How much vitamin D should I take. Doctor John Cambell talks.

Dr John Campbell and Professor Angus Dalgleish begin from a point they say is no longer in doubt: vitamin D is essential for immunity. In their view, the old argument about whether vitamin D matters is over. What remains is a practical question: how much does an individual actually need, and what blood level should we aim for if we want more than just prevention of rickets?

Why the gap?

They argue that most official recommendations were designed decades ago for one narrow goal: preventing rickets in children. That requires only a tiny amount of vitamin D. By contrast, they say, the immune system appears to require dramatically higher levels. Campbell notes that doses around 400 IU (often quoted in public health advice) may be enough to prevent rickets, but he believes they are unlikely to do anything meaningful for immunity.

Instead of starting with a fixed “one-size” dose, both men say vitamin D should be treated like a titrated medicine, similar to insulin in diabetes or drugs used for high blood pressure. The central idea is to work backwards from a target blood level of 25-hydroxyvitamin D, the standard lab marker. Campbell talks about aiming for a blood level between 100 and 150 nanomoles per litre and says he personally treats around 150 as an ideal. He claims that, looking back at COVID-19 data, people whose 25-hydroxyvitamin D levels were above 100 nanomoles per litre “don’t come to harm” from the infection, whereas lower levels are associated with more severe disease. He presents vitamin D level as a kind of practical proxy for immune robustness.

This view sits above the thresholds used by many public health bodies, which often regard 50 nanomoles per litre as sufficient for most people and warn that very high levels may carry risks. Campbell and Dalgleish argue that these cut-offs are too low and are based on bone health alone, not on the broader roles of vitamin D in immunity and disease prevention. They also suggest that official safe upper limits for daily intake are conservative and not strongly evidence-based, though most agencies currently place long-term safety around 4,000 IU per day for the general population.

What is an International Unit anyway?

To explain how he thinks about dose, Campbell goes back to the original definition of an “International Unit” of vitamin D. Historically, one unit was defined as the daily amount needed by a 10-gram mouse. If 10 grams needs one unit, a 60-kilogram human, on a simple body-weight scale, would need around 6,000 units a day. On that logic, he describes 6,000 IU per day as a plausible physiological intake for a 60-kilogram adult, and 3,000 IU per day as a very conservative starting point. Dalgleish adds that, based on his own body weight, he personally takes around 8,000 IU per day and suggests that someone weighing 120 kilograms might need 12,000 IU daily, while stressing that dose should always be judged against actual blood results.

They emphasise that individual requirements vary widely. Genetics, the gut microbiome, body composition and other factors can all influence how much vitamin D a given intake will produce in the bloodstream. Two people taking the same dose could end up with very different blood levels. Their practical recommendation is to start with a reasonable daily dose—Campbell suggests 3,000 IU for most adults—test blood levels after several months, and then increase or decrease the dose depending on whether the level has reached the target range. In their words, “you judge the dose by the response it’s had.”

Obesity is one factor they highlight repeatedly. Vitamin D is fat-soluble, and Campbell says that in people with obesity, newly produced or supplemented vitamin D tends to be soaked up by fat tissue and does not appear in the bloodstream to the same extent. If you expose an obese person and a lean person to the same amount of sunlight or UV light, he says, the obese person may show only about half the blood level of vitamin D. The conclusion is that people with obesity often require significantly higher supplement doses to achieve the same 25-hydroxyvitamin D concentration.

Skin pigmentation and latitude are another focus. Darker skin reduces UVB penetration and slows vitamin D production in the skin. In the UK’s northern climate, the pair say, women of Black African and South Asian origin are at particular risk of deficiency, especially during pregnancy, and their children are more likely to develop rickets. They argue that these groups should be proactively screened and supported but often are not. Even fair-skinned people are not guaranteed to reach high levels through sun exposure alone. Dalgleish describes spending much of one summer in the sun, stopping supplements for five to six months and then having his blood tested at the end of the season. Despite good sun exposure, his level was around 75 nanomoles per litre—better than deficiency, but still below the 100–150 nanomoles per litre range they regard as optimal.

What about immunity?

