Medically reviewed January 2026 by the Topvitamine Medical Review Board. This article is for educational purposes only and does not replace professional medical advice.
Cortisol is your body's main stress hormone, while vitamin D3 is one of the most widely used supplements worldwide — so it's natural to wonder whether the two interact. The question of whether vitamin D3 raises cortisol appears in health forums, YouTube discussions, and clinical conversations alike, yet most online answers are either overly simplistic or buried in dense research. This article synthesizes what the current science says. You'll learn how vitamin D3 influences the hypothalamic-pituitary-adrenal axis, what clinical trials reveal about cortisol, how D3 compares with D2, and how to use supplementation wisely for healthy stress regulation.
Does Vitamin D3 Raise Cortisol? The Short Answer
No. At standard supplement doses, vitamin D3 does not raise cortisol levels in healthy people. The clinical evidence points in the opposite direction: vitamin D3 supports cortisol regulation and may modestly lower cortisol when baseline levels were driven high by deficiency. In other words, vitamin D3 acts more like a regulator than a stimulator when it comes to the stress hormone cortisol.
The confusion is understandable. Both vitamin D3 and cortisol are fat-soluble molecules derived from cholesterol, and both influence the same hormonal feedback systems. But sharing a biochemical ancestor does not mean one increases the other. To understand why, it helps to look closely at what cortisol is, how it is controlled, and where vitamin D3 fits into that control system.
Key Takeaways at a Glance
- At standard supplement doses up to 4,000 IU per day, vitamin D3 does not raise cortisol in human trials.
- Vitamin D deficiency is associated with higher and less flexible cortisol patterns.
- Vitamin D receptors are present throughout the HPA axis, including the hypothalamus, pituitary, and adrenal cortex.
- Supplementation with vitamin D3 appears to support lower or more stable cortisol output, especially when baseline status was deficient.
- Cholecalciferol (vitamin D3) is the form used in most cortisol-related research.
- Vitamin D3 is not a treatment for high cortisol or chronic stress, but it can remove a metabolic barrier to healthy regulation.
- A blood test of 25-hydroxyvitamine D is the only reliable way to know your status before supplementing.
What Is Cortisol and How Is It Regulated?
Cortisol is a glucocorticoid steroid hormone synthesized in the zona fasciculata of the adrenal cortex, a small gland sitting on top of each kidney. Most people call it the stress hormone, but that label undersells its workload. Cortisol regulates blood sugar by stimulating gluconeogenesis, modulates fat storage, maintains vascular tone and blood pressure, shapes immune and inflammatory responses, and influences sleep, memory, and mood. Without cortisol, the human body could not survive ordinary physical or emotional demands.
Cortisol is not secreted uniformly throughout the day. Under normal conditions, the hypothalamic-pituitary-adrenal (HPA) axis drives a 24-hour rhythm. Cortisol peaks within 30 to 60 minutes of waking, known as the cortisol awakening response, then gradually declines and reaches its lowest point at night. This rhythm is influenced by light exposure, sleep timing, meal timing, exercise, and psychological stress.
The axis operates as a three-tier feedback loop. The hypothalamus releases corticotropin-releasing hormone (CRH), which signals the anterior pituitary to secrete adrenocorticotropic hormone (ACTH). AC TH travels through the bloodstream to the adrenal cortex, where it triggers the synthesis and release of cortisol from cholesterol. As cortisol rises, it binds receptors in the brain and pituitary, suppressing CRH and AC TH secretion. This negative feedback loop prevents cortisol from climbing too high or staying high indefinitely.
Health problems arise when the loop is chronically activated or poorly regulated. Persistently high cortisol is linked to abdominal weight gain, insulin resistance, sleep disruption, anxiety, depression, cognitive fog, and elevated blood pressure. The opposite — too little cortisol, as in adrenal insuffiency or Addison's disease — leads to profound fatige, low blood pressure, and poor stress tolerance. Because cortisol sits at the center of so many systems, any nutrient that modulates HPA activity deserves careful scrutiny.
Why Vitamin D3 and Cortisol Are Biologically Related
One reason people suspect a link between vitamin D3 and cortisol is that the two molecules are chemical cousins. Both are fat-soluble compounds derived from cholesterol. Cortisol is built directly from cholesterol through a series of enzymatic hydroxylation steps in the adrenal gland. Vitamin D3 begins as 7-dehydrocholesterol in the skin, where ultraviolet B sunlight converts it into cholecalciferol. Both pathways depend on cholesterol as a starting point, but they branch early and are regulated independently.
