Why are so many people diagnosed with multiple sclerosis deficient in vitamin D?

And what is this deficiency trying to tell us?

Vitamin D deficiency is remarkably common in MS. Studies from different parts of the world have reported deficiency in the majority of people studied, with rates reaching 73 percent in one population and even higher in others.

That is a clue we shouldn’t ignore.

The usual explanation is simple: people with MS may get less sunlight because of heat sensitivity, fatigue, reduced mobility, or spending more time indoors.

Those factors certainly matter.

But they may not explain the whole story.

Research has also found links between vitamin D status and inflammation, medications, genetics, the vitamin D receptor, and the enzymes the body needs to activate and use vitamin D.

Then there is an even more intriguing possibility.

 

Zoom Deeper Discussion

Could infection itself be affecting vitamin D levels or interfering with the way our cells respond to vitamin D?

That question matters because vitamin D is not simply a nutrient for strong bones.

It is deeply involved in immune defense.

Our immune cells use vitamin D to help recognize and respond to invading organisms. Vitamin D influences antimicrobial peptides, immune signaling, inflammation, and the activity of genes involved in defending us against viruses, bacteria, fungi, and parasites.

So perhaps the important question is not simply:

“Why do people with MS have low vitamin D?”

Perhaps we should also be asking:

“What happens to our immune system’s ability to control infections when vitamin D is low, and could those infections then make the vitamin D problem even worse?”

That possibility changes the conversation.

Instead of viewing vitamin D deficiency as an isolated nutritional problem that can always be solved by taking more vitamin D, it may be more useful to see it as part of a larger biological puzzle.

And when we start putting those pieces together, the connection between vitamin D, immune function, infection, and MS becomes much harder to ignore.

 

Vitamin D Deficiency Is Extremely Common in MS

Low vitamin D is seen again and again in people diagnosed with multiple sclerosis.

Studies from different parts of the world have reported very high rates of deficiency. One Saudi study found vitamin D deficiency in 73 percent of people with MS. Other studies and reviews have reported rates approaching 88 percent or even higher in certain populations.

Research consistently shows that people with low vitamin D are more likely to develop MS, and some studies also link lower vitamin D levels with more active disease after diagnosis.

That does not mean vitamin D supplementation has been proven to prevent or treat MS.

Those are different questions.

The risk and deficiency literature shows a strong relationship between low vitamin D and MS. The treatment literature is much less settled, and supplementation trials have produced mixed results.

So why are vitamin D levels often low?

There are several possible explanations.

People with MS may spend less time outdoors because heat can temporarily make neurological symptoms worse. Fatigue, weakness, mobility problems, or wheelchair use can also reduce sunlight exposure.

Some medications may affect vitamin D metabolism.

Inflammation itself may influence vitamin D levels.

Genetic differences can affect the vitamin D receptor and the enzymes needed to activate or break down vitamin D.

Research has also raised the possibility that chronic infections may interfere with vitamin D regulation and signaling.

The evidence suggests vitamin D deficiency in MS may develop through several overlapping factors rather than one simple cause.

 

The MS Seasonal Pattern Is Hard to Ignore

There is also an interesting seasonal pattern.

In one study of 415 people with MS, vitamin D levels were lowest in January and February. The modeled prevalence of relapses peaked about two months later, in March and April.

This does not prove that falling vitamin D caused those relapses.

But the researchers found an inverse association between seasonal vitamin D levels and MS disease activity.

A much larger international analysis involving more than 32,000 MS relapses also found an early-spring relapse peak.

This raises an important question:

Could the winter drop in sunlight and vitamin D be one factor that leaves the immune system more vulnerable in the months that follow?

Vitamin D deficiency may not simply come before MS.

In some people, it may also become worse because of MS.

That means vitamin D deficiency could be both a contributing factor and a consequence of the disease process.

 

Vitamin D Is Not Just About Bones

Most people first learn about vitamin D because of calcium and bone health.

Vitamin D helps the intestines absorb calcium and phosphorus. These minerals are essential for building and maintaining strong bones.

When vitamin D is too low, calcium absorption falls. Over time, this can contribute to weaker bones.

