Vitamin D overdose: where meeting your needs ends and high-dose therapy begins
The same molecule can be an everyday food supplement or a powerful intervention in your calcium balance. The difference is the dose. And the question of whether anyone is watching.
Vitamin D is not a vitamin in the classical sense. It is a prohormone that reaches deep into the calcium control loop. And anything that reaches deep can also reach deep in the wrong direction. Not because it is malicious. But because it is strong.
At some point you started taking vitamin D. Maybe because of a lab value, maybe because of a podcast, maybe simply because the winter was long. First 1,000 units. Then 5,000, because somewhere online it said that was too little. Then at some point 10,000, because someone said that was what they did too.
And at some point comes the moment when you ask yourself: can this actually become too much?
Yes. It can. Rarely, but it can. And the more interesting question is not whether it can become too much, but why a vitamin of all things becomes dangerous at all. With vitamin C you excrete a large part of the excess through the kidney again. With vitamin D the body lacks exactly that route.
This is exactly where you can see what I try to explain across this whole guide: a nutrient is not a switch with two positions. It is a player in a control loop. And whoever turns one screw in a control loop always moves more than that one screw.
What you will find here
- Why fat-soluble and storable makes the difference
- How hypercalcaemia develops mechanistically
- Which symptoms can point to too much vitamin D
- What EFSA and the BfR name as an upper level
- Why, as far as we know today, the sun cannot overdose you
- The bolus question: why more at once was not better
- Magnesium and K2 as players in the same loop
- Where meeting your needs ends and high-dose therapy begins
Why a vitamin of all things can become dangerous
Picture two bathtubs. One has an open drain. You can pour in as much as you like, it runs off. The other one has a plug in it. Whatever you put in stays.
Vitamin C, the B vitamins, folate: those are the tubs with the open drain. They are water-soluble. A large part of whatever is too much leaves through the kidney.
That does not make it harmless either. Very high doses of vitamin C can raise oxalate formation and thereby favour kidney stones, particularly when kidney function is already reduced. Vitamin B6 in high dosage over a longer time can damage nerves, and that does not always fully reverse. Water-soluble therefore does not mean without consequences. It only means the body has more ways to get rid of an excess. With vitamin D it lacks exactly that route.
Vitamin D, A, E and K are the other kind. They are fat-soluble. They do not dissolve in the water of the blood, they are stored in fatty tissue and in the liver. They have a plug.
How strong that plug can be is shown by a pharmacokinetic review by Glenville Jones. In the body, vitamin D3 has a half-life of about two months. The transport metabolite 25-OH vitamin D, which is the value your laboratory measures, sits at around 15 days. The active hormone 1,25-dihydroxyvitamin D, by contrast, at only about 15 hours.
Glenville Jones of Queen's University in Canada collected what is known about the mechanisms of vitamin D toxicity. His starting point: fat solubility explains the distribution into fatty tissue and the slow turnover.
The division of roles is interesting. Earlier assumptions held that the active hormone 1,25-dihydroxyvitamin D triggers the hypercalcaemia. That idea has been replaced. Two other routes are discussed today: either 25-OH vitamin D at very high concentration can overcome its disadvantage at the receptor and act directly at the cell nucleus. Or the total amount of all vitamin D metabolites displaces the active hormone from its transport protein, so that more free hormone becomes available.
Important for context: a large part of what is known about the mechanisms of vitamin D toxicity comes from animal experiments. In humans there are mainly individual case reports.
What that means for you: it is not the measured value alone that decides, but what it does inside the calcium control loop. As the threshold above which toxicity would be expected, Jones names a 25-OH level above 750 nanomoles per litre, but out of caution he recommends an upper limit of 250 as a safety margin.
Jones G. Am J Clin Nutr. 2008. DOI: 10.1093/ajcn/88.2.582SOn top of that comes the second point that sets vitamin D apart from almost every other food supplement: it is not a vitamin in the original sense of the word. By definition a vitamin is something the body cannot make itself. Vitamin D it does make itself, in the skin, from cholesterol, with sunlight as the tool. Biochemically it is a secosteroid and it behaves like a hormone.
You are not taking a vitamin. You are taking a hormone precursor.
That is not a reason for fear. It is a reason for respect. With a hormone you automatically ask about dose, duration and monitoring. Those three questions are missing surprisingly often with vitamin D.
And now you know why the word overdose plays any role at all with vitamin D, while with vitamin C it hardly bothers anyone.
The mechanism: how too much vitamin D can tip the calcium balance
Almost everything that happens in vitamin D poisoning does not happen through the vitamin. It happens through calcium.
The calcium level in the blood is one of the most tightly regulated values in your body. It is only allowed to move within a narrow window, because heart rhythm, nerve excitability and muscle contraction depend on it. Three adjusting screws hold it there: uptake in the gut, deposition and release in bone, and excretion through the kidney.
Vitamin D acts on two of those three screws.
Sylvia Christakos and her group at Rutgers University summarised what is known about the action of vitamin D in the intestine. The core job of the active hormone 1,25-dihydroxyvitamin D is to increase calcium uptake from the gut.
The route there runs through transport proteins. Among other things, the hormone increases the calcium channel TRPV6 on the intestinal cell, the binding protein calbindin, which ferries calcium through the cell, and the calcium pump on the far side. Together they form a kind of three-part conveyor chain.
What that means for you: whoever takes in a lot of vitamin D turns that conveyor chain up. With a normal starting status that is a good thing. With a very high continuous intake, more calcium can reach the blood than the control loops can absorb.
Christakos S et al. J Steroid Biochem Mol Biol. 2019. DOI: 10.1016/j.jsbmb.2019.105501The second screw is bone. At high concentration, vitamin D can stimulate the breakdown of bone substance, that is, mobilise calcium out of the depot. For the body this is an emergency reaction to secure the blood level. With an oversupply from outside it runs in the wrong direction: the gut is already delivering too much, and the bone adds more on top.
Both together can end in hypercalcaemia. And that is what does the actual damage.
Too much vitamin D does not make you ill because it is vitamin D. It can make you ill because it can put too much calcium into circulation. The damage can happen where that calcium ends up: in the kidney, in the vessel, in the heart rhythm.
Why the kidney is affected so often follows almost by itself. It has to get rid of the excess. In doing so the calcium concentration in the urine rises, and dissolved calcium can form crystals. Kidney stones can develop from that. If calcium is deposited in the kidney tissue itself, this is called nephrocalcinosis, and it can impair filtration.