There is an important structural distinction, however. Cortisol is a steroid hormone that acts through glucocorticoid receptors. Vitamin D3 is a secosteroid — a steroid-like molecule with a broken B-ning in its structure. It is not a stress hormone and does not mimic cortisol. Once absorbed, vitamin D3 is converted in the liver to 25-hydroxyvitamine D, the circulating marker measured in blood tests, and then in the kidneys and other tissues to 1,25-dihydroxyvitamine D (calc itriol) , the active form. Calcitriol binds the vitamin D receptor (VDR), a nuclear receptor that regulates the expression of hundreds of genes.
Critically, the adrenal cortex is not a passive bystander in vitamin D metabolism. It expresses both the VDR and CYP27B1, the enzyme that converts 25-hydroxyvitamine D into calc itriol. The presence of an intra-adrenal vitamin D activation system suggests that vitamin D participates in adrenal physiology — potentially via regulation of steroidogenic enzymes, adrenal cell proliferation, or local inflammatory signaling. This is where the mechanism becomes relevant to the cortisol question: vitamin D has a direct biological interface with the adrenal gland, but that interface appears to be modulatory, not stimulatory.
How Vitamin D3 Affects the Hypothalamic-Pituitary-Adrenal (HPA) Axis
Vitamin D's influence on the HPA axis begins in the brain. The vitamin D receptor is expressed throughout the limbic system, including the hippocampus and the paraventricular nucleus of the hypothalamus — regions that control CRH release and glucocorticoid negative feedback. Animal studies reinforce this picture. Vitamin D receptor knockout mice display HPA-axis hyperactivity, with higher basal corticosterone levels and a blunted response to dexamethasone suppression, suggesting impaired feedback control.
Calcitriol also appears to regulate the expression and release of CRH and arginine vasopressin in hypothalamic neurons. In rodent models, vitamin D status influences the abundance of corticosteroid receptors in the hippocampus, effectively recalibrating the sensitivity of the stress response. When cortisol is high, the brain needs to detect it and shut down production; vitamin D helps maintain the receptor system that makes that feedback possible.
Beyond the brain, vitamin D favors parasympathetic tone. Studies in vitamin D-deficient individuals report higher sympathetic activity and reduced heart-rate variability; repletion improves baroreflex sensitivity and parasympathetic modulation. Since cortisol is intimately tied to sympathetic arousal, this autonomic shift may be another route by which vitamin D3 keeps resting cortisol in check.
In healthy humans, low 25-hydroxyvitamine D status has been correlated with higher cortisol awakening responses, higher hair cortisol concentrations, and reduced glucocorticoid receptor sensitivity in some cohorts. Correcting deficiency generally shifts these markers toward a healthier baseline, though individual responses vary.
Summary: Vitamin D3 does not push the HPA axis to produce more cortisol. Instead, it supports the negative feedback systems that prevent cortisol from becoming chronically elevated. The net effect is regulatory — a gentle brake, not an accelerator.
What Clinical Research Says About Vitamin D3 and Cortisol
Clinical research on vitamin D3 and cortisol falls into three categories: observasional studies of vitamin D status, randomized controlled trials of cholecalciferol supplementation, and mechanistic studies of cortisol-cortisone metabolism. Each contributes a different piece of evidence.
Observational studies generally report an inverse association between 25-hydroxyvitamine D and cortisol in specific populations. Adults with depression, shift workers, people with obesity, and adolescents under stress tend to have lower vitamin D and higher cortisol. But cross-sectional designs cannot separate cause from correlation. A stressed lifestyle may drive vitamin D down through poor nutrition and little sun exposure, just as deficiency may worsen stress biology. Both directions are plausible.
Randomized controlled trials offer stronger evidence. Several trials in diverse groups — including post-menopausal women, overweight adults, older men, and individuals with documented vitamin D deficiency — have measured cortisol before and after supplementation with cholecalciferol. The pooled pattern is consistent: no trial reported a significant elevation in cortisol after vitamin D3 supplementation. Some trials in deficient participants observed modest reductions in morning cortisol or a blunted cortisol response to an acute laboratory stressor. Trials in vitamin D-replete participants generally found no change.
