Scroll through any health feed at the moment and you will not get far before somebody mentions vitamin D. Podcasters call it the "sunshine vitamin". Supplement companies build entire ranges around it. Your GP may have quietly added it to your last blood test. Friends compare their numbers the way people once compared step counts. For something that was, until fairly recently, filed under "bones and rickets", vitamin D has become one of the most talked-about molecules in medicine.
As a cardiology clinic in London, we are asked about it constantly: Does low vitamin D cause heart disease? Should I take it? How much? Is my level of 38 a problem? Can I have too much? Those are good questions, and the honest answers are more interesting, and more nuanced, than either the hype or the backlash suggests.
This guide walks through what vitamin D actually is, why the UK is a genuinely difficult place to make enough of it, what the evidence says about the heart, how to read your own blood test, and what a sensible, evidence-based approach looks like for most adults. It is long, deliberately so, because the short versions are usually where the misunderstandings come from. Use the headings to jump to what matters to you.
Vitamin D is technically a misnomer. A vitamin is something your body cannot make and must obtain from food. Vitamin D does not fit that definition: given enough sunlight on bare skin, a healthy body manufactures it from a cholesterol derivative sitting in the outer layers of the skin. In that sense it behaves far more like a hormone than a nutrient, and it is increasingly described as one.
The process runs in stages. Ultraviolet B (UVB) light, a narrow band of sunlight between roughly 290 and 315 nanometres, strikes 7-dehydrocholesterol in the skin and converts it into pre-vitamin D3, which quickly rearranges into vitamin D3 (cholecalciferol). That molecule is biologically inert. It travels to the liver, where it is converted to 25-hydroxyvitamin D, written 25(OH)D and sometimes called calcidiol. This is the storage form and the one your blood test measures, because it has a half-life of two to three weeks and reflects your overall supply from sun, food and supplements.
The final activation step happens mainly in the kidneys, where 25(OH)D is converted to 1,25-dihydroxyvitamin D, or calcitriol, the active hormone. Calcitriol binds to the vitamin D receptor, a protein found in the nucleus of cells in almost every tissue in the body. When it does, it switches genes on and off. Estimates vary, but somewhere between 200 and 2,000 genes are thought to be directly or indirectly regulated by vitamin D. That breadth is the real reason it has attracted so much attention: a molecule that talks to that many genes in that many tissues is bound to show up in studies of almost every disease.
There are two dietary forms worth knowing about. Vitamin D3 (cholecalciferol) is the form made in skin and found in animal foods and most supplements. Vitamin D2 (ergocalciferol) comes from plants and fungi and is found in some fortified foods and vegan supplements. Both work, but D3 raises and sustains blood levels more efficiently, which is why most guidelines, including those in the UK, prefer it.
Vitamin D's reputation was built on bones. Its discovery in the 1920s followed the realisation that cod liver oil and sunlight both cured rickets, the softening and bowing of children's bones that was rampant in smoky industrial cities. For most of the twentieth century, that was the story: vitamin D helps you absorb calcium, calcium builds bone, end of chapter.
Several things changed that. First, the discovery in the 1980s and 1990s that the vitamin D receptor is present in immune cells, heart muscle, blood vessel walls, the pancreas and the brain forced scientists to ask what it was doing there. Second, large observational studies began reporting that people with low 25(OH)D levels had higher rates of almost everything: cardiovascular disease, type 2 diabetes, several cancers, autoimmune disease, depression, respiratory infections and earlier death. Third, blood testing for 25(OH)D became cheap and widely available, and the results were startling. Depending on the threshold used, somewhere between one in five and one in two British adults were "low" during winter.
Then came the pandemic. Early in 2020, researchers noticed that populations and individuals with low vitamin D seemed to fare worse with COVID-19. The association was real, though later trials found that giving vitamin D did not reliably change outcomes. Regardless, the coverage put vitamin D in front of millions of people who had never thought about it, and many started testing and supplementing.
Layered on top of all this is a broader cultural shift towards "optimisation": wearable devices, at-home blood panels, longevity podcasts and social-media doctors, all of whom love a single measurable number that can be nudged with a cheap daily capsule. Vitamin D fits the brief perfectly. It is measurable, modifiable, inexpensive, and almost everyone in Britain is lower than they would like in February.