For calcium the body has a regulation with several feedback arms: parathyroid hormone, calcitonin, active vitamin D, the kidney. That regulation is stable as long as intake stays within a usual range.
A very high continuous intake can override it. That is why, when supplementing, I do not only ask about the benefit, but always also about which other wheels start turning along with it.
And now you know why, with a suspected overdose, it is not the vitamin D value alone that counts, but always the calcium alongside it.
Vitamin D overdose: symptoms that are easily missed
Here is the uncomfortable part of this topic: the symptoms are so unspecific that almost nobody thinks of the supplement on their own.
You are tired. You are constantly thirsty. You feel sick in the morning. You have to get up at night. Your head feels like cotton wool. Who would think first of the vitamin D drops that have been sitting in the cupboard for six months?
A Polish and Canadian group around Ewa Marcinowska-Suchowierska collected the clinical signs of vitamin D toxicity. Their list reads like a cross-section of everyday complaints.
The authors name as the most frequent signs: confusion, apathy, repeated vomiting, abdominal pain, increased urination, intense thirst and dehydration. All of them arise through the severe hypercalcaemia.
As the typical laboratory sign of an overdose from supplements they name a 25-OH vitamin D level above 150 nanograms per millilitre, that is above 375 nanomoles per litre. At the same time they stress that real poisoning is rare and usually arises from the accidental or improper intake of extremely high pharmacological doses.
One point stayed with me while reading. The group describes a vitamin D hypersensitivity: in some people even a dose considered safe for the general population can lead to a hypercalcaemia that is initially without symptoms, because their vitamin D metabolism is regulated differently.
Marcinowska-Suchowierska E et al. Front Endocrinol. 2018. DOI: 10.3389/fendo.2018.00550The same complaints can have many other causes, and some of them are more urgent than a vitamin D overdose. Intense thirst together with frequent urination and tiredness can also be the first sign of a diabetes that has not been recognised yet. That needs to be checked quickly.
A raised calcium level can also come from a parathyroid gland producing too much parathyroid hormone, or from a tumour disease. Both appear elsewhere in this article only as a risk group for an overdose. They can just as well be the cause of the same complaints.
So the rule is: these complaints belong in a medical assessment, not in stopping the supplement and waiting. Stop the preparation if that seems sensible to you, but in addition have blood glucose, calcium and parathyroid hormone measured.
| Sign | How it can arise | Why it gets missed, and what else to think of |
|---|---|---|
| Intense thirst, frequent urination | Calcium can disturb the concentrating ability of the kidney | Often read as stress. Conversely it can also point to a diabetes that has not been recognised yet, or to another cause of hypercalcaemia, so always have it checked |
| Nausea, vomiting, loss of appetite | Calcium can slow down gut motility | Dismissed as an upset stomach |
| Constipation | A more sluggish gut at a high calcium level | A very common everyday symptom without a clear suspicion |
| Muscle weakness, exhaustion | Calcium influences the excitability of nerve and muscle | Fits a hundred other causes, which is why it belongs in an assessment rather than an interpretation |
| Confusion, listlessness | Described in pronounced hypercalcaemia | In older people it is easily put down to age. New confusion always belongs in a prompt medical assessment |
| Kidney stones, weak kidney function | Calcium excretion and deposition in kidney tissue | Often only shows up in the laboratory or on ultrasound |
How extreme the amounts have to be before it really becomes critical is shown by two cases from Tübingen.
A group at Tübingen University Hospital described a 53-year-old woman and a 33-year-old man with a life-threatening hypercalcaemic crisis after self-chosen, very highly dosed vitamin D intake. Cumulatively the amounts were between 2.5 and 10 million International Units over several months.
The 25-OH vitamin D levels were 663 and 1,289 nanomoles per litre, against a reference range of 50 to 175. Neither forced excretion nor bisphosphonates were enough to control the recurring hypercalcaemia. Only procedures such as plasma exchange and special forms of dialysis brought the values down.
The sentence that occupied me most: until calcium and vitamin D levels were nearly normal again, 355 and 109 days respectively had passed. That is the price of fat solubility. Whoever stops the supplement has to wait until the store in the fatty tissue has run down, and that can take months.
For context: these are two individual documented cases. No risk for the general population can be derived from two cases. They only show that this range exists.
Heister DJ et al. J Nephrol. 2023 (online 2022). DOI: 10.1007/s40620-022-01543-2A second case report from Brazil shows the other variant: a 24-year-old man injected himself with a veterinary medicine containing high doses of vitamins A, D and E for aesthetic reasons. He arrived with abdominal pain, nausea, vomiting and exhaustion. His creatinine was 3.1 milligrams per decilitre, his calcium 13.6, his 25-OH value above 150 nanograms per millilitre. Even 30 days after successful treatment the vitamin D level was still clearly raised.
A review by Sebastian Aberger and colleagues describes what counts in such situations: stop the intake, stabilise the fluid balance and treat the calcium level medically. Waiting alone is not enough with a marked hypercalcaemia.
These cases are extremes. They are explicitly not a description of what happens at 2,000 or 4,000 units daily.
I am showing them to you for a different reason: they make visible that the dose-response relationship with vitamin D is real. There is an amount at which the substance tips. Exactly where is individual. That it exists is not up for negotiation.
Persistent nausea, intense thirst and tiredness while taking vitamin D are not a reason to wait and see. If vomiting, confusion or clearly increased urination come on top, please have it checked medically without delay and take your preparation along to the appointment.
With marked confusion, repeated vomiting or a racing or stumbling heartbeat, this belongs in an immediate medical examination. In an emergency, call 112.
And now you know why, with persistent nausea, thirst and tiredness while taking vitamin D, not only a look at the calcium makes sense, but also an appointment with the doctor who knows you and your medication.
Where the authorities draw the line, and what 20,000 IU really means
Now come the numbers. I am giving them to you deliberately as what they are: reference values from authorities for the general population. Not a personal dose recommendation.
In 2023 the European Food Safety Authority revised its assessment of the tolerable upper intake level for vitamin D. The document is unusually worth reading, because it lays open how such a limit comes about in the first place.
The EFSA panel on nutrition and novel foods searched systematically for the most important adverse effects of an excessive vitamin D intake: persistent hypercalcaemia, persistently raised calcium excretion in the urine, as well as falls, fractures and bone density.
Persistently raised calcium excretion in the urine was chosen as the critical endpoint, because it can be an earlier sign than hypercalcaemia in the blood. From two randomised trials in humans a lowest observed adverse effect level of 250 micrograms per day was derived. An uncertainty factor of 2.5 was then applied.