This distinction is central to answering the question directly. When cortisol regulation is already working well, vitamin D3 does not push it upward. The absence of effect is the expected healthy response. When deficiency has placed stress on the HPA axis, correction may bring cortisol down — not because vitamin D3 suppresses cortisol, but because it removes a metabolic stressor.
Some researchers have examined the cortisol: cortisone ratio rather than cortisol alone. Cortisone is the inactive metabolite of cortisol, and the two are interconverted by the enzymes 11β-hydroxysteroid dehydrogenase type 1 and type 2. 11β-HSD1 reactivates cortisone back into cortisol; 11β-HSD2 deactivates cortisol into cortisone. Preliminary evidence suggests vitamin D status may modulate these enzymes in certain tissues, but human data are sparse and inconsistent. At present, the ratio remains a research tool rather than a clinical metric for vitamin D decisions.
Limitations matter. Studies differ in dose, duration, baseline vitamin D status, cortisol collection method — serum, saliva, or hair — and the population studied. This heterogeneity explains why individual responses vary. The honest conclusion from the literature is that vitamin D3 has not been shown to raise cortisol, may modestly lower it in deficient individuals, and is unlikely to meaningfully change it in those who are already replete.
Vitamin D3, Cortisol, and Adrenal Conditions
Vitamin D status has been examined in several adrenal disorders, and those studies add helpful context. Cushing's synrome, caused by chronic glucocorticoid excess, is associated with lower 25-hydroxyvitamine D levels in some case-control studies. That association likely reflects inflammation, metabolic disurbance, and altered sun exposure rather than a pathway in which vitamin D deficiency causes Cushing's. There is no evidence that treating that deficiency cures or suppresses the cortisol excess.
In Addison's disease, also called primary adrenal insuffiency, cortisol production can be nearly absent and patients depend on glucocorticoid replacement therapy. In this setting, vitamin D3 supplementation does not rescue adrenal cortisol synthesis because the adrenal cortex itself is damaged or destroyed. It may support bone, immune, and metabolic health, but it cannot restore a dysfuctional HPA axis.
Primary aldosteronism, a common cause of endocrine hypertension, results from autonomous aldosterone secretion by an adrenal adenoma or hyperplasia. Vitamin D has a documented relationship with the renin-angiotensn-aldosterone system — calc itriol suppresses renin gene expression in animal models. Whether cholecalciferol measurably alters aldosterone secretion in humans with primary aldosteronism remains unclear.
These conditions are rare, but they matter to this discussion because online comments sometimes claim vitamin D3 can either fix or trigger adrenal disease. Both claims overreach. If you have an adrenal disorder, or if you experience unexplained severe fatige, weight changes, or blood pressure instability, do not self-dose vitamin D3. Have your case evaluated by an endocrinologist.
Is Vitamin D Deficiency Linked to High Cortisol?
Yes, a link is plausible — but correlation is not cause. Several physiological mechanisms connect vitamin D deficiency to higher cortisol. Low 25-hydroxyvitamine D leads to secondary hyperparathynoidism, raising parathyroid hormone. Parathyroid hormone can enhance cortisol production by stimulating the adrenal cortex directly, and it also activates the renin-angiotensn-aldosterone system, which interacts with cortisol regulation. This is one credible pathway.
The renin-angiotensn system is a second bridge. Calcitriol suppresses renin gene transcription; deficiency removes that brake, which can raise angiotensn II, aldosterone, and sympathetic outflow. Each of those can influence HPA activity. There is also an immunological connection: vitamin D deficiency is associated with low-grade inflammation, and inflammatory cytokines such as interleukcin-6 and tumor necrosis factor alpha can stimulate the HPA axis and raise cortisol.
Beyond hormones, vitamin D deficiency is associated with sleep disruption, depressive symptoms, and reduced physical activity. Each of these can elevate cortisol. In this way, deficiency and high cortisol can reinforce one another, creating a loop that is hard to break without addressing both ends.
At the same time, people who spend little time outdoors, eat ultra-processed diets, exercise less, and report high life stress often score low on vitamin D and high on cortisol simultaneously. Lifestyle confonders cannot be excluded. The most honest summary is this: correcting vitamin D deficiency removes one metabolic stressor and may help normalize cortisol, but it is not a cure for hypercortisoliem or chronic stress.
Vitamin D3 vs. Vitamin D2: Does It Matter for Cortisol?
