Seasonal vitamin D: why your winter dose is not your summer dose
Every autumn, the same public health message goes out: take a vitamin D supplement through winter. In the UK, the NHS recommends 10 micrograms daily from October to March. It is a sensible population-level nudge, and for many people it is probably better than nothing. But the framing, a single dose, for everyone, for a defined calendar window, obscures most of what actually determines whether a person's vitamin D status is adequate at any given point in the year.
The reality is that two people following identical supplement routines through an identical winter can arrive at spring with vitamin D levels that differ by a factor of two or more. That gap is not random. It is shaped by biology, and understanding the main variables that drive it makes the difference between a supplementation approach that is calibrated to your situation and one that is based on a population average that may not apply to you at all.
Why winter is genuinely different
Vitamin D is unusual among nutrients because the body's primary source is not food but sunlight, specifically, a narrow band of ultraviolet radiation called UVB. When UVB hits the skin, it converts a cholesterol precursor into previtamin D3, which is then processed by the liver and kidneys into the active form the body uses.
The problem in winter, particularly at northern latitudes, is geometric. The sun sits lower in the sky, which means sunlight travels through a much greater thickness of atmosphere before reaching the ground. UVB radiation is scattered and absorbed during that journey. By the time sunlight arrives at the surface in the UK between October and March, the UVB component is effectively absent for most of the day, and often entirely absent depending on the time and cloud cover.
This is not a matter of degree, it is close to a binary. Studies measuring cutaneous vitamin D synthesis at UK latitudes have found that meaningful skin production is effectively negligible for practical purposes for roughly five months of the year, regardless of how much time a person spends outdoors. Being outside on a bright February afternoon in London does not produce appreciable vitamin D. The light is there; the relevant wavelength mostly is not.
This matters because it means the body's stores from summer sun exposure, whatever they are, have to carry a person through winter, supplemented by whatever they take. Those stores are not the same for everyone, and they deplete at different rates. A person who entered October with a 25(OH)D level of 75 nmol/L is in a meaningfully different position to someone who entered at 40 nmol/L, even if both take 10mcg daily through to March.
Why the same dose works differently in different people
The variation in how people respond to the same supplement dose is one of the more consistently documented findings in the vitamin D literature, and it has several distinct explanations.
Skin pigmentation
Melanin, the pigment responsible for skin colour, is a natural filter of UVB radiation. This is part of its biological role: darker skin evolved in high-UVB environments where limiting vitamin D synthesis to a safe level was adaptive. In lower-UVB environments, the same protective mechanism becomes a liability.
The practical consequence is substantial. Research comparing vitamin D synthesis rates across skin tones has found that individuals with darker skin require longer sun exposure to produce the same amount of vitamin D as those with lighter skin. Estimates vary widely depending on UV index, body surface area exposed, and study methodology, some research has reported differences of several times the required exposure time, though the range across studies is broad. This applies to sun exposure, but it also has downstream effects on the stores that arrive at winter and on how much supplementation is needed to compensate.
This is one reason why vitamin D deficiency is disproportionately common in people of South Asian and Black African or Caribbean heritage living at northern latitudes. The mismatch between the skin's UVB filtering and the available sunlight is larger, the deficit going into winter is typically greater, and a standard 10mcg supplement may not be sufficient to maintain adequate status through the winter months. It is worth noting that behaviour and environment also shape this, patterns of time outdoors, clothing, and occupation all interact with the biological variables, but the underlying melanin effect is real and documented across multiple study designs.
Body composition and fat mass
Vitamin D is a fat-soluble compound, which means it is stored in adipose tissue. This has two consequences that are relevant here.
The first is that higher body fat mass means a larger reservoir for vitamin D to distribute into. When a person with a higher fat mass takes a supplement or is exposed to sunlight, the vitamin D produced is distributed across a greater volume of tissue, which is consistently associated with lower circulating blood levels for a given dose compared to someone with lower fat mass. Whether this is primarily explained by volumetric dilution across a larger body mass or by active sequestration in adipose tissue is still debated, but the association between higher BMI and lower serum 25(OH)D is consistent across studies and holds after accounting for other variables including sun exposure and dietary intake.
The second consequence is that in people with higher fat mass, vitamin D can accumulate in adipose tissue during summer and be released more slowly during winter. This is sometimes described as a buffering effect, and while it provides some protection against acute deficiency, it also means that the relationship between supplementation, sun exposure, and circulating levels is less direct and harder to predict.
The practical implication is that higher doses may be needed to achieve the same circulating level in individuals with higher body fat, and that standard dose recommendations based on population averages will systematically underserve this group.
Baseline status entering winter
Perhaps the most straightforward variable is where a person starts. Someone who enters October with a circulating 25(OH)D level of 30 nmol/L, already at the lower end of what is considered adequate, and someone who enters at 80 nmol/L are not in equivalent positions. Both may take the same supplement through winter, but one is compensating for an existing deficit while the other is maintaining a level that already provides a reasonable buffer. Population studies suggest that 25(OH)D levels typically decline by somewhere in the range of 20 to 30 nmol/L across the winter months in unsupplemented adults, though there is considerable inter-individual variation around that figure.
