but controlled interventions fail to deliver the same magnitude of effect.

The mechanism here likely involves circadian signaling. Light entering the eyes influences the suprachiasmatic nucleus, the brain’s master clock, which in turn regulates the hypothalamic-pituitary-gonadal axis. Bright-light exposure has been shown to acutely suppress cortisol, the body’s primary stress hormone, which chronically elevated levels of can suppress testosterone production. So part of the link between light and testosterone may simply be that adequate light exposure helps keep cortisol in check and circadian rhythms running smoothly.

Time Outdoors Matters, Even After Controlling for Everything Else

One of the most interesting recent findings comes from a study that asked a deceptively simple question: is just spending more time outside associated with higher testosterone? Using NHANES data, researchers found that each additional hour spent outdoors per day was associated with about a 9 ng/dL increase in serum testosterone and a 14% decrease in the odds of having clinically low testosterone. The striking part is what they controlled for: age, income, education, BMI, physical activity (both self-reported and measured by accelerometer), diabetes, vitamin D levels, and dietary habits. Even after accounting for all of those, the outdoor-time association persisted.¹³

This is cross-sectional data, so it cannot prove causation. But the fact that the association survived adjustment for physical activity and vitamin D concentration makes it harder to dismiss as just a proxy for exercise or sun-derived vitamin D. Something about being outdoors, whether it is UVB on the skin, bright visible light through the eyes, reduced psychological stress, or some combination, appears connected to testosterone in a way that existing measured confounders do not fully explain.

What Happens in Animals

In many animal species, photoperiod (the daily ratio of light to darkness) is the dominant regulator of seasonal reproduction and testosterone secretion. Male hamsters exposed to short days for ten weeks showed reduced testicular size, lower plasma testosterone, and diminished sexual behavior.¹⁴ Subtropical goats showed testosterone secretion that tracked directly with day length: short days enhanced testosterone, and long days inhibited it, reflecting their breeding season’s alignment with autumn and winter.¹⁵ Tree sparrows exposed to various light-dark cycles showed testicular growth and increased testosterone only under cycles their internal clocks interpreted as “long days.”¹⁶

These animal models confirm that light-driven pathways to the reproductive axis are biologically real and ancient. But humans are not photoperiodic breeders in the same way hamsters, goats, and sparrows are. We reproduce year-round, and the degree to which residual photoperiodic sensitivity influences human testosterone is still debated. The inconsistent seasonal data in human studies probably reflects the fact that modern humans live under artificial lighting, variable schedules, and cultural conditions that dilute whatever photoperiodic signal our physiology might otherwise respond to.

The Melatonin and Cortisol Angle

Two hormones that light exposure directly influences, melatonin and cortisol, both interact with testosterone production. Melatonin, which the pineal gland produces in darkness and suppresses in response to light, acts as a local modulator in testicular cells. Research indicates melatonin influences Leydig cell endocrine activity and Sertoli cell proliferation and energy metabolism, both of which feed into testosterone synthesis. The relationship is not a simple suppression or boost: melatonin appears to be a regulatory player whose effects depend on timing and concentration.

Cortisol’s relationship to testosterone is more straightforward. Chronically elevated cortisol suppresses the hypothalamic-pituitary-gonadal axis, and bright-light exposure has been shown to acutely reduce cortisol levels compared to dim-light conditions. If you are chronically under-exposed to bright light (spending most of your day indoors under dim artificial lighting), this could contribute to higher baseline cortisol and, indirectly, lower testosterone. Getting adequate bright light may not boost testosterone so much as remove a brake on it.

Why Testicle Sunning and Perineum Sunning Are Counterproductive

Social media trends advocating direct genital sun exposure as a testosterone hack deserve their own section, because they are not just unsupported: they risk doing the opposite of what their proponents claim. A study analyzing public interest in “testicle tanning” noted that excessive UV radiation exposure to the genital area is associated with higher rates of genital tumor formation and decreased sperm counts, since spermatogenesis depends on temperatures lower than the body’s core.¹⁷ Similarly, researchers examining the perineum-sunning trend found no evidence that perineal skin has any special ability to generate more vitamin D than other skin areas, and no human evidence that sunning this specific area improves hormone regulation, mood, or libido.¹⁸

The thermal angle makes the problem worse. For optimal sperm production, testicular temperature needs to sit about 2 to 6°C below core body temperature. Heat stress directly damages testicular tissue and reduces testosterone synthesis. Chronic heat stress can abnormally increase aromatase activity in Leydig cells, which converts testosterone into estradiol, creating a hormonal imbalance that works against everything the testicle-sunning advocates claim to want.¹⁹ In short, the testes are external for a reason: they need to stay cool. Deliberately heating them with direct sunlight undermines their function.

What Actually Helps

If the evidence points anywhere, it is toward a simple and admittedly unsexy recommendation: spend more time outside during the day. Not sunbathing strategically, not exposing specific body parts to UV light, not timing supplement protocols. Just being outdoors, where you get bright visible light through your eyes, moderate UVB on your arms and face, physical movement, and relief from the cortisol-raising effect of spending all day in a dim indoor environment. The NHANES data showing an independent association between outdoor time and testosterone, even after controlling for exercise and vitamin D, suggests that the benefits may come from the combination rather than from any single isolable factor.¹³

That said, the effect sizes being discussed are modest. An extra hour outdoors being associated with about 9 ng/dL of testosterone is not trivial, but it is not going to move someone from clinically low to normal range on its own. For men with genuinely low testosterone, outdoor time is worth incorporating as one piece of a broader picture that includes adequate sleep, healthy body weight, resistance exercise, and medical evaluation when appropriate. For men with normal testosterone who are looking for an edge, spending more daylight hours outdoors is a reasonable and low-risk habit, but expecting it to produce dramatic hormonal changes is not supported by the current evidence.

Effects on Female Hormones

Most of the research and public interest on this topic focuses on men, but UV exposure also appears to influence female reproductive hormones, in different directions. A European multicenter study of postmenopausal women found that greater UV radiation exposure was associated with lower levels of estradiol and estrone, and higher levels of follicle-stimulating hormone and luteinizing hormone.²⁰ This pattern is consistent with UV exposure having gonadotropin-stimulating effects through the hypothalamic-pituitary axis, though the downstream hormonal consequences differ between men and women due to differences in gonadal function. The mouse study on UVB and the skin-brain-gonad axis observed enlarged ovaries and extended estrus in female mice, which aligns with the idea that UVB activates the reproductive axis broadly rather than boosting any one specific hormone.⁹ The female hormonal response to UV is understudied compared to the male side, and what evidence exists is cross-sectional or from animal models.