That is especially important in MS because some people already have reduced physical activity, muscle weakness, balance problems, or an increased risk of falling.

But focusing only on bones greatly underestimates what vitamin D does.

Vitamin D also acts more like a hormone than a typical vitamin.

The active form of vitamin D enters cells and binds to a protein called the vitamin D receptor, or VDR.

Once this happens, vitamin D can influence the activity of many genes.

Some of those genes are directly involved in immune defense.

 

Your Immune System Uses Vitamin D to Fight Invaders

Your immune system is not simply waiting for something to attack.

It is constantly identifying threats, communicating between different types of immune cells, controlling inflammation, killing infected cells, and trying to prevent invading organisms from gaining a foothold.

Vitamin D is involved in many of these functions.

Immune cells including macrophages, monocytes, dendritic cells, B cells, and T cells contain vitamin D receptors.

That tells us something important.

The immune system is designed to respond to vitamin D.

When vitamin D reaches these cells and activates its receptor, it can influence how those cells behave.

One important effect is the production of antimicrobial peptides.

These are small defensive molecules that help the body respond to infectious organisms.

One of the best studied is cathelicidin.

Vitamin D helps turn on genes involved in producing cathelicidin and other antimicrobial defenses.

These substances are part of our innate immune system, the fast-acting defense system we rely on when viruses, bacteria, fungi, and parasites enter the body.

Vitamin D also helps regulate inflammation.

This is important because an effective immune response needs balance.

Too little response can allow an infection to persist.

Too much uncontrolled inflammation can damage healthy tissue.

Vitamin D helps immune cells communicate and coordinate that response.

So when vitamin D is deficient, we are not simply talking about a nutrient for bone health being low.

We may also be talking about one part of the immune defense system functioning below its full capacity.

 

Vitamin D Does Not Simply “Boost” the Immune System

You will often hear that vitamin D “boosts” immunity.

That description is too simple.

A healthy immune system does not need to be constantly boosted. It needs to respond appropriately.

Vitamin D appears to help with both sides of that equation.

It supports antimicrobial defenses while also helping regulate inflammatory immune responses.

For example, vitamin D can influence regulatory T cells. These cells help keep immune activity under control after a threat has been addressed.

Vitamin D can also affect inflammatory signaling molecules and the activity of other immune cells.

This is better described as immune regulation.

The goal is not simply more immune activity.

The goal is an immune system that can recognize a threat, respond effectively, contain the infection, and then calm the inflammatory response when the job is done.

 

What Does This Have to Do With MS?

This is where the vitamin D discussion becomes much more important.

MS is usually described as a disease in which immune cells become activated against myelin in the brain and spinal cord.

But that description leaves a critical question unanswered:

Why is the immune system activated in the first place?

Research into MS increasingly points to major changes in the microbial environment of the body.

Dysbiosis in MS

Multiple studies have found that people with MS have differences in their microbiome compared with people without MS.

This imbalance is called dysbiosis.

Researchers have identified changes in specific groups of bacteria that maintain the intestinal barrier and influence immune regulation.

Dysbiosis can affect immune signaling, microbial metabolites, and the permeability of the gut lining.

The finding is important because the gut contains one of the largest collections of microbes and immune cells in the human body. Changes there can influence immune activity far beyond the digestive tract.

Infectious Organisms Have Also Been Investigated in the Central Nervous System of MS

The infection question in MS goes back more than a century, and the organisms investigated are not limited to one type of pathogen.

Researchers and pathologists have reported findings involving bacteria, fungi, protozoa, and parasitic worms.

Filarial worms: Pathologist Dr. Alan MacDonald has reported microscopic structures he identified as filarial nematodes and microfilariae in cerebrospinal fluid from people with MS.

Tapeworm larvae: Dr. MacDonald also published a small study examining cerebrospinal fluid from 10 people with MS. He reported larval cestodes, or tapeworm larvae, in all 10 samples, with several developmental stages represented. Juvenile developing tapeworm forms were reported in two patients, along with hooklets, cyst-like larval structures, and other features used to identify cestodes.