So the conversation is loud for understandable reasons. The task for the rest of this article is to separate the parts of it that are well supported from the parts that are wishful thinking.
If you live in the United Kingdom, your relationship with vitamin D is dictated by geography. London sits at about 51.5° north; Edinburgh at almost 56°. At these latitudes, the sun is so low in the sky between roughly October and March that the UVB wavelengths needed to make vitamin D are almost entirely filtered out by the atmosphere before they reach the ground. You can stand outside all day on a bright January afternoon and make effectively none.
A useful rule of thumb is the "shadow rule": if your shadow is longer than you are tall, the sun is too low for meaningful vitamin D production. In London, that is true for the whole day for about five months of the year, and for all but the middle of the day in spring and autumn.
Even in summer, several factors get in the way. Cloud cover reduces UVB substantially. Glass blocks it completely, so sitting by a sunny window does nothing. Sunscreen with an SPF of 30 cuts production by more than 95 per cent when applied properly. Clothing, obviously, blocks it. Many of us work indoors during the hours when UVB is strongest and go outside in the early morning or evening when it is weakest. And skin pigmentation matters a great deal: melanin is a natural sunscreen, so people with darker skin need considerably longer in the sun to make the same amount of vitamin D, and consistently show lower average levels in UK surveys.
The result is a pronounced seasonal roller-coaster. Population studies in the UK show average 25(OH)D peaking in late summer and troughing in late winter and early spring, with the trough commonly dipping into the insufficient range for a large proportion of adults. The interactive chart below illustrates the pattern.
The practical implication is stark and is the reason the UK government, unusually, recommends a supplement for the entire population. Since 2016, following a review by the Scientific Advisory Committee on Nutrition (SACN), Public Health England and now the NHS advise that everyone in the UK should consider taking 10 micrograms (400 IU) of vitamin D daily during autumn and winter, and that certain groups should take it all year round. Those groups include people who are rarely outdoors, those who are frail or housebound, people who cover most of their skin when outside, people with darker skin, and children aged one to four. Babies under one who are breastfed should receive a daily drop supplement of 8.5 to 10 micrograms.
This is the section our patients care most about, so it deserves a careful treatment. Cardiology's interest in vitamin D is not far-fetched. The vitamin D receptor is present in cardiac muscle cells, in the smooth muscle of artery walls and in the endothelial cells that line blood vessels. In laboratory studies, calcitriol suppresses the renin-angiotensin system (a key regulator of blood pressure), reduces inflammation, inhibits the proliferation of vascular smooth muscle that contributes to arterial stiffening, and influences how the body handles calcium in vessel walls. There are, in other words, plausible mechanisms by which low vitamin D could be bad for the cardiovascular system.
Observational studies have been consistent. People with low 25(OH)D levels have higher rates of high blood pressure, coronary artery disease, heart failure, stroke, atrial fibrillation and cardiovascular death. A frequently cited analysis of the Framingham Offspring cohort found that participants with 25(OH)D below 37.5 nmol/L had roughly a 60 per cent higher risk of a first cardiovascular event over five years than those with higher levels. Meta-analyses pooling dozens of studies have found similar dose-response patterns, with risk rising steadily as levels fall below about 50 nmol/L.
The problem, as every epidemiologist will tell you, is confounding. The people with the lowest vitamin D are also disproportionately the people who are older, heavier, less physically active, more likely to smoke, more likely to have chronic kidney disease, and less likely to spend time outdoors. Every one of those factors independently damages the heart. Fat tissue also sequesters vitamin D, so obesity lowers blood levels directly. Is low vitamin D causing heart disease, or is it simply a marker of a lifestyle and body composition that cause heart disease? Observational data cannot answer that.
To answer it, you need randomised controlled trials, and over the past decade we have had several large ones.
