Edinburgh sits at approximately 56 degrees north latitude. Oslo is 59 degrees. Helsinki is 60. The physics of UVB radiation at these latitudes means that from approximately October to March — five months of the year — the sun's angle is too low for UVB to penetrate the atmosphere at the wavelengths required for vitamin D synthesis in human skin. Not reduced. Not diminished. For practical purposes of vitamin D production, the winter sun in Scotland is non-functional.
During the brief window when UVB is theoretically available — April to September — cloud cover, indoor working patterns, glass windows (which block UVB entirely), clothing, modern sunscreen use, and the specific time of day required (sun angle above 45 degrees, which in Scotland is only available for limited hours even in summer) combine to ensure that most Scots are accumulating substantially less vitamin D from sun exposure than the population guidance implies.
How skin makes vitamin D
When UVB radiation strikes the skin, it converts 7-dehydrocholesterol — a cholesterol precursor — into pre-vitamin D3. This compound is then converted to cholecalciferol (D3) by body heat. Vitamin D is made inside living skin cells, not on the surface, and the last step happens within hours (Tian 1993), so washing after sun isn’t thought to wash it away. (Tian XQ et al., J Biol Chem 1993, PMID 8392061; grade: mechanistic.)
What GrassrootsHealth shows — the data that changes the conversation
GrassrootsHealth is a public health research organisation that has conducted one of the largest ongoing prospective studies of vitamin D status in a real-world population — the D*Action project. Tens of thousands of participants across multiple countries have submitted vitamin D blood tests alongside detailed data on sun exposure, supplement use, body weight, and health outcomes. The D*calculator they have developed is the most sophisticated publicly available tool for estimating what an individual at a given latitude needs to reach a target blood level.
The GrassrootsHealth data also addresses the question of optimal blood levels empirically — looking at health outcomes across their participant population rather than deriving thresholds from bone health alone. Their findings consistently suggest that health outcomes across immune function, cancer risk, cardiovascular health, and all-cause mortality continue to improve up to approximately 100–125 nmol/L, with no clear additional benefit beyond 150 nmol/L and potential concerns above that range.
The evolutionary context — the dietary compensation that modern living cancelled
The relationship between latitude and vitamin D is not a design flaw. It is a design feature that has been undermined by modern living.
Populations living at high latitudes for thousands of generations did not die of vitamin D insufficiency in the numbers that modern insufficiency rates would predict. The reason is dietary adaptation. The traditional diets of high-latitude populations — Scottish, Scandinavian, Inuit, Northern Russian — were exceptionally rich in the dietary sources of vitamin D that partially compensate for limited UVB exposure.
Herring, mackerel, salmon, cod, and other fatty fish contain vitamin D3 in meaningful quantities. Cod liver oil — a traditional staple across northern European populations — is one of the most concentrated dietary sources of both vitamin D and vitamin A. Organ meats, particularly liver, contain D3 alongside a cofactor matrix that supports its conversion and utilisation. Full-fat dairy from pasture-raised animals — including butter and traditionally made cheese — contributed to vitamin D intake across seasons.
The Scottish traditional diet of herring, oatmeal, liver, full-fat dairy, and occasional game was not arriving at that composition by accident. It was the result of thousands of years of adaptation to an environment that provided limited sunshine for five months of the year. The diet solved the problem that the latitude created. Modern living — processed foods, seed oils, refined carbohydrates, reduced organ meat consumption, factory-farmed animals fed indoors — has cancelled that adaptation. The sun restriction remains. The dietary compensation has largely gone.
There is also an open question about whether populations that have lived at high latitudes for many generations have developed some degree of adaptation at the level of VDR sensitivity or conversion efficiency — becoming more efficient at using whatever vitamin D is available. The evidence here is limited but the question is legitimate. The individual variation in vitamin D status and response to supplementation observed clinically is consistent with this possibility, alongside the known genetic VDR polymorphisms that affect receptor sensitivity independently of latitude.