Candida and other fungi: Researchers have detected fungal antigens, fungal DNA, and antibodies against several Candida species in the cerebrospinal fluid of some people with MS. Other studies have reported fungal markers in the blood of MS patients.

Malaria-related protozoa: The connection between MS and malaria-like protozoan parasites has been investigated for more than a century, with dozens of scientific reports examining striking similarities in neurological symptoms, disease distribution, pathology, and response to antimalarial drugs. Historical research reviewed by Kissler reported antibodies to malaria parasites in 30 to 40 percent of MS patients and malaria parasites themselves in about 20 percent, while other researchers described MS-like neurological disease associated with malaria and reported improvement in some patients treated with quinine. The breadth of the historical, epidemiological, pathological, and treatment evidence makes malaria-like protozoan infection an important part of the infectious-disease research in MS.

Babesia: Babesia is another tick-borne parasite that infects red blood cells. Published reports show that people with MS, particularly those receiving strong B-cell-suppressing treatments, can develop severe babesiosis.

Borrelia: The bacterial connection has a much longer history. Spirochete-like organisms were reported in MS brain and spinal cord tissue decades before Borrelia burgdorferi was formally identified as the cause of Lyme disease. Modern research confirms that Borrelia can enter the nervous system, and neuroborreliosis can produce neurological symptoms and MRI abnormalities that sometimes resemble MS. Historical and more recent researchers have continued investigating whether Borrelia or related spirochetes may contribute to disease in a subset of people diagnosed with MS.

This research provides much broader evidence of dysbiosis and raises a legitimate question:

Could chronic microbial imbalance and persistent infection keep the immune system activated in MS?

That question becomes especially important when we consider vitamin D, because vitamin D is one of the tools the immune system uses to recognize, regulate, and respond to microbial threats.

 

Could Infection Interfere With Vitamin D?

This question takes us one step further.

Many of vitamin D’s effects depend on its ability to bind to the vitamin D receptor.

Think of vitamin D as a key and the vitamin D receptor as the lock.

You can have vitamin D circulating in the blood, but the signal still has to reach and activate the receptor inside the cell.

Research across several very different types of infections suggests this pathway may be affected in more than one way.

Borrelia can greatly reduce Vitamin D receptor expression

Laboratory research involving Borrelia burgdorferi, the bacterium that causes Lyme disease, found that live Borrelia greatly reduced vitamin D receptor expression in monocytes, important immune cells.

Even dead bacterial fragments reduced receptor expression, although less dramatically than live bacteria.

This raises the possibility that infection and inflammation may affect the way vitamin D is regulated in the body.

Parasites

Research has also found associations between parasitic infections and low vitamin D.

A recent study of children with intestinal parasites found vitamin D deficiency in a large majority of children infected with Giardia lamblia and in many of those infected with Blastocystis.

Significant associations were also reported with other parasites, including Entamoeba coli and the roundworm Ascaris lumbricoides.

These studies suggest parasitic infection and vitamin D status may be connected in ways that go beyond simply not eating enough vitamin D or getting enough sunlight.

Viruses

Similar associations between low vitamin D and infection have been reported with viruses including influenza, Epstein-Barr virus, and COVID-19.

Here again, there is an important complication.

Inflammation during an acute infection can lower circulating vitamin D levels relatively quickly.

That makes it difficult to know whether low vitamin D weakened the body’s defenses before the infection, whether the infection and inflammatory response lowered vitamin D afterward, or whether both processes are occurring together.

The Bigger Pattern

Taken together, this research suggests that infection and vitamin D may influence each other in several different ways.

Some pathogens may interfere directly with vitamin D signaling or receptor expression.

Other infections are strongly associated with low circulating vitamin D.

Inflammation itself may also alter vitamin D metabolism and blood levels.

A broader review has proposed that certain bacteria living inside human cells may disrupt vitamin D regulation of the immune system, potentially contributing to persistent infection and ongoing inflammation.

This research shows that the relationship between infection and vitamin D is biologically more complex than simply asking whether someone gets enough sunshine or takes a supplement.

That creates a very different question.

Instead of only asking:

“How much vitamin D am I taking?”

we may also need to ask:

“Why is my body not using or regulating vitamin D normally?”