The VITAL trial, published in the New England Journal of Medicine in 2019, randomised almost 26,000 American adults over 50 to 2,000 IU of vitamin D3 daily or placebo and followed them for a median of 5.3 years. The primary cardiovascular outcome, a composite of heart attack, stroke and cardiovascular death, was not reduced. Nor was the rate of invasive cancer, the other primary endpoint.
The ViDA trial in New Zealand gave over 5,000 adults a monthly high dose (100,000 IU) or placebo for around three years. No reduction in cardiovascular events was seen.
The D-Health trial in Australia, with more than 21,000 participants taking 60,000 IU monthly, reported in 2023. It found no significant effect on cardiovascular events overall, although a secondary analysis suggested a modest and statistically borderline reduction in major cardiovascular events, particularly among people already taking statins or other cardiovascular medication. The authors themselves were cautious about over-interpreting this.
Trials targeting blood pressure specifically, including several using doses of 2,000 to 4,000 IU daily in people with hypertension and low vitamin D, have generally shown either no effect or a very small reduction in blood pressure of one or two millimetres of mercury, which is clinically negligible. Trials in heart failure have not shown improvements in survival, although one, VINDICATE, found modest improvements in the heart's pumping function on echocardiography.
Why do strong associations dissolve in trials? Several explanations are likely operating together.
The first is the confounding we have already described: low vitamin D is largely a marker rather than a cause. The second is a design issue. Most trial participants were not actually deficient at baseline; the average 25(OH)D in VITAL was about 77 nmol/L, well above the sufficiency threshold. Topping up people who are already replete would not be expected to help, in the same way that giving iron to people who are not anaemic does nothing. There is a reasonable argument that trials have not adequately tested the hypothesis that correcting true deficiency (below 25 or 30 nmol/L) reduces cardiovascular risk, because it is ethically difficult to leave genuinely deficient people on placebo for years.
The third is that vitamin D may be doing something real but small, an effect that is swamped by the larger drivers of heart disease such as blood pressure, cholesterol, smoking, diabetes and inactivity. A small benefit would require truly enormous trials to detect.
Where does that leave a cardiologist? Our view, which reflects that of the major cardiovascular societies, is this:
If you are concerned about your own cardiovascular risk, a low vitamin D level is a reason to have a broader conversation rather than simply to buy a supplement. Our healthy heart screening looks at the factors that trials have actually shown matter: blood pressure, cholesterol and lipid sub-fractions, blood glucose, weight, an ECG and, where appropriate, an echocardiogram.
Because vitamin D has such a broad footprint in the body, it is worth briefly summarising the evidence in other areas, since this is where much of the enthusiasm comes from.
This is the bedrock. Vitamin D is essential for absorbing calcium from the gut, and severe deficiency causes rickets in children and osteomalacia (soft, painful bones) in adults. In older people, particularly those in care settings with low baseline levels, combined vitamin D and calcium supplementation modestly reduces hip and other fractures. Vitamin D also plays a role in muscle function; deficiency is associated with proximal muscle weakness, and correcting it in deficient older adults may reduce falls. Notably, very high intermittent doses (for example, 500,000 IU once a year) have paradoxically increased falls and fractures in trials, one of several reasons that steady daily dosing is preferred.
Vitamin D modulates both the innate and adaptive immune systems. A well-conducted 2017 meta-analysis of individual patient data from 25 trials found that daily or weekly vitamin D supplementation reduced the risk of acute respiratory infections, with the largest benefit in people who were very deficient to begin with. Subsequent larger trials have been less impressive, and the COVID-19 trials, as noted, were largely disappointing. A reasonable summary is that correcting deficiency probably offers a modest reduction in respiratory infections, but supplementing people who are already replete does little.
One of the more intriguing findings from VITAL was a secondary analysis showing a roughly 22 per cent reduction in newly diagnosed autoimmune disease (such as rheumatoid arthritis, psoriasis and polymyalgia rheumatica) over five years in the vitamin D group. This is consistent with a long-standing observation that multiple sclerosis is more common at higher latitudes. It needs confirmation, but it is one of the few areas where a randomised trial has pointed towards a real preventive effect.