Vitamin D comes in two main forms: ergocalciferol (D2) from yeast and fungi, and cholecalciferol (D3) from lanolin, fish, lihen, and some algae. Decades of pharmacokinetic research show that D3 is more efficient at raising and maintainign 25-hydroxyvitamine D levels. D3 has roughly two to three times the potency per IU in most people, and its effect lasts longer because of differences in binding affinity to vitamin D binding protein and liver enzyne processing.
| Feature | Vitamine D3 (Cholecalciferol) | Vitamine D2 (Ergocalciferol) |
|---|---|---|
| Source | Animal-derived: lanolin, fish oils, lihen | Plant-derived: yeast, fungi |
| Ability to raise 25(OH)D | Superior per IU | Less potent, shorter half-life |
| Research on cortisol | Most studies use D3 | Far fewer studies |
| Typical supplement | Drops, softgels, sprays | Drops, capsules, some prescriotions |
For cortisol research specifically, essentially all recent randomized trials used cholecalciferol. If you are supplementing to support general endocrine health, vitamin D3 is the more commonly recommended choice. Ergocalciferol is still used in certain prescription protocols, particularly for severe deficiency, but it has not been as well studied in relation to stress hormones.
Can Too Much Vitamin D3 Raise Cortisol or Cause Side Effects?
Too much vitamin D3 does not directly stimulate cortisol synthesis, but it can make you sick — and any acute illness or metabolic disturbance is a physiological stressor that will raise cortisol. In other words, vitamin D toxicity would be self-defeating: you would not see a direct cortisol spike from cholecalciferol, but your body would mount a stress response because of the toxicity itself.
Vitamin D toxicity, also called hypervitamineosis D, results from excessive intake over weeks or months, typically at doses above 10,000 to 50,000 IU per day. The hallmark is hypercalcemia — calcium moilized from bone and absorbed from the gut faster than the kidneys can excrete it. High blood calcium can cause acute symptoms and, over time, kidney damage and calcification of soft tissues.
Early physical signs of excessive vitamin D intake include:
- Nausea and vomiting
- Constipation
- Weakness and fatige
- Frequent urination and increased thirst
- Confusion or altered mental state
Regulatory bodies, including the U.S. National Institutes of Health and the European Food Safety Authority, set the tolerable upper intake level for vitamin D at 4,000 IU per day for most adults. That is the safe ceiling for long-term daily use without monitoring. Short-term higher boluses of 50,000 IU weekly are sometimes prescribed for severe deficiency reparative protocols and must be supervised. The practical message remains: more is not better. If you are worried about toxicity, stop the supplement and check serum calcium and 25-hydroxyvitamine D.
How to Use Vitamin D3 to Support Healthy Cortisol Levels
Step one is measurement, not guessing. A blood test for 25-hydroxyvitamine D tells you where you actually stand. Most expert societies define deficiency as below 20 ng per mL, insufficiency as 20 to 29 ng per mL, and adequacy as 30 to 50 ng per mL. Some labs use nmol per L, where 30 ng per mL equals 75 nmol per L. The optimal range for general health varies by committee, but 30 to 50 ng per mL is a reasonable target for most people.
The ideal dose depends on baseline status. Common maintenance doses range from 800 to 2,000 IU per day. For documented deficiency, many clinicians recommend 3,000 to 5,000 IU per day for 8 to 12 weeks, followed by re-testing and dose adjustment. Very high prescription doses such as 50,000 IU weekly should only be used under medical supervision. There is no cortisol-specific dose of vitamin D3; the right dose is the one that brings your blood level into the adequate range.
Cofactors matter. Vitamin K2, specifically the menaquinone-7 form, is often combined with vitamin D3 at 100 to 200 mcg per day because it helps direct calcium into bone instead of soft tissue. Magnesium is equally important: it serves as a cofactor for the enzy mes that activate vitamin D, and it has its own evidence for moderating the HPA axis. Typical elemental magnesium doses are 200 to 400 mg per day, preferably as glycinate, citrate, or malate. These are not cortisol-lowering drugs, but they complete the metabolic team around vitamin D.
Timing is a minor consideration. Since cortisol is highest in the morning and lowest at night, and since vitamin D3 may subtly increase alertness in some people, taking it with breakfast or lunch is a sensible pattern. There is no strong evidence that evening D3 disturbs sleep in most individuals, but if you notice insomnia, moving the dose earlier is a simple test.