VDR genetics — why the same blood level means different things in different people
The honest position on supplementation
After everything in this post, the clinical position I hold on vitamin D supplementation for people living in Scotland is straightforward — even if getting there required this much context to justify it.
Test first. A 25-OH-D measurement before supplementing tells you where you are and gives you a baseline against which to assess response. It takes the guesswork out of dose selection and makes the intervention evidence-based rather than assumed.
Address cofactors simultaneously. Magnesium (bisglycinate or glycinate) and vitamin K2 (MK-7) are not optional additions to vitamin D supplementation. They are prerequisites for conversion, VDR function, and appropriate calcium direction.
The UK advice, and my working range. The UK advice is 10 µg (400 IU) a day from October to March (SACN 2016). It's set to keep almost everyone above 25 nmol/L (10 ng/mL), the level linked to bone and muscle health, and for that job it works. My working range is higher, 75–125 nmol/L (30–50 ng/mL), but that's my practice, not a guideline: large trials haven't shown that aiming higher improves mood, immunity or cancer risk (see Vitamin D: Supplement of the Month). If you start low, reaching any higher level takes more than 400 IU, and how much depends on where you start, so test first rather than guess. Doses are set individually after testing, with your other medicines checked.
The body was not designed to receive vitamin D as an isolated high-dose capsule. Skin synthesis produces vitamin D gradually, alongside warmth, nitric oxide production, and other photochemical events. The supplement is a seasonal corrective for a design problem created by the mismatch between our latitude and our modern lifestyle — not a permanent replacement for a system that was never intended to be supplemented. Chronic very high-dose supplementation (10,000 IU+ daily indefinitely) lacks the evidence base to justify it as a population-level recommendation, and creates cofactor imbalance risks that are rarely discussed alongside the advocacy for high targets.
Retest at 12–16 weeks. Vitamin D responds relatively slowly to supplementation. Testing too early produces misleading results. Testing at 12–16 weeks allows you to assess whether the dose has achieved the target and adjust accordingly. This is not optional — it converts supplementation from guesswork into a clinical intervention with a measurable outcome.
Individual variation is the rule, not the exception. The same dose produces different blood levels in different people based on body weight, gut absorption, baseline level, VDR genetics, and cofactor status. What works for one person at your latitude is not necessarily what will work for you. The data — not the average — should guide the decision.
"We were not designed to consume high-dose isolated nutrients in order to survive. We were designed to live in environments that provided what we needed — and to eat the foods that those environments offered. Supplementation is the corrective for the gap between that design and the life we're actually living. Not a replacement for understanding why the gap exists."
The food-first position — what's actually available
Dietary vitamin D from food alone cannot compensate for the Scottish UVB deficit in winter. That is the honest answer. 100g of wild Atlantic salmon provides approximately 400–700 IU. Mackerel, herring, and sardines are in a similar range. A teaspoon of cod liver oil provides 400–1,000 IU depending on the product. Egg yolks from pasture-raised hens contribute 40–100 IU each. Full-fat dairy contributes modest amounts. A diet that genuinely prioritises these sources daily will provide 1,000–2,000 IU from food — meaningful but insufficient on its own to reach functional optimal levels for someone starting low at a Scottish latitude in October.
This is not an argument against food-first. It is an argument for understanding what food-first can and cannot achieve at this latitude in this season, so that the supplementation discussion is grounded in realistic expectations rather than either dismissal or excessive reliance on capsules.
Eat the fatty fish. Reconsider the cod liver oil your grandparents used. From late March or April to the end of September, most people in the UK can make vitamin D from short daily sun exposure on uncovered skin, without burning (NHS). From October to March, the UK advice is 10 µg (400 IU) a day (SACN 2016). If you want to know where you are, test.
Know your actual vitamin D status — not population guidance
25-OH-D is part of the blood chemistry in the TDG Five-Test Programme, read alongside calcium, magnesium, inflammatory markers, PTH where needed (an add-on), and the full metabolic picture. The number in context — not the number alone — is where the clinical decision lives.
See the TDG Programme →