Low vitamin D is associated with depression and, in some studies, with cognitive decline. Trials of supplementation for depression have been mixed and mostly negative, with any benefit confined to people who were deficient. Seasonal affective disorder is often attributed to vitamin D, but the evidence points more towards light exposure acting via the eyes and circadian rhythm than towards vitamin D itself.
The D2d trial randomised over 2,400 adults with pre-diabetes to 4,000 IU daily or placebo. It did not significantly reduce progression to type 2 diabetes overall, although a later pooled analysis of three trials suggested a small reduction of around 15 per cent in relative risk, again concentrated in people with lower baseline levels. Vitamin D is not a diabetes treatment, but this is another area where correcting deficiency may help at the margins.
Observational data linking low vitamin D to colorectal and other cancers is strong; trial data is weaker. VITAL found no reduction in cancer incidence but did report a possible reduction in cancer deaths, particularly after the first two years, and meta-analyses of several trials support a modest reduction in cancer mortality of around 10 to 15 per cent. Whether this is real remains debated.
Adequate vitamin D in pregnancy supports fetal bone development, and deficiency in pregnancy is linked to low birth weight and, in infants, to rickets and hypocalcaemic seizures. The NHS advises pregnant and breastfeeding women to take 10 micrograms daily, and all babies who are breastfed or having less than 500 ml of formula a day to receive a supplement from birth.
If you have had your vitamin D checked, you will have been given a number, usually in nanomoles per litre (nmol/L) in the UK. American and some private labs report in nanograms per millilitre (ng/mL); to convert, multiply ng/mL by 2.5 to get nmol/L. A result of 20 ng/mL is therefore about 50 nmol/L.
Interpreting that number is where much of the confusion lies, because different organisations draw the lines in different places. In the UK, the thresholds used by SACN, NICE and most NHS laboratories are:
The US Endocrine Society and some private health providers use higher cut-offs, describing 50 to 75 nmol/L as insufficient and 75 nmol/L or above as optimal. This is the origin of many worried enquiries from patients who have been told they are "low" at 60 nmol/L by one source and "fine" by another. Both statements are defensible; they simply reflect different definitions. Our practical view is that anyone consistently above 50 nmol/L, including in late winter, is doing well, and that 75 to 125 nmol/L is a comfortable range if you are supplementing anyway. There is no evidence that levels above about 125 nmol/L offer any additional benefit, and some observational studies suggest a U-shaped curve with slightly worse outcomes at very high levels.
Use the gauge below to see where your own result sits.
Insufficient: Between 25 and 50 nmol/L many people benefit from a daily 10–25 µg (400–1,000 IU) supplement, especially through the autumn and winter. This tool is for general education and is not a substitute for advice from your own doctor.
A few more points about testing. Timing matters enormously: a result from August and a result from February can differ by 20 to 30 nmol/L in the same person, so a single reading is a snapshot rather than a verdict. A late-winter test is the most informative, because it catches you at your lowest. If you start a supplement, allow at least three months before re-testing, as it takes that long for levels to plateau.
Routine testing of healthy people is not recommended by the NHS, partly on cost grounds and partly because the answer, in winter, is almost always to take the standard supplement whatever the result. Testing is appropriate if you have symptoms of deficiency (bone pain, muscle weakness, unexplained fatigue), a condition that affects absorption, chronic kidney disease, osteoporosis, or if your doctor is considering high-dose treatment.
In the UK, essentially everyone is at risk of insufficiency in winter, but some groups are far more likely to be genuinely deficient year-round:
If you belong to one or more of these groups, the NHS advice is to take a daily supplement throughout the year, not only in winter.
Vitamin D is unusual among nutrients in that very few foods contain meaningful amounts, and the UK does not fortify staple foods on the scale that, say, the United States, Canada or Finland do. The best natural sources are oily fish: salmon, mackerel, sardines, herring and trout. Cod liver oil is exceptionally rich but also delivers a large dose of vitamin A, which limits how much can be safely taken. Egg yolks, red meat and liver contain small amounts. Mushrooms exposed to UV light (some supermarkets now sell these, labelled as such) can contain useful quantities of vitamin D2. Fortified foods in the UK include most breakfast cereals, margarine and fat spreads (fortification of these was mandatory until 2013 and remains widespread), some yoghurts and most plant-based milks.
