Clinical article · Vitamin D · Latitude 59.3°N
Vitamin D in a Swedish winter —
why sunlight isn't enough
and why uptake varies
Short answer. At Stockholm's latitude of 59.3°N the sun sits too low above the horizon between October and March for sufficient UVB to reach ground level. During those months no meaningful vitamin D is produced in the skin — regardless of how much time is spent outdoors. Since 25(OH)D has a half-life of two to three weeks, summer stores are usually depleted at some point over the winter.
The question is rarely whether vitamin D is needed through a Nordic winter, but why two people on the same dose end up at different levels. The answer lies in the absorption pathway and in the genetics of hydroxylation and transport.
Latitude
Vitamin D winter is a
physical limit, not a lifestyle question
Cutaneous vitamin D synthesis begins when UVB radiation in the 290–315 nm range strikes 7-dehydrocholesterol in the skin. The molecule converts to previtamin D3 and then thermally to cholecalciferol. The entire process depends strictly on radiation in that specific wavelength band reaching the skin surface.
It does not do so year-round. The lower the sun sits, the longer the path radiation takes through the atmosphere, and UVB is filtered far more heavily than UVA. Above roughly 50°N the winter solar angle is insufficient — and Stockholm lies at 59.3°N. From October to March there is therefore no meaningful synthesis in the skin, however long one stays outside. Winter sun delivers UVA, warmth and light, but not vitamin D.
Even during the summer months synthesis is modified by skin pigmentation, age — 7-dehydrocholesterol content in skin declines over the years — clothing, sunscreen and time of day. Someone working indoors through the middle of the day has a shorter effective season than the calendar suggests.
The half-life sets the timeline. 25-hydroxyvitamin D has a half-life of roughly two to three weeks. A store built up in July is therefore effectively gone by February. That is why measured levels in a Nordic population are lowest at the end of winter, and why deficiency is often only discovered then.
Absorption
Fat-soluble means uptake depends
on more than the dose
Cholecalciferol is fat-soluble. Orally administered vitamin D must therefore be emulsified with the help of bile salts, taken up in micelles in the small intestine, packaged into chylomicrons in the enterocyte and transported via the lymphatic system before it reaches circulation. Only then is it 25-hydroxylated in the liver into the form measured as status.
Every step in that chain can be limiting. Reduced bile flow or cholestasis reduces micelle formation. Inflammatory bowel disease, coeliac disease and other conditions with impaired fat absorption reduce uptake. Previous bariatric surgery shortens the absorptive length. And a supplement taken on an empty stomach, without fat in the meal, is absorbed less well than the same dose taken with food.
In obesity a further phenomenon applies: vitamin D distributes into adipose tissue, meaning a larger volume of distribution produces a lower serum concentration at the same intake. The level is low without the intake necessarily being so.
This is why "how much should I take" is a worse question than "what is limiting uptake in me". It is the same logic that governs the form of other supplements: the number on the label says nothing about what actually arrives.
Individual variation
Why the same dose produces
different levels
After absorption, status is determined by hydroxylation and transport — and both vary genetically.
CYP2R1 encodes the hepatic 25-hydroxylase. Variants affect how efficiently cholecalciferol is converted to 25(OH)D. GC encodes vitamin D binding protein, which binds the majority of circulating vitamin D; variants affect what proportion is free and therefore available for cellular uptake. VDR encodes the receptor, and variants affect how strongly target tissue responds to a given level.
The consequence is clinical rather than academic. Two people with identical intake and identical sun exposure can arrive at different 25(OH)D, and two people with the same measured level can have different biological responses. It is also why a normal value does not always exclude functional deficiency — and why follow-up should be done by measurement rather than assumption.
To see your own profile, CYP2R1, GC and VDR are among the genes analysed in MethylDetox, and intracellular status complements the serum value in CMA.
Clinical consequence
When the gut is the bottleneck
injection is a different tool
If the limiting step is absorption, raising the oral dose rarely helps. A single intramuscular high dose bypasses the gut entirely and acts as a depot released slowly over about three months.
In a comparative trial, 100% of the group receiving intramuscular administration achieved sufficient levels at twelve weeks, which was superior to oral administration in the same study (Agarwal et al., 2024). This is particularly relevant in verified deficiency, in impaired fat absorption, and where adherence to a daily tablet is uncertain across six months of darkness.
It also explains why vitamin D cannot be given in a standard vitamin drip: cholecalciferol is practically insoluble in water and cannot be dissolved in an aqueous infusion solution in any meaningful quantity. That argument is developed separately →
Vitamin D (D3) injection 100,000 IU — indication, interval and price →
Frequently asked questions
Questions about vitamin D
and the Nordic winter
Cutaneous vitamin D synthesis requires UVB radiation in the 290–315 nm range. At Stockholm's latitude of 59.3°N the solar elevation is too low during the winter months for sufficient UVB to reach ground level — it is filtered out in the atmosphere. The period is therefore known as vitamin D winter and runs in practice from October to March. During those months no meaningful cutaneous synthesis occurs, regardless of time spent outdoors.
25-hydroxyvitamin D has a half-life of roughly two to three weeks. Stores built up over summer are therefore usually depleted at some point during late autumn or winter, which is why measured levels in a Nordic population are lowest in February and March.
Vitamin D is fat-soluble and requires bile salts and micelle formation to be absorbed in the small intestine, after which it is packaged into chylomicrons and transported via the lymphatic system. Impaired fat absorption, cholestasis, inflammatory bowel disease, coeliac disease, previous bariatric surgery or taking a supplement without fat in the meal all reduce uptake. In obesity part of the vitamin D is additionally sequestered in adipose tissue, lowering the serum level at the same dose.
Yes. Variants in CYP2R1 affect hepatic 25-hydroxylation, variants in GC affect vitamin D binding protein and therefore how much is free and available, and VDR variants affect the receptor response in target tissue. Two people with the same intake and the same sun exposure can therefore reach different levels and respond differently to the same dose.
25-hydroxyvitamin D is formed in the liver and is the form measured to assess status. The active form, 1,25-dihydroxyvitamin D, is then produced in the kidney and locally in several tissues. Status testing refers to 25(OH)D; the active form is hormonally regulated and does not reflect stores.
A single intramuscular high dose of 100,000 IU bypasses intestinal absorption entirely and acts as a depot released slowly over about three months. In a comparative trial 100% of the group receiving intramuscular administration achieved sufficient levels at twelve weeks (Agarwal et al., 2024). This is particularly relevant in verified deficiency, in impaired fat absorption, and where adherence to a daily tablet is uncertain.
Not in a standard aqueous vitamin drip. Cholecalciferol is fat-soluble and practically insoluble in water, so it cannot be dissolved in an aqueous infusion solution in any meaningful quantity. Vitamin D is given intramuscularly in an oil-based form.
Measurement is recommended but is not a requirement for booking. A licensed physician always performs an individual assessment. Where symptoms are pronounced or a risk factor is known, treatment may begin alongside testing, and intracellular analysis can complement the picture where the serum value is insufficient.
Reference. Agarwal N, et al. (2024). Comparison of intramuscular versus oral vitamin D supplementation. J Basic Clin Physiol Pharmacol. doi:10.1515/jbcpp-2024-0018