Baseline status at the start of winter is determined by everything that happened through spring and summer: how much sun exposure there was, what was eaten, whether supplements were taken, and all of the individual biological factors discussed here. It is also affected by the previous winter, people who become significantly depleted and do not fully recover by summer will carry a lower baseline into the next winter than those who do.
This creates a compounding dynamic that a fixed-dose, fixed-season recommendation does not account for. The same 10mcg for five months may be appropriate maintenance for one person and inadequate correction for another, depending on what they are starting from.
Genetics
There is meaningful genetic variation in how people produce, transport, and use vitamin D, and this variation contributes to differences in circulating levels that cannot be explained by sun exposure, diet, or supplementation alone.
Two gene regions are particularly relevant. The VDR gene encodes the vitamin D receptor, the protein through which active vitamin D exerts most of its effects in cells. Variants in this gene affect how sensitively cells respond to vitamin D, which means that two people with identical circulating levels may experience different biological effects depending on their VDR genotype.
The CYP gene family, particularly CYP2R1 and CYP27B1, encode enzymes responsible for converting vitamin D into its active form. Variants in these genes affect conversion efficiency, and people with less efficient conversion may need higher circulating levels of the precursor form to achieve the same biological effect as those with more efficient conversion.
These are not exotic rare variants. Relevant polymorphisms in both VDR and CYP2R1 are common in most populations, and their contribution to variation in vitamin D status has been documented in genome-wide association studies. The effect size per individual variant is modest, genetics contributes meaningful variation at the population level but does not override the effects of sun exposure and supplementation in any single person. What it does mean is that the response to a given dose is not uniform, and that genetic factors may contribute to differences in how effectively a given circulating level translates into biological effect, even if the clinical implications of specific variants have not been precisely established.
The summer side of the equation
The standard framing treats summer as a solved problem, as if sun exposure through spring and summer reliably produces adequate status that then needs topping up in winter. This is not always the case.
A substantial proportion of people in the UK arrive at October already below the threshold considered adequate, based on population studies of serum 25(OH)D levels. This reflects several converging factors: indoor working patterns that limit midday sun exposure even in summer, the same skin pigmentation and body composition variables that affect winter response, and the relatively modest UVB intensity even at peak summer in northern regions compared to lower latitudes. Sunscreen use is sometimes cited as a major contributor, though real-world application is typically inconsistent and rarely blocks all UVB, it is a factor but probably a smaller one than the others.
A survey of serum 25(OH)D levels in UK adults has consistently found a substantial proportion with levels below 50 nmol/L even at the end of summer, the point at which stores should be at their annual peak. For those people, the winter supplement conversation is not about maintaining a reasonable level but about correcting one that was already marginal.
This is one reason why a small number of clinicians and researchers have argued that year-round supplementation at modest doses makes more sense for many people than the October-to-March window, not because summer sunlight is irrelevant, but because not everyone achieves adequate status from it even under reasonable conditions.
What testing actually tells you
A serum 25(OH)D test, available from GPs in the UK when there is clinical reason, or through private testing, measures the main circulating form of vitamin D and is the standard way to assess status. The result gives a snapshot of where you are, and testing at the end of winter and at the end of summer gives a more complete picture of how your levels move across the year.
The main reference points used clinically are: below 25 nmol/L is generally considered deficient; 25 to 50 nmol/L is insufficient; above 50 nmol/L is considered adequate for most purposes. Some guidance suggests 75 nmol/L or above as a more conservative target, though this threshold is debated and not universally adopted in clinical or public health recommendations.
What testing cannot tell you is what dose you need to get from where you are to where you want to be, because that depends on the individual response variables discussed above. Two people starting at 35 nmol/L taking the same supplement may reach different levels after three months, the relationship between dose and circulating level is not linear or uniform, and response tends to be larger at lower baseline levels and smaller as levels rise. This is where the individual variation compounds: it is not just about where you start but about how efficiently you convert and respond to what you take.
Testing does at least remove the guesswork about the starting point, which is meaningful. Supplementing without knowing your baseline is not necessarily wrong, at modest doses, the risk of over-supplementation is low, but it does mean you cannot tell whether what you are taking is sufficient, insufficient, or more than needed.
What can reasonably be concluded
The public health recommendation to supplement vitamin D through winter is broadly sensible, and for a population-level nudge it is better calibrated than most. But it is built on a set of implicit assumptions, about baseline status, about skin tone, about body composition, about genetics, that do not hold equally across the population.
For people at northern latitudes with darker skin, higher fat mass, or a history of low vitamin D status, a standard 10mcg recommendation through winter is likely to be insufficient. For people who arrive at October already depleted from a summer that did not produce adequate synthesis, the same dose addresses only part of the gap. For people with genetic variants that affect conversion or receptor sensitivity, the relationship between dose and outcome is less predictable than the recommendation implies.
None of this means that supplementation is not worth doing, for most people at northern latitudes through winter, it is. It means that the dose, the timing, and the adequacy of the approach depend on individual factors that a universal recommendation cannot account for. Testing, particularly at the end of winter when levels are at their lowest, provides a more reliable basis for calibrating what is needed than the calendar alone.
Where evidence is limited or outcomes are uncertain, conclusions should be treated as provisional and subject to revision as the evidence base develops.
Key references
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