The chart makes the difficulty clear. A portion of wild salmon or mackerel can deliver most of a day's 400 IU, but few people eat oily fish daily, and farmed salmon, which is what most of us buy, contains less than half the vitamin D of wild fish. The typical UK diet provides around 100 to 150 IU (2.5 to 4 micrograms) a day, well short of the 400 IU reference intake. This is not a failure of willpower; it is simply not possible to eat your way to sufficiency on a normal British diet without oily fish several times a week. That is the arithmetic behind the national supplement recommendation.
That said, eating oily fish twice a week is worth doing regardless, because it also supplies omega-3 fatty acids, which have their own modest cardiovascular evidence base and are a central part of the Mediterranean-style eating pattern that has the strongest support for heart health.
Sun exposure is the most efficient way to make vitamin D, and it carries no risk of overdose because the skin destroys excess pre-vitamin D. But it also causes skin ageing and skin cancer, so the question is how much is enough.
Research from the University of Manchester, which has studied this specifically in UK conditions, suggests that for people with lighter skin, around 10 to 15 minutes of midday sun (between about 11am and 3pm) on the face, forearms and lower legs, several times a week between late March and September, is enough to maintain adequate levels through summer and build a modest store for autumn. People with darker skin may need 25 to 40 minutes or longer for the same effect. This is short of the time it takes to burn for most people, and burning should always be avoided; there is no vitamin D benefit to staying out longer once the skin has done its work.
The key insight is that short, regular, unprotected exposures are more effective and safer than long ones. Sunscreen, when used as most people actually use it (thinly and inconsistently), reduces vitamin D production less than laboratory studies suggest, and studies of people using sunscreen on sunny holidays have found their levels still rose considerably. So sun-safety advice and vitamin D advice are not really in conflict: enjoy brief exposure, then protect yourself.
Sunbeds are not a sensible source of vitamin D. Most emit predominantly UVA, which does not make vitamin D but does cause skin damage, and their use is associated with a significantly increased risk of melanoma.
For most adults in the UK, the answer is straightforward: 10 micrograms (400 IU) of vitamin D3 daily from October to March at a minimum, and all year if you fall into any of the higher-risk groups. This is the dose recommended by the NHS and is available for pennies a day from any supermarket or pharmacy.
Some clinicians, ourselves included, are comfortable with adults taking 25 micrograms (1,000 IU) daily, particularly if they are overweight, have darker skin, or have previously tested in the insufficient range. This dose reliably lifts most people above 50 nmol/L, is very safe, and is well within the UK upper limit. Doses of 50 micrograms (2,000 IU) a day are commonly used and also safe for healthy adults, though they are more than most people need.
The UK safe upper level for long-term daily intake in adults is 100 micrograms (4,000 IU). This is not a target; it is a ceiling, and there is no reason for a healthy adult to approach it without medical supervision.
Some practical notes on taking supplements:
If a blood test shows a level below 25 nmol/L, or below 30 with symptoms, your doctor will usually prescribe a loading regimen, typically a total of around 300,000 IU over six to ten weeks (for example, 50,000 IU once a week for six weeks, or 20,000 IU twice weekly for seven weeks), followed by a daily maintenance dose of 800 to 2,000 IU. This should be done under medical supervision. In people with a history of kidney stones, sarcoidosis, certain lymphomas or hyperparathyroidism, vitamin D must be handled with particular care, and calcium levels should be checked before and during treatment.
Yes, and this is the part of the current enthusiasm that concerns us. Because vitamin D is fat-soluble and stored in the body, it accumulates, and because the marketing has shifted from "avoid deficiency" to "optimise", doses of 5,000, 10,000 or even 50,000 IU daily are being taken by people who have read about them online.
Vitamin D toxicity is rare from sun and food, but it is a real risk from supplements. It causes hypercalcaemia: too much calcium in the blood. Symptoms include nausea, vomiting, constipation, excessive thirst and urination, confusion, muscle weakness and, in severe cases, kidney damage, kidney stones and cardiac arrhythmias. It generally requires sustained daily intake of 10,000 IU or more, or blood levels above 250 nmol/L, but individual susceptibility varies, and case reports of toxicity from "wellness" doses have risen sharply over the past decade. Some UK hospitals have reported a several-fold increase in referrals for vitamin D–related hypercalcaemia.