The result: a tolerable upper intake level of 100 micrograms of vitamin D equivalents per day for adults, including pregnant and breastfeeding women, and for adolescents from 11 to 17 years. For children from 1 to 10 years it is 50 micrograms, for infants from 6 to 12 months 35 and for infants up to 6 months 25 micrograms. EFSA notes that European populations as a rule do not exceed this amount, with one exception: regular users of highly dosed food supplements.
EFSA NDA Panel. EFSA J. 2023. DOI: 10.2903/j.efsa.2023.8145Let us convert that, because your packaging shows International Units and not micrograms. One microgram of vitamin D corresponds to 40 International Units.
| Reference figure | Amount | In International Units |
|---|---|---|
| EFSA upper level, adults and adolescents from 11 | 100 µg per day | 4,000 IU per day |
| EFSA upper level, children 1 to 10 years | 50 µg per day | 2,000 IU per day |
| EFSA upper level, infants 6 to 12 months | 35 µg per day | 1,400 IU per day |
| EFSA upper level, infants up to 6 months | 25 µg per day | 1,000 IU per day |
| EFSA: lowest dose with an observed effect | 250 µg per day | 10,000 IU per day |
| BfR proposed maximum for food supplements | 20 µg per day | 800 IU per day |
| DGE estimated value without endogenous synthesis | 20 µg per day | 800 IU per day |
In Germany, infants usually receive a low, medically defined daily dose for rickets prophylaxis. That is something different from any other number in this article.
If you are unsure whether you are using the right preparation or the right number of drops, please ask at the paediatric practice before you change anything. Accidental overdoses in infants almost always arise from a wrongly chosen product strength or a wrongly counted number of drops. Highly dosed adult preparations do not belong in infants' hands.
Two rows of this table regularly cause confusion, so here is the logic behind them in brief. The German Federal Institute for Risk Assessment proposes a maximum of 20 micrograms per day for freely available food supplements. That is not a toxicity value. It is a consumer protection value: it is meant to ensure that someone who also eats fortified foods and combines several products does not slide unintentionally above the tolerable upper level.
Which brings us to the question many people have in mind at this point: what about 20,000 units?
In Germany there are prescription-only preparations with 20,000 International Units per capsule. They are frequently prescribed once a week. That works out at roughly 2,850 units per day, so below the EFSA upper level.
Prescription-only means: you get these capsules after a medical assessment, with an indication and as a rule with a laboratory value beforehand. Anyone obtaining them by other routes leaves out exactly the part that makes the prescription safe.
20,000 units daily over months is something completely different. That is five times the upper level and twice the dose from which a persistently raised calcium excretion has been described in studies. Amounts like that do not belong in self-medication, they belong in a medically supervised setting with laboratory monitoring.
If you are unsure about your packaging: it always says whether it is a daily or a weekly dose. That one glance can clear up a lot.
And now you know why a number on its own is never dangerous. It only becomes dangerous together with the question: per day or per week, for how long, and in whom.
Why, as far as we know today, the sun cannot overdose you, but real food is not enough either
There is an observation that surprises many people: cases of vitamin D poisoning from sunlight have not been described so far, not even in people who spend a great deal of time outdoors for work. That is a strong argument, but it is an argument from the absence of reports, not a proof.
Behind it there is probably a built-in brake.
Ann Webb and Michael Holick investigated in Boston what happens to vitamin D3 that has already formed in the skin and stays exposed to sunlight. They worked both with human skin and with a model system.
The result: vitamin D3 turned out to be extremely light-sensitive. As soon as it forms in the skin, further sunlight rapidly breaks it down into a series of photoproducts, among them 5,6-trans-vitamin D3 and the suprasterols I and II.
What that means for you: the skin appears to limit itself. Important for context: this is a photochemical study on human skin outside the body and on a model system. It carries the mechanism, not the clinical claim that poisoning from the sun is impossible. Together with the absence of corresponding case reports, though, the two fit well: the documented poisonings come from preparations, not from the sun. That does not change the fact that sunburn, skin ageing and skin cancer risk remain serious topics in their own right.
Webb AR, DeCosta BR, Holick MF. J Clin Endocrinol Metab. 1989. DOI: 10.1210/jcem-68-5-882The same safety applies to food. Small oily fish such as herring and sardine, egg yolk, mushrooms that have seen sunlight: they supply vitamin D, but in amounts from which no poisoning follows. Anyone wanting to overdose through food would have to eat quantities nobody eats.
For me what follows from this is first of all an attitude, not a warning. Real food from good sources and good husbandry is always the first choice. Not out of romance, but because a food delivers nutrients in a matrix of cofactors that a capsule does not rebuild. No supplement replaces nutrition, sleep, movement, sun and relationship.
And still: with vitamin D this principle runs into a physical limit at our latitudes.
Berlin lies at around 52 degrees northern latitude. From October to March the sun stands so low here that the short-wave UVB radiation needed for vitamin D formation barely reaches the skin. That is down to the length of the path through the atmosphere. It is not an opinion about how healthy sun is.
This was measured by Ann Webb, Lois Kline and Michael Holick. They exposed human skin to sunlight on cloudless days in Boston at 42 degrees and in Edmonton at 52 degrees northern latitude. In Edmonton, so at Berlin's latitude, no vitamin D precursor was formed from October through March. Important for context: this is a photochemical study on skin outside the body, not a clinical endpoint. For the order of magnitude of the winter gap it is informative all the same.
On top of that come living conditions that did not exist in this form fifty years ago: indoor work, screen time, consistent sun protection, a high share of highly processed foods with a lot of energy and little micronutrient density, environmental exposures and chronic stress, which can raise the consumption of protective substances.
Medication plays a part too. For some antiepileptics and for glucocorticoids it is described that they can speed up the breakdown of vitamin D. For proton pump inhibitors a reduced uptake of vitamin B12 and magnesium is discussed, and for metformin an effect on vitamin B12 status as well. All of these substance groups are prescription-only. How relevant this is in an individual case varies, and it can be measured.
One thing matters to me here: this is not an argument against these medicines, and certainly not a reason to stop or reduce them on your own. It is an argument for measuring the corresponding values from time to time during longer use and discussing this with the doctor who prescribed them.
There is also a discussion about whether intensive agriculture and depleted soils may have reduced the micronutrient density of plant foods over the decades. The data on this is mixed. I list it as an open question, not as an established fact.