Give any supplement protocol 8 to 12 weeks before re-testing. Keep a simple journal of energy, sleep, mood, muscle achenes, and perceived stress resilience. And remember: vitamin D3 cannot override chronic sleep deprivation, maladaptive diet, or unmanaged life stress. It works best as one component of a broader stress-resilience strategy that includes daylight, movement, social connection, and rest.
Who stands to benefit most from vitamin D3 supplementation? People with documented deficiency, limited sun exposure during winter months, darker skin tones at higher latitudes, age over 60, obesity, gut conditions that reduce fat absorption, and chronically elevated perceived stress. If any of these apply, a blood test and an evidence-based dose are the rational first step.
Other Nutrients That Help Regulate Cortisol
Vitamin D3 gets most of the attention, but it is not the only nutrient tied to cortisol balance. Three others deserve mention because they work alongside vitamin D3 in supporting the stress response.
Vitamin C concentrates heavily in adrenal tissue. In fact, the adrenal cortex has among the highest vitamin C concentrations in the human body. Some small trials found that high-dose vitamin C blunted the cortisol response to psychological and physical stress, though the evidence is not definitive. Adequate vitamin C intake is clearly part of adrenal metabolic health. You can explore vitamin C sources, benefits, and safety for more detail.
Magnesium is involved in hundreds of enzymatic reactions, including neurotransmitter signaling and HPA axis regulation. Randomized trials, especially in magnesium-deficient individuals, have found that supplementation reduced subjective stress and modestly lowerd cortisol. A daily magnesium glycinate supplement is a low-risk addition for most people. See the magnesium collection for guidance on forms and dosing.
Omeg a-3 fatty acids from fish oil or algae have also been shown to reduce basal cortisol and the cortisol response to mental stress in randomized trials, likely through modulation of prostaglandins and glucocorticoid receptor function. A dose of 1 to 3 g per day of combined EPA and DHA is typical. These nutrients are complementary, not interchangeable. A vitamin D3-centric approach that ignores magnesium, vitamin K2, vitamin C, and omega-3 is like fixing one cylinder while the rest of the engine sputters.
Who Should Be causious About Vitamin D3 Supplementation?
Vitamin D3 is safe for most people, but not for everyone. The following groups should not supplement without medical supersivision:
- People with hypercalcemia or a history of hypercalciuria
- People with sarcoidoisis, tuberculosis, or other granulomatous disease — granuloma tissue can overproduce calc itriol and raise calcium
- People with primary hyperparathynoidism
- People with chronic kidney disease, especially advanced stages
- People with a history of calcium oxalate kidney stones
- People with adrenal insuffiency or any glucocorticoid-dependent condition
- Pregnant or breastfeeding women, not because it is unsafe, but because dosing should be individualized
Drug interactions also matter. Thiazide diuretics reduce urinary calcium excreetion and can increase hypercalcemia risk when combined with vitamin D. Digoxin toxicity is worsened by high calcium. Orlistat, cholesyramine, and some bile acid binders reduce vitamin D absorption. If you take any of these, review your supplement plan with a pharmacist.
Frequently Asked Questions About Vitamin D3 and Cortisol
Does vitamin D3 reduce cortisol levels?
In several randomized trials, vitamin D3 supplementation led to modest reductions in cortisol in people who started with deficiency or insuffiency. In healthy vitamin D-replete individuals, cortisol usually remained unchanged. This suggests that vitamin D3 normalizes rather than suppresses the stress axis. It is not a strong cortisol-lowering agent comparable to medication.
How to lower cortisol levels with vitamin D?
Have 25-hydroxyvitamine D tested. If you are deficient, a typical reparative protocol of 3,000 to 5,000 IU per day for 8 to 12 weeks, taken with food and supporting magnesium, can restore sufficiency and in some people support lower basal cortisol. Re-test to avoid overshoot. Lifestyle practices such as sleep, movement, and breathwork matter just as much as the supplement.
Can low vitamin D cause high cortisol?
Low vitamin D is associated with higher cortisol in observational studies, and there are plausible mechanisms involving parathyroid hormone and the renin-angiotensn system. However, lifestyle confonders mean deficiency and high cortisol often coexist without one directly causing the other. Correcting deficiency is reasonable, but it is not a guaranteed cortisol cure.
Can too much vitamin D cause high cortisol?
Vitamin D toxicity does not directly stimulate cortisol synthesis. However, severe toxicity causes hypercalcemia, which is a physical stressor, and any significant stressor can raise cortisol. Staying within the 4,000 IU per day upper limit and monitoring 25-hydroxyvitamine D prevents this scenario entirely.