If infection, inflammation, receptor function, or another part of the vitamin D signaling pathway is being affected, simply increasing the amount of vitamin D may not address the original problem.

 

Vitamin D Deficiency May Create a Vicious Cycle

Consider how these pieces could interact.

A person develops low vitamin D.

Their antimicrobial immune defenses may become less effective.

A persistent virus, bacterium, fungus, or parasite may then become more difficult for the immune system to control.

The infection may contribute to ongoing immune activation and inflammation.

That inflammation may affect vitamin D metabolism or signaling.

MS symptoms such as fatigue, heat sensitivity, and mobility problems may then lead to even less sun exposure.

Vitamin D levels may fall further.

Now the person may be caught in a cycle:

Low vitamin D → weaker antimicrobial defense → persistent immune activation → more inflammation → poorer vitamin D status

Research has not proven that this exact sequence explains every case of MS.

But the individual relationships within this cycle have scientific support, and the model gives us a more complete way to think about vitamin D deficiency than simply blaming a lack of sunshine.

 

This May Help Explain the Confusing Vitamin D Studies

There is another reason this matters.

Studies consistently show an association between low vitamin D and MS.

Yet when researchers give people with established MS larger amounts of vitamin D, the results have often been far less dramatic than the association would seem to predict.

Some studies have found changes in immune markers or fewer new MRI lesions.

But major trials of high-dose vitamin D have not consistently produced large improvements in relapse rates, disability, or overall disease activity.

That may seem contradictory.

It is not necessarily.

Imagine seeing smoke coming from a house.

The smoke is important because it tells you something is wrong.

But removing the smoke does not necessarily extinguish the fire.

Vitamin D deficiency may work in a similar way.

Correcting the deficiency is important.

But if chronic infection, inflammation, altered vitamin D receptor function, epigenetic changes, lacking health promoting microbes or other problems are contributing to the deficiency, raising the blood level alone may not resolve everything happening underneath it.

 

The Vitamin D Receptor May Be Part of the Story

There is another layer worth understanding.

Not everyone processes or responds to vitamin D in exactly the same way.

Research has also found altered epigenetic regulation of the vitamin D receptor gene in people with MS.

Epigenetics refers to changes that influence how strongly genes are turned on or off without changing the underlying DNA code. This may be caused by disruptions to the microbiome.

This matters because a person could theoretically have an acceptable vitamin D blood level while still having disrupted signaling inside the cell.

That does not mean everyone with MS has vitamin D resistance and that it can’t be resolved.

It means the vitamin D pathway is more complicated than the number shown on a blood test.

 

More Vitamin D Is Not Always Better

If vitamin D is this important, it is easy to assume that taking much more must be better.

That does not follow from the evidence.

Some protocols use tens of thousands of international units of vitamin D every day.

The best-known example is the Coimbra Protocol, developed by Brazilian neurologist Dr. Cícero Coimbra.

The protocol is based on the theory that some people with autoimmune diseases have resistance to vitamin D and therefore require extremely high doses to create a biological response.

There are reports of patients doing well under this protocol.

There is also a published safety study involving more than 300 patients in which long-term toxicity was not observed when patients followed strict calcium restriction, high fluid intake, and continuous medical monitoring.

But there are also documented cases of serious harm in people taking extremely high doses.

Reported complications include severe hypercalcemia, kidney injury, kidney failure, calcium deposits in the kidneys, weakness, and other serious problems.

Even randomized trials using high doses below typical Coimbra levels have generally failed to show dramatic improvement in the major clinical outcomes of MS.

It means the goal should not automatically be to take more and more.

The better questions are:

How much vitamin D does this person actually need?

Why did the deficiency develop?

And is the vitamin D pathway functioning normally?

 

Vitamin D May Be One Piece of a Much Larger MS Puzzle

Vitamin D deserves far more attention than it gets when we discuss immune function.

It is essential for bone health, but its role does not stop there.

Vitamin D helps regulate immune cells.

It supports antimicrobial defenses.

It influences inflammatory responses.

It affects gene expression.