Not because supplementation is fashionable, but because the conditions have changed, targeted topping up can be more often justified today. That is an argument for precision, not for arbitrariness.
And now you know why the sentence “just get outside more” in a Berlin January is well meant, but of physically limited help.
The bolus question: why more at once was not better
Now comes the part that convinced me most on the professional level. Not because it is dramatic, but because it is so unexpected.
At first the idea sounds sensible: people forget tablets. So why not give one large dose at once and then have peace? That is exactly what was investigated. Several times. And the results pointed in a direction nobody had counted on.
Kerrie Sanders and her group in Australia gave 2,256 women aged 70 and over, who were considered to be at high risk of fracture, a single dose of 500,000 International Units of vitamin D3 or placebo every autumn or winter. Over three to five years.
The vitamin D group had 171 fractures against 135 in the placebo group. The fall rate was 83.4 against 72.7 per 100 person-years, the ratio was 1.15 with a confidence interval of 1.02 to 1.30. For fractures the ratio was 1.26 with a confidence interval of 1.00 to 1.59, so only just statistically notable. A striking pattern in time, which the authors however only examined afterwards: in the first three months after the dose the risk of falling was most clearly raised.
What that means for you: a very high single dose is not the same as the same amount spread out. The body appears to react differently to peaks than to a steady flow.
Sanders KM et al. JAMA. 2010. DOI: 10.1001/jama.2010.594That was 2010. You could have taken it for an outlier. Six years later a second trial from Zurich arrived at the same picture, with clearly lower doses.
Heike Bischoff-Ferrari and her team studied 200 people aged 70 and over who had already fallen. Three groups, each monthly: 24,000 International Units, 60,000 units, or 24,000 units plus calcifediol.
The higher doses reached a 25-OH level above 30 nanograms per millilitre more reliably. For lower extremity function that brought no advantage. With falls it even tipped: 66.9 percent in the 60,000 group and 66.1 percent in the combination group fell within one year, against 47.9 percent in the 24,000 group.
Important for context: this is a small trial, and falls were a secondary endpoint. But it does not stand alone, it fits a pattern.
Bischoff-Ferrari HA et al. JAMA Intern Med. 2016. DOI: 10.1001/jamainternmed.2015.7148The largest bolus trial came from New Zealand. In the ViDA trial 5,108 adults between 50 and 84 years received a starting dose of 200,000 units and then 100,000 units monthly, on average over 3.4 years. The result: no protection against falls, the ratio was 0.99. For non-vertebral fractures it was 1.19, not statistically secured. Notable in the same trial, analysed by Malihi and colleagues: kidney stones and hypercalcaemia did not occur more often under this bolus regimen than under placebo. That only means that in this trial those two safety events did not occur more often. It does not mean that bolus dosing is without risk. For falls and fractures the same family of trials pointed in the other direction.
And then there is one more piece of work that made me think, because it used daily doses, exactly the way most people take vitamin D.
Lauren Burt and her group in Calgary divided 311 healthy adults between 55 and 70 years without osteoporosis into three groups: 400, 4,000 or 10,000 International Units of vitamin D3 daily over three years. Important for transferability: the participants were explicitly well supplied with vitamin D at the start of the trial.
An advantage for the higher doses had been expected. The opposite was measured. Bone density at the radius fell on average by 1.2 percent in the 400 group, by 2.4 percent in the 4,000 group and by 3.5 percent in the 10,000 group. For bone strength there were no significant differences.
How should that be read? Cautiously. The authors themselves write that the findings do not support a benefit of high doses for bone health and that further research is needed to clarify whether they do harm. For me that is not an alarm signal, but a very good argument against the assumption that more is automatically better.
Burt LA et al. JAMA. 2019. DOI: 10.1001/jama.2019.11889If you want to see the whole picture, you will find it in a large synthesis. Mark Bolland and colleagues evaluated 81 randomised trials with 53,537 participants. For fractures overall they found a relative risk of 1.00, for hip fractures 1.11, for falls 0.97. Between high and low doses there was no difference. Their conclusion was clear: for muscle and bone they see little justification for broad vitamin D supplementation.
With vitamin D, more is not more. Beyond a certain point, more is simply more.
This data does not say that vitamin D is useless. It says something more cautious: whoever is already well supplied appears to gain little from more. In the large American VITAL trial with 25,871 adults there were no lower rates of cancer or cardiovascular events under 2,000 units daily than under placebo.
A benefit could lie above all where a genuine deficiency is topped up, and less where an already good value is stacked higher. That is my reading of the data, not a statement of the meta-analysis itself. It found no difference between high and low doses.
That is one view among several, and other experts weigh the data differently. My reasoned position is: measure first, then decide.
And now you know why, on the subject of vitamin D, I would rather talk about regularity than about height.
Magnesium and K2: the players in the same control loop
If you search online for vitamin D, you will inevitably stumble over two companions: magnesium and vitamin K2. Both are often presented with great certainty as compulsory. I would like to show you what is well founded about that and where the data becomes thinner than it sounds.
Let us start with magnesium, because there the biochemistry is clearest.
Anne Marie Uwitonze and Mohammed Razzaque gathered how magnesium and vitamin D are connected. Their core point is mechanistic and rather elegant.
Vitamin D from skin or capsule is inactive at first. It is converted in the liver into 25-OH vitamin D and in the kidney into the active hormone. This review describes that the enzymes of vitamin D metabolism use magnesium as a cofactor. That is a description from biochemistry, not a health claim about magnesium supplements.
What that means for you: a low magnesium status could explain why some people barely move their laboratory value while taking vitamin D. What is established is the mechanism, not the clinical benefit of a routine combination. A large randomised trial on this is missing.
Uwitonze AM, Razzaque MS. J Am Osteopath Assoc. 2018. DOI: 10.7556/jaoa.2018.037With vitamin K2 the chain of argument is longer, and that is exactly why it is worth taking apart honestly.
Vitamin K contributes to normal blood clotting and to the maintenance of normal bones. Those are the two claims authorised for vitamin K in Europe.
Beyond that, research discusses that vitamin K can bring certain proteins into an active form by allowing them to bind calcium. Two of them are interesting here: osteocalcin in bone and matrix Gla protein in the vessel wall. In laboratory work, matrix Gla protein is ascribed a role in the calcium metabolism of the vessel wall, and without enough vitamin K it stays in an inactive form. Whether a benefit for the vessels follows from that in humans has not been established, and a health claim about it would not be permissible under European law either.