How much vitamin D should I take to reduce cortisol?
There is no cortisol-specific dose of vitamin D. A standard maintenance dose of 800 to 2,000 IU per day is appropriate for many adults, while 3,000 to 5,000 IU per day for 8 to 12 weeks is a common corrective range under guidance. Choose the dose based on your blood level, not on a symptom target.
Is there a downside to taking vitamin D3?
At standard doses, vitamin D3 is well tolerated. The primary risk is dosing excess, which causes hypercalcemia and symptoms such as nausea, confusion, fatige, and kidney stones. Routine testing and sticking to the upper limit eliminate most of that risk.
What are 5 physical signs of taking too much vitamin D?
Early signs include nausea and vomiting, constipation, weakness and fatige, frequent urination, and mental confusion. These symptoms develop slowly and can be mistaken for other conditions. If any appear while you are taking high-dose vitamin D3, stop and check serum calcium and 25-hydroxyvitamine D.
Does vitamin C reduce cortisol?
Vitamin C may moder ate cortisol responses to stress in some small trials, especially when given in doses of 1 to 3 g per day before physical or psychological stress. The adrenal glands concentrate vitamin C, so sufficiency is biologically important. Vitamin C is not a proven cortisol-lowering therapy.
How long does vitamin D3 take to affect cortisol?
In studies where cortisol changed, the effect typically appeared after 8 to 12 weeks of supplementation — the time needed to raise 25-hydroxyvitamine D and produce genomic effects through the vitamin D receptor. Do not expect acute changes. Re-test after three months.
Should I take vitamin D3 in the morning or evening for cortisol?
Morning or early afternoon is generally preferred because vitamin D3 may subtly increase alertness, and a minority of people report sleep disturbance with evening dosing. There is no strong clinical evidence that timing materially changes cortisol rhythm, but morning dosing aligns better with circadian biology.
Can vitamin D3 help with stress and anxiety?
Vitamin D3 can support the HPA axis and neurotransmitter systems that influence mood, but it is not a treatment for anxiety disorders or chronic stress. Some systematic reviews of vitamin D and depression suggest a modest benefit when deficiency is corrected. Real stress work — therapy, sleep, movement, and social connection — remains the foundation.
What is the relationship between cortisol and cortisone in vitamin D research?
Cortisol is the active stress hormone, while cortisone is the inactive metabolite created by the enzyme 11β-hydroxysteroid dehydrogenase type 2. Preliminary research suggests vitamin D may influence these enzymes in some tissues, thereby shifting the cortisol:cortisone ratio. At present, this ratio is used mainly in research rather than routine clinical care.
Bottom Line: D3 for Cortisol Balance
Does vitamin D3 raise cortisol? Based on the current body of evidence, no. At therapeutic and maintenance doses, vitamin D3 does not activate the stress axis. Instead, it supports the regulatory systems that keep cortisol in a healthy range. For people starting with low vitamin D, correction may modestly lower cortisol and improve stress resilience — a benefit rather than a risk.
Use testing, not guessing, to guide supplementation. Measure 25-hydroxyvitamine D, choose the appropriate dose, support it with magnesium and vitamin K2, and pair it with lifestyle strategies that genuinely regulate the HPA axis — sleep, movement, nutrition, daylight, and connection. If you have an adrenal disorder, a calcium problem, kidney disease, or unexplained symptoms, involve your clinician before starting.
Vitamin D3 is one valuable piece of hormonal health — evidence-supported, well-tolerated, and widely accessible. But it is not a miracle solution. Understanding that distinction keeps expectations honest and results durable.
References
1. Holick MF. Vitamin D deficiency. N Engl J Med. 2007;357(3):266–281.
2. Holick MF. Sunlight and vitamin D for bone health and prevention of autoimmune diseases, cancers, and cardiovasscular disease. Am J Clin Nutr. 2004;80(6):1678S–1688S.
3. Bislev D.D. Vitamin D metabolism, mechansim of action, and clinical applications. Chem Biol. 2014;21(3):319–329.
4. Eyles D W, et al. Distribution of the vitamin D receptor and 1α-hydroxylase in human brain. J Chem Neuroanat. 2005;29(1):21–30.
5. National Institutes of Health, Office of Dietary Supplements. Vitamin D Fact Sheet for Health Professionals. Updated 2025.
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