From a cardiologist's perspective, hypercalcaemia is not trivial. Very high calcium levels shorten the QT interval on the ECG and can trigger arrhythmias. Chronically elevated calcium is also, in observational data, associated with vascular calcification, the exact opposite of what people taking high doses are hoping to achieve. And as noted, several large studies have hinted at a U-shaped relationship, with mortality risk rising again at very high 25(OH)D levels.
The message is simple. Vitamin D behaves like most things in physiology: deficiency is harmful, sufficiency is good, and excess is harmful again. Aim for the middle, and if you are taking more than 4,000 IU a day, do so only with a doctor's guidance and blood monitoring.
Not worried, but it is worth acting on. That sits in the insufficient range on UK criteria. A daily supplement of 400 to 1,000 IU through the autumn and winter will very likely bring you above 50 nmol/L within a few months. Combine it with getting outside at midday when the weather allows.
The trials say no, or at least not meaningfully. Correcting deficiency is worthwhile for other reasons, but if your blood pressure or cholesterol is raised, those need addressing directly. Our pages on hypertension and high cholesterol explain how we assess and treat them.
Low vitamin D is associated with a higher incidence of AF in observational studies, and a small number of studies have suggested that deficiency may increase the risk of AF recurrence after cardioversion or ablation. The evidence is not strong enough to recommend vitamin D as an AF treatment, but it is reasonable to check and correct deficiency in anyone with AF. Be aware that very high doses causing hypercalcaemia can themselves trigger arrhythmias.
Not in a way that matters. Some research has explored whether vitamin D levels influence statin-related muscle aches, with mixed results, and correcting deficiency in people with muscle symptoms is a reasonable step. The D-Health trial's hint that vitamin D might benefit people already on cardiovascular medication is intriguing but unconfirmed.
If you are simply deciding whether to take the standard winter supplement, no; take it regardless. If you have symptoms, risk factors for deficiency, or want to know your late-winter baseline before deciding on a dose, a single test in February or March is informative and inexpensive.
Take it if you are deficient or insufficient, or if you fall into any of the high-risk groups, at a standard dose. Do not expect it to substitute for your antiplatelet therapy, statin, blood pressure medication or cardiac rehabilitation, all of which have strong trial evidence for preventing further events. If you would like your overall risk reviewed, we are happy to see you at the clinic.
Fatigue is a common symptom of genuine deficiency, and correcting it often helps. But fatigue has many causes, including anaemia, thyroid problems, sleep apnoea, depression and heart disease, and it should not be assumed to be vitamin D until those have been considered. If tiredness comes with breathlessness, chest pain or palpitations, please have your heart assessed.
Pulling all of this together, here is what we would suggest for the typical healthy adult living in Britain:
Vitamin D deserves attention, and the UK's recommendation that everyone supplements through the winter is one of the more sensible pieces of public health advice of recent years: the deficiency is real, widespread, cheap to fix and genuinely harmful to bones and muscles. Where the conversation has gone astray is in promising that a capsule will protect against heart disease, cancer, depression and infection. The trials have looked hard for those benefits and, at population level, have not found them. That does not mean vitamin D is useless; it means that, once you are sufficient, the heavy lifting for your heart is done by the things that have always done it: not smoking, moving your body, eating well, keeping your blood pressure and cholesterol under control, and sleeping enough.
So take your winter vitamin D. Get outside when the sun is high enough to cast a short shadow. And if you are worried about your heart, come and talk to someone who can measure the things that actually predict it. You can book a consultation with My Heart Clinic online or by telephone, and our heart screening packages are designed exactly for people who want a clear, evidence-based picture of their risk rather than another supplement.
This article is for general information and does not constitute individual medical advice. If you have symptoms, an existing medical condition, or are taking prescribed medication, please discuss vitamin D supplementation with your GP or specialist before starting or changing your dose.