Rogier Caluwé and colleagues in Belgium studied 200 people on chronic dialysis, a group with pronounced vascular calcification. They received 360, 720 or 1,080 micrograms of menaquinone-7 three times a week over eight weeks.
The inactive form of matrix Gla protein fell in a dose-dependent way, by 17, 33 and 46 percent in the three groups. The baseline values were not related to vitamin K1 intake, but they were to menaquinone intake.
Important for context: what was measured is a biomarker, not the calcification itself and not heart attacks. The step from “the marker improves” to “vessels stay healthier” is exactly the step that has not been established yet.
Caluwé R et al. Nephrol Dial Transplant. 2014. DOI: 10.1093/ndt/gft464The widespread story goes: vitamin D brings calcium into the body, vitamin K2 makes sure it lands in bone and not in the vessel wall. That is mechanistically plausible and a nice image.
So far it is a hypothesis. For the combination of vitamin D3 and K2, large trials with hard clinical endpoints in humans are missing. If someone presents this combination to you as established, it is worth asking what that rests on.
If you take vitamin K antagonists, that is phenprocoumon or warfarin, every additional vitamin K intake acts directly on the effect of your anticoagulation. That is not a theoretical interaction, that is precisely the mechanism these medicines are built on.
In this situation vitamin K should only ever be added after speaking with your doctor and with close monitoring of the clotting value. For the newer direct oral anticoagulants this does not apply in the same way, but a conversation makes sense there too.
And now you know why I do not sell magnesium and K2 as a compulsory programme, but as what they are: reasoned players with data of differing quality.
Where meeting your needs ends and high-dose therapy begins
Now we are at the core. And I would like to start this section with a distinction that gets lost across the whole field of supplementation.
There are two completely different things that are both called “taking vitamin D”.
Meeting your needs
The doses you buy online or in the drugstore. They fill a gap, nothing more. No therapeutic effect is to be expected from them, and that is entirely fine.
Order of magnitude: what the authorities name for the general population. DGE estimated value 800 units daily, EFSA upper level 4,000.
Therapeutic high dosing
Clearly higher doses, used in a targeted way, limited in time, under medical supervision and with laboratory monitoring. Whether a nutrient at this order of magnitude actually has a therapeutic benefit differs from substance to substance, and for vitamin D it has not been established in humans so far.
What is certain is the reverse: from this order of magnitude on, a nutrient reaches so deep into control loops that monitoring is no longer a formality but a precondition. I am describing this second world here so that you know the difference, not because I am recommending it to you.
Order of magnitude: a multiple of the upper level. Without monitoring of calcium, parathyroid hormone and kidney values this is risky.
This distinction is made in orthomolecular medicine, and it holds far beyond vitamin D. Niacin in gram doses was used as a lipid medicine for a long time, until large trials failed to confirm the hoped-for benefit and side effects became visible. That belongs to the story too: a substance can act like a medicine at high dose and still be abandoned as a therapy. For the liver, gram doses of niacin are explicitly not harmless. High-dose thiamine in Wernicke encephalopathy is an emergency treatment. High-dose zinc in Wilson's disease is a long-term therapy under medical control. In all these cases the same pattern applies: the same substance, two different applications, separated only by the dose and the setting.
With vitamin D this principle can be shown with a concrete example. I describe it here explicitly as an illustration, not as a recommendation.
The Brazilian neurologist Cicero Coimbra described a therapeutic approach in which people with autoimmune disease, above all with multiple sclerosis, receive very high vitamin D doses. A paper by Dirk Lemke and colleagues describes daily doses in the range of tens of thousands up to more than 100,000 International Units, up to 1,000 units per kilogram of body weight. Parathyroid hormone in serum serves as the steering variable for finding the dose.
Ulrich Amon and co-authors published safety data from 319 people treated this way over a period of up to 3.5 years. The mean daily dose was around 35,000 International Units and scattered very widely, with a standard deviation of about 21,800 units. It was accompanied by a strictly low-calcium diet and a daily fluid intake of at least 2.5 litres. From more than 6,100 individual laboratory values, the mean values for serum calcium, creatinine and estimated kidney function were within the normal range. For calcium excretion in 24-hour urine the mean of 6.9 millimoles per 24 hours was close to the upper reference limit and scattered widely. A share of those treated is likely to have had a raised excretion.
How should that be placed? These are observational data from specialised centres with close supervision. They are not randomised trials with clinical endpoints, and there was no control group. It also matters that the evaluation comes from authors who themselves run a centre certified for this protocol. The statement is: under these very specific conditions the safety parameters largely stayed within range. It is not: the approach is effective.
Amon U et al. Nutrients. 2022. DOI: 10.3390/nu14081575 · Lemke D et al. Front Immunol. 2021. DOI: 10.3389/fimmu.2021.655739This is an experimental therapeutic approach. It is not an established standard, it is not recommended in any guideline for the treatment of multiple sclerosis, and it does not replace disease-modifying therapy.
Without medical supervision it is dangerous, because hypercalcaemia with kidney damage can develop. The published safety data come explicitly from centres with structured supervision, a low-calcium diet, a defined fluid intake and regular laboratory monitoring.
One more thing that often gets lost: in these dosages vitamin D is prescription-only in Germany, and its use in multiple sclerosis is an off-label use. That means the preparation is not authorised for this application. In practice this has consequences: as a rule neither statutory nor private health insurance covers the costs, manufacturer liability falls away, and responsibility lies entirely with the treating doctor, with a correspondingly high duty to inform and document.
Anyone considering something like this should not decide it via a blog article, and nobody should do it alone. An existing disease-modifying therapy must under no circumstances be stopped or reduced on one's own initiative for this.
I am not recommending this approach here. I am showing it to you because it makes the dose principle as clearly visible as almost no other example: the same substance is a food supplement at 800 units and an intervention that resets a whole control loop at 50,000 units.
Classical neurology treats multiple sclerosis with immune therapies that have been tested in large randomised trials. That is important, well established and in many cases what influences the course most strongly. An integrative view adds questions about vitamin D status, gut, sleep, the stress axis and nutrition. It does not replace the established treatment.
And now you know why the question “is vitamin D dangerous” without a dose is as unanswerable as the question of whether water is dangerous.
The four lenses: why vitamin D plays along everywhere at once
In clinical psychoneuroimmunology we look at a topic through four lenses. With vitamin D that is not a detour, it is simply receptor biology: the vitamin D receptor is found in a great many tissues, not only in gut and bone.