The discussion then turns to immunity more broadly. Campbell argues that there is no simple, routine blood test that captures overall immune competence, and suggests that vitamin D level functions as a practical surrogate. In his view, higher vitamin D levels are associated with fewer infections, such as influenza and COVID-19, while low levels correlate with more frequent infections and a range of other diseases. Mechanistically, he highlights T-lymphocytes (T-cells), which are central to the adaptive immune response and, he says, heavily dependent on vitamin D for proper activation. He contrasts structurally normal white blood cell counts with functionally weak cells that are “physiologically suboptimal” when vitamin D is lacking.

To illustrate the consequences of immune suppression, Campbell refers to AIDS, where damage to T-cells leads to unusual infections, malignancies, heart disease and dementia. He uses this to underline how critical immune function is to many different disease processes and argues that widespread subclinical immune weakness today—reflected in ambulance delays and crowded hospitals—is partly driven by inadequate vitamin D status. He calls for large-scale vitamin D optimisation as “a public health imperative,” particularly in the wake of successive viral seasons that may deplete individuals’ vitamin D stores.

Pregnancy and neurological disease add another dimension. Campbell notes long-standing epidemiological observations that babies born in spring at higher latitudes have a greater risk of developing multiple sclerosis in adult life than babies born in autumn. One common interpretation is that autumn-born babies had mothers who were in late pregnancy during summer, with better vitamin D status, while spring-born babies had mothers who were in late pregnancy in winter, when skin production of vitamin D is minimal. From this, he concludes that no baby should be born vitamin D deficient and that every woman attending antenatal clinics should have her vitamin D level checked and treated if low.

He links low vitamin D in pregnancy with complications such as pre-eclampsia and argues that sufficient vitamin D supports maternal health, optimises fetal development and ensures the newborn starts life with adequate stores as it meets a world full of viruses and bacteria. Chronic vitamin D deficiency, he adds, appears to be one of several factors in dementia and other neurological conditions, with the strongest association seen in multiple sclerosis.

Where does vitamin D come from?

The conversation also looks at where vitamin D actually comes from. In humans and other land animals, UVB light converts a cholesterol-like molecule in the skin, 7-dehydrocholesterol, into vitamin D3. This hormone is then partially activated in the liver and fully activated within target cells. Campbell points out that this system did not begin with humans: plankton at the surface of the sea produce 7-dehydrocholesterol as a primitive sunscreen. UV light turns this into vitamin D, which for plankton is essentially a waste product. As plankton are eaten by fish and fish by other animals, vitamin D moves up the food chain. Land animals also produce vitamin D in their skin, and humans obtain some vitamin D from meat and especially from oily fish.

Most commercial vitamin D3 supplements, he explains, are derived from sheep. Sheep produce vitamin D in their skin in exactly the same way humans do. When they are shorn in summer, the greasy lanolin from the wool contains vitamin D. This is extracted and purified into supplement form. In that sense, Campbell says, we are not really taking a “vitamin” at all but an animal hormone, much like taking thyroxine from animal sources in the treatment of an underactive thyroid.

Vitamin D confusion

He also addresses a common practical confusion: vitamin D doses on labels can vary widely—1,000 IU, 4,000 IU, 10,000 IU—yet the capsules often look identical. The reason is that the active ingredient is present in microscopic quantities. One unit weighs only around 25 billionths of a gram, so almost all the capsule’s volume is carrier oil such as olive oil. The amount of vitamin D by mass and volume is tiny, even at higher IU doses, which is why visual appearance is not a reliable guide to strength.

In summary

Campbell and Dalgleish’s position is that vitamin D requirements for robust immunity are much higher than those needed merely to avoid rickets and likely higher than many current guideline intakes. They advocate targeting a blood level above 100 nanomoles per litre, starting most adults on at least 3,000 IU per day, adjusting doses based on blood testing and increasing intake for those with obesity, darker skin, limited sun exposure, frequent infections or pregnancy. This is a more aggressive and personalised approach than standard public-health advice, which typically focuses on lower thresholds for sufficiency, smaller daily doses and routine testing only in higher-risk groups.

There is ongoing scientific debate about how high vitamin D levels should be for optimal health, how much benefit extra supplementation brings once frank deficiency is corrected and how risks and benefits balance at higher intakes over the long term. The discussion between Campbell and Dalgleish represents one end of that debate, arguing for higher targets and more intensive use of supplementation.

This article reports their views and the data they cite. It is not personal medical advice. People considering vitamin D supplements—especially at doses above standard recommendations, or those with existing health conditions, pregnancy or kidney disease—should seek guidance from a qualified health professional and use blood testing to monitor their levels over time.

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