Nervous system
Calcium steers the excitability of nerve and muscle. If the level rises too high, excitability can fall. That could explain why the specialist literature describes confusion, apathy and muscle weakness in pronounced hypercalcaemia, rather than over-excitation.
Metabolism
Vitamin D is fat-soluble and is stored in fatty tissue. With a higher body fat percentage more of it can distribute there, which can push the measurable blood levels down. The activation itself needs magnesium as a cofactor in liver and kidney.
Hormone system
Vitamin D is part of a hormone axis with parathyroid hormone and calcitonin. When calcium rises, parathyroid hormone is suppressed. That is why a low parathyroid hormone together with high calcium is an important warning signal, and why parathyroid hormone serves as a steering variable in high-dose protocols.
Immune system
Immune cells carry the vitamin D receptor and can activate vitamin D themselves. This is exactly where a risk lies: in granulomatous diseases such as sarcoidosis, immune tissue can produce active vitamin D in an uncontrolled way and thereby trigger hypercalcaemia, even without a high intake.
These four lenses explain why vitamin D turns up in such different contexts: in bone, in infections, in mood, in autoimmunity. Not because it would be a cure-all. But because a hormone whose receptor sits almost everywhere can also make itself felt almost everywhere.
This is not about a laboratory value. It is about whether you get up in February and feel alive. Whether your immune system carries you through the winter. Whether your bone in twenty years still does what you want from it.
And it is about something that matters to me even more: that you know what you are doing. Taking a supplement without knowing the control loop it reaches into is not self-efficacy. It is hope in a capsule. Knowledge is the difference.
Three levers you can put into practice today
No protocols, no brands, no weekly plans. Three things that are in your hands.
Lever 1: add up what you are actually taking
- Put everything on the table that contains vitamin D. The single product, the multivitamin, the omega-3 capsule with an added extra, the fortified drink.
- Note the amount for each in International Units and whether it applies per day or per week. This is exactly where most unintended doubling-up happens.
- Compare the total with the EFSA upper level of 4,000 units daily for adults. That amount is an upper limit, not a target. For freely available supplements the German BfR even proposes only 800 units. If your total is above it, that is a good reason to raise it at your next visit to your general practice.
Lever 2: measure instead of guessing, and measure the right thing
- The sensible baseline value is 25-OH vitamin D. A single value without calcium beside it says little about safety at higher doses.
- At higher doses, serum calcium belongs alongside it, sensibly complemented by parathyroid hormone and creatinine. EFSA classed calcium excretion in the urine as the earliest warning signal, so a 24-hour urine test can make sense with a longer high intake.
- Agree the choice of parameters with the doctor who knows your history and your medication. These values are only meaningful together.
Lever 3: set yourself an end point before you start
- Put into one sentence what you want to achieve and how you would notice it. A laboratory value is one goal, a feeling is one too. Both are legitimate, but they should be named.
- At the start, set a date for a check. As a rule, supplements are a time-limited intervention with a goal and a review appointment, not a lifelong subscription.
- There are well-founded exceptions: vitamin D in winter at our latitudes is one, as is B12 after stomach surgery or a targeted substitution in chronic malabsorption. Exceptions are exactly that, and they are justified, not self-evident.
People should be particularly attentive if they have granulomatous diseases such as sarcoidosis or tuberculosis, certain lymphomas, primary hyperparathyroidism, a history of kidney stones, reduced kidney function or known variants in the breakdown pathway CYP24A1. Severe liver disease can play a role too, because the first conversion step to 25-OH vitamin D takes place in the liver. In all of these situations even a usual dose can do more than expected.
Interactions to keep in mind: vitamin K antagonists and vitamin K. Simultaneous calcium intake matters especially. Calcium preparations, calcium and vitamin D combinations and fortified foods can raise the calcium level further. In the Women’s Health Initiative with 36,282 women, the combination of calcium and vitamin D was linked with a raised risk of kidney stones. Thiazide diuretics can raise the calcium level as well. With digitalis preparations particular caution applies: hypercalcaemia under digitalis can trigger life-threatening cardiac arrhythmia. Some antiepileptics and glucocorticoids can influence vitamin D metabolism. None of these prescription-only medicines may be stopped or reduced on your own account because of this, that belongs in a conversation with the prescribing practice.
In pregnancy and breastfeeding the same upper levels apply as for other adults, but the decision belongs in a conversation with the doctor providing care. In children the upper levels are lower.
This text does not replace a medical examination or individual advice. It is meant to help you ask better questions, not to replace answers.
And now you know why the most honest answer to the question “how much vitamin D is too much” starts with a question in return: how much are you taking right now, for how long, and who is looking at it with you?
Frequent questions about vitamin D overdose
At what dose do we speak of a vitamin D overdose?
Real vitamin D poisoning is rare and as a rule only develops from a very high intake over a longer period.
Specialist reviews describe a 25-OH vitamin D level above 150 nanograms per millilitre, that is above 375 nanomoles per litre, together with hypercalcaemia as the typical hallmark. In 2023 EFSA set the tolerable upper intake level for adults at 100 micrograms per day, which corresponds to 4,000 International Units.
It was derived from studies in which a persistently raised calcium excretion in the urine appeared from about 250 micrograms daily, so around 10,000 International Units. Between the upper level and acute poisoning there is a wide span. But it is not an empty safety buffer: it is precisely within that span, from about 250 micrograms daily, that the persistently raised calcium excretion was observed from which the limit was derived in the first place. The upper level is therefore not a number to exceed with an easy mind, it is an upper limit with a reason behind it.
These figures are reference values for authorities, not a personal dose recommendation.
What symptoms can too much vitamin D cause?
Almost all of the complaints described arise through the raised calcium level, not through the vitamin itself.
The specialist literature names nausea, repeated vomiting, loss of appetite, abdominal pain, intense thirst, frequent urination, dehydration, muscle weakness, constipation, confusion and apathy. In severe cases kidney stones, calcium deposits in kidney tissue, cardiac arrhythmia and a decline in kidney function can occur.
The tricky part: thirst, tiredness and nausea are completely unspecific. If you do not connect them with the supplement, you may look for the cause somewhere else for a long time. The reverse holds just as much: these complaints can have many other causes. Intense thirst with frequent urination and tiredness can also be the first sign of a diabetes that has not been recognised yet, and a raised calcium level can also come from the parathyroid gland or from a tumour disease. So they belong in a medical assessment, not in stopping the supplement and waiting.
Important: if such complaints persist while you are taking vitamin D, please have them checked medically without delay and take your preparation along to the appointment. With repeated vomiting, confusion or a racing or stumbling heartbeat, this belongs in an immediate medical examination.
Are 20,000 IU of vitamin D a day dangerous?
20,000 International Units are well above the EFSA upper level of 4,000 units daily and above the amount from which a persistently raised calcium excretion was observed in studies.
The distinction matters: 20,000 units once a week as a medically prescribed preparation work out at roughly 2,850 units per day and are frequently prescribed in Germany. 20,000 units every single day over months are something entirely different and do not belong in self-medication.
In the documented poisoning cases the cumulative amounts were in the range of millions of units over months. Anyone considering such a high intake needs medical supervision with calcium, parathyroid hormone and kidney values in the laboratory.
Can you get too much vitamin D from the sun?
According to what we know today, no. The skin has a built-in brake.
A group around Michael Holick showed as early as 1989 that sunlight itself breaks down the vitamin D3 formed in the skin as soon as it accumulates. Inactive photoproducts arise, such as 5,6-trans-vitamin D3 and the suprasterols I and II. That is an elegant piece of self-protection: production limits itself.
Sunburn, skin ageing and skin cancer risk are untouched by this and remain serious topics in their own right. But vitamin D poisoning from the sun has not been described so far. Overdoses come almost exclusively from capsules, drops or injections.
How quickly does a vitamin D overdose resolve?
Much more slowly than most people expect.
Vitamin D is fat-soluble and is stored in fatty tissue. The half-life of vitamin D3 in the body is about two months, that of the transport metabolite 25-OH vitamin D around 15 days.
In two documented poisoning cases from Tübingen it took the people affected 355 and 109 days respectively until calcium and vitamin D levels were close to the normal range again. In a Brazilian case report the level was still clearly raised 30 days after treatment.
In severe hypercalcaemia, stopping the supplement alone is not enough, it is treated medically.
Do you really need magnesium and vitamin K2 alongside vitamin D?
There is a good biochemical rationale for both, and for both there is no large randomised trial showing a benefit of the combination in humans.
Magnesium appears to be needed as a cofactor for the enzymes that convert vitamin D in the liver and the kidney, and without enough magnesium the activation can run more sluggishly. Vitamin K contributes to normal blood clotting and to the maintenance of normal bones. Beyond that it is discussed that it can bring matrix Gla protein and osteocalcin into an active form. In laboratory work, matrix Gla protein is ascribed a role in the calcium metabolism of the vessel wall. Whether a benefit for vessels or bone follows from that has not been proven in humans.
The idea that K2 steers calcium into bone and away from the vessel wall is mechanistically plausible and is discussed as a hypothesis. In humans it has not yet been proven for clinical endpoints.
Important exception: anyone taking vitamin K antagonists such as phenprocoumon or warfarin may only add vitamin K after speaking with their doctor.
What is the Coimbra protocol and is it safe?
The Coimbra protocol is an experimental therapeutic approach in autoimmune disease, above all in multiple sclerosis.
Vitamin D doses in the range of tens of thousands up to more than 100,000 International Units daily are used, in the publication by Lemke and colleagues up to 1,000 units per kilogram of body weight. It is accompanied by strict calcium restriction, a high fluid intake and close monitoring of parathyroid hormone, calcium in serum and in 24-hour urine as well as kidney values.
An evaluation of 319 treated people reported mean values within the normal range over up to 3.5 years. Important for context: these are observational data from specialised centres, not randomised trials with clinical endpoints, and there was no control group. The evaluation also comes from authors who themselves run a centre certified for this protocol. In these dosages vitamin D is prescription-only, and its use in multiple sclerosis is an off-label use with the corresponding consequences for cost coverage and liability. An existing disease-modifying therapy must not be stopped or reduced on one’s own initiative for this.
The approach is not guideline-supported, it is not an established standard, and without medical supervision it is dangerous, because hypercalcaemia can develop. I describe it here as an illustration of the dose principle, not as a recommendation.
Who has a raised risk of a vitamin D overdose?
People with granulomatous diseases such as sarcoidosis or tuberculosis should be particularly attentive, because there immune cells can produce active vitamin D themselves.
The same goes for people with certain lymphomas, with primary hyperparathyroidism, with reduced kidney function and with variants in the gene CYP24A1, the breakdown pathway for vitamin D. Specialist reviews additionally describe a so-called vitamin D hypersensitivity, in which hypercalcaemia can appear even at usual doses.
Anyone taking several combination products at the same time can also add up without noticing. If you belong to one of these groups, you should not supplement vitamin D without medical supervision.
Which blood values indicate a vitamin D overdose?
The decisive combination is 25-OH vitamin D together with calcium and parathyroid hormone.
A high 25-OH value on its own is not yet poisoning. It becomes critical when serum calcium rises at the same time and parathyroid hormone is suppressed.
In 2023 EFSA classed the persistently raised calcium excretion in the urine as the earliest warning signal, ahead of hypercalcaemia in the blood. That is why a 24-hour urine test for calcium belongs alongside higher doses. Creatinine and the estimated kidney function as well as phosphate are useful additions.
A baseline value before starting and a check after some weeks to months makes sense.
Is one high single dose better than small daily doses?
The study data tend to speak against it.
In a randomised trial in 2,256 women aged 70 and over, a single annual dose of 500,000 International Units led to more falls and more fractures than placebo, especially in the first three months after it was given. In a trial in 200 older people with a previous fall, more participants fell on 60,000 units monthly than on 24,000 units.
A large New Zealand trial with 5,108 people found no protection against falls or fractures on 100,000 units monthly. The most plausible explanation is the short-term peak levels after a very large single dose.
For everyday life that means: steady rather than in bursts, and agree the dose with your doctor.
How this topic connects with the others
Vitamin D never stands alone. It hangs on calcium, on magnesium, on vitamin K and on the question of why you are supplementing at all. These paths lead further.
Supplements
The guide this article belongs to
You are hereTaking vitamin D properly
Magnesium, K2 and the question of fat alongside
Vitamin D deficiency in winter
Why the sun here is barely enough from October to March
Vitamin K2 and D3
Where the calcium travels in the body
Orthomolecular medicine
Why the dose changes everything
When supplementing makes sense
Control loops, and why more is not better
Which magnesium
The mineral that plays along in the same metabolic pathway
Hormone Guide
Vitamin D as a prohormone in the bigger picture
Sources
- EFSA Panel on Nutrition, Novel Foods and Food Allergens (NDA). Scientific opinion on the tolerable upper intake level for vitamin D, including the derivation of a conversion factor for calcidiol monohydrate. EFSA J. 2023;21(8):e08145. DOI: 10.2903/j.efsa.2023.8145 [Authority Document]
- Marcinowska-Suchowierska E, Kupisz-Urbańska M, Łukaszkiewicz J, Płudowski P, Jones G. Vitamin D Toxicity, A Clinical Perspective. Front Endocrinol (Lausanne). 2018;9:550. DOI: 10.3389/fendo.2018.00550 [Review]
- Jones G. Pharmacokinetics of vitamin D toxicity. Am J Clin Nutr. 2008;88(2):582S-586S. DOI: 10.1093/ajcn/88.2.582S [Review]
- Aberger S, Schreiber N, Pilz S, Eller K, Rosenkranz AR, Kirsch AH. Targeting Calcitriol Metabolism in Acute Vitamin D Toxicity, A Comprehensive Review and Clinical Insight. Int J Mol Sci. 2024;25(18):10003. DOI: 10.3390/ijms251810003 [Review]
- Heister DJ, Bohnert BN, Heyne N, Birkenfeld AL, Artunc F. Two cases of severe vitamin D intoxication treated with therapeutic plasma exchange and high cut-off hemodialysis. J Nephrol. 2023;36(5):1461-1467. DOI: 10.1007/s40620-022-01543-2 [Case, n=2]
- Ronsoni MF, Santos HCD, Colombo BS et al. Hypercalcemia and acute renal insufficiency following use of a veterinary supplement. J Bras Nefrol. 2017;39(4):467-469. DOI: 10.5935/0101-2800.20170082 [Case]
- Christakos S, Li S, De La Cruz J, Shroyer NF, Criss ZK, Verzi MP, Fleet JC. Vitamin D and the intestine, Review and update. J Steroid Biochem Mol Biol. 2019;196:105501. DOI: 10.1016/j.jsbmb.2019.105501 [Mechanism Review]
- Webb AR, DeCosta BR, Holick MF. Sunlight regulates the cutaneous production of vitamin D3 by causing its photodegradation. J Clin Endocrinol Metab. 1989;68(5):882-887. DOI: 10.1210/jcem-68-5-882 [In vitro, human skin]
- Sanders KM, Stuart AL, Williamson EJ et al. Annual high-dose oral vitamin D and falls and fractures in older women, a randomized controlled trial. JAMA. 2010;303(18):1815-1822. DOI: 10.1001/jama.2010.594 [RCT, n=2,256]
- Bischoff-Ferrari HA, Dawson-Hughes B, Orav EJ et al. Monthly High-Dose Vitamin D Treatment for the Prevention of Functional Decline, A Randomized Clinical Trial. JAMA Intern Med. 2016;176(2):175-183. DOI: 10.1001/jamainternmed.2015.7148 [RCT, n=200]
- Khaw KT, Stewart AW, Waayer D et al. Effect of monthly high-dose vitamin D supplementation on falls and non-vertebral fractures, secondary and post-hoc outcomes from the randomised, double-blind, placebo-controlled ViDA trial. Lancet Diabetes Endocrinol. 2017;5(6):438-447. DOI: 10.1016/S2213-8587(17)30103-1 [RCT, n=5,108]
- Malihi Z, Lawes CMM, Wu Z et al. Monthly high-dose vitamin D supplementation does not increase kidney stone risk or serum calcium, results from a randomized controlled trial. Am J Clin Nutr. 2019;109(6):1578-1587. DOI: 10.1093/ajcn/nqy378 [RCT, n=5,110]
- Burt LA, Billington EO, Rose MS, Raymond DA, Hanley DA, Boyd SK. Effect of High-Dose Vitamin D Supplementation on Volumetric Bone Density and Bone Strength, A Randomized Clinical Trial. JAMA. 2019;322(8):736-745. DOI: 10.1001/jama.2019.11889 [RCT, n=311]
- Bolland MJ, Grey A, Avenell A. Effects of vitamin D supplementation on musculoskeletal health, a systematic review, meta-analysis, and trial sequential analysis. Lancet Diabetes Endocrinol. 2018;6(11):847-858. DOI: 10.1016/S2213-8587(18)30265-1 [Meta-analysis, k=81, n=53,537]
- Manson JE, Cook NR, Lee IM et al. Vitamin D Supplements and Prevention of Cancer and Cardiovascular Disease. N Engl J Med. 2019;380(1):33-44. DOI: 10.1056/NEJMoa1809944 [RCT, n=25,871]
- Jackson RD, LaCroix AZ, Gass M et al. Calcium plus vitamin D supplementation and the risk of fractures. N Engl J Med. 2006;354(7):669-683. DOI: 10.1056/NEJMoa055218 [RCT, n=36,282]
- Uwitonze AM, Razzaque MS. Role of Magnesium in Vitamin D Activation and Function. J Am Osteopath Assoc. 2018;118(3):181-189. DOI: 10.7556/jaoa.2018.037 [Review]
- Caluwé R, Vandecasteele S, Van Vlem B, Vermeer C, De Vriese AS. Vitamin K2 supplementation in haemodialysis patients, a randomized dose-finding study. Nephrol Dial Transplant. 2014;29(7):1385-1390. DOI: 10.1093/ndt/gft464 [RCT, n=200]
- Amon U, Yaguboglu R, Ennis M, Holick MF, Amon J. Safety Data in Patients with Autoimmune Diseases during Treatment with High Doses of Vitamin D3 According to the Coimbra Protocol. Nutrients. 2022;14(8):1575. DOI: 10.3390/nu14081575 [Cohort, n=319]
- Lemke D, Klement RJ, Schweiger F, Schweiger B, Spitz J. Vitamin D Resistance as a Possible Cause of Autoimmune Diseases, A Hypothesis Confirmed by a Therapeutic High-Dose Vitamin D Protocol. Front Immunol. 2021;12:655739. DOI: 10.3389/fimmu.2021.655739 [Review]
- Webb AR, Kline L, Holick MF. Influence of season and latitude on the cutaneous synthesis of vitamin D3, exposure to winter sunlight in Boston and Edmonton will not promote vitamin D3 synthesis in human skin. J Clin Endocrinol Metab. 1988;67(2):373-378. DOI: 10.1210/jcem-67-2-373 [In vitro, human skin]
- Bundesinstitut für Risikobewertung. Höchstmengenvorschläge für Vitamin D in Lebensmitteln inklusive Nahrungsergänzungsmitteln. BfR opinion, Berlin. bfr.bund.de [Authority Document]