And when vitamin D is deficient, the immune system may be less able to respond effectively to invading organisms.

For people with MS, that raises important questions.

Why is deficiency so common?

Is it simply because of less sunlight?

Is inflammation lowering vitamin D?

Are genetic or epigenetic changes affecting the vitamin D receptor?

Could persistent infections be interfering with vitamin D signaling or regulation?

And if infection is part of the disease process for some people, could low vitamin D make it harder for the immune system to keep those organisms under control?

These are not small questions.

They shift the conversation away from simply asking how much vitamin D someone should take.

The deeper question becomes:

Why is the body deficient, and what is preventing the immune system from doing its job properly?

Correcting vitamin D deficiency is important.

But it may be only one part of understanding the much bigger connection between immune function, chronic infection, vitamin D signaling, and multiple sclerosis.

There are real solutions to recover from parasites today!

To restore health, we must focus on treating the cause of inflammation, which are parasites. First, identify the enemy (parasites), then support the body and treat the parasites while following a holistic approach. When parasitic infections are treated effectively, we can overcome inflammation or disease.

If you’re frustrated with the fact that our standard of care STILL doesn’t offer a real solution for treating MS and other diseases, then click on the link below to watch Pam Bartha’s free masterclass training and discover REAL solutions that have allowed Pam and many others to live free from MS and other diseases.

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References:

Balasooriya NN, Elliott TM, Neale RE, Vasquez P, Comans T, Gordon LG. The association between vitamin D deficiency and multiple sclerosis: an updated systematic review and meta-analysis. Mult Scler Relat Disord. 2024;90:105804. doi:10.1016/j.msard.2024.105804.
Link: https://pubmed.ncbi.nlm.nih.gov/39180838/
Key finding: Pooled analysis of 14 case-control studies (4,130 cases, 4,604 controls) found vitamin D deficiency associated with 54% higher odds of MS (OR 1.54, 95% CI 1.05–2.24). In the 7 studies that excluded supplement users, the odds ratio rose to 2.19 (95% CI 1.44–3.35).

Li Y, Xu Y, Liu Z, Ma L, Wang Y, Cai Y. Vitamin D status, supplementation, and multiple sclerosis: a systematic review and meta-analysis. Front Immunol. 2026;17:1775270. doi:10.3389/fimmu.2026.1775270.
Link: https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2026.1775270/full  
Key finding: MS patients had significantly lower serum 25(OH)D than controls, most pronounced during relapse and in secondary progressive MS. No statistically significant seasonal fluctuation was found. High-dose vitamin D3 supplementation significantly reduced annualized relapse rate; low-dose supplementation did not.

Spelman T, Gray O, Trojano M, et al. Seasonal variation of relapse rate in multiple sclerosis is latitude dependent. Ann Neurol. 2014;76(6):880-890. doi:10.1002/ana.24287.
Link: https://pubmed.ncbi.nlm.nih.gov/25283272/
Key finding: Analysis of 32,762 relapses from 9,811 patients across 30 countries found relapse onset follows an annual sinusoidal pattern, with spring peaks and autumn troughs in both hemispheres. Every 10° of latitude from the equator was linked to a 28.5-day shorter lag between UV trough and relapse peak (95% CI 3.29–53.71, p=0.028).

Taha R, Abureesh S, Alghamdi S, Hassan RY, Cheikh MM, Bagabir RA, Almoallim H, Abdulkhaliq A. The relationship between vitamin D and infections including COVID-19: any hopes? Int J Gen Med. 2021;14:3849-3870. doi:10.2147/IJGM.S317421. Link: https://pmc.ncbi.nlm.nih.gov/articles/PMC8318784/
Key finding: Reviews how vitamin D regulates innate and adaptive immunity and modulates antiviral and antibacterial inflammatory responses, covering tuberculosis, influenza, HIV, and SARS-CoV-2 infections.

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.
Link: https://pmc.ncbi.nlm.nih.gov/articles/PMC9033096/
Key finding: In 319 autoimmune disease patients followed up to 3.5 years on a mean vitamin D3 dose of 35,291 IU/day, combined with a strict low-calcium diet and at least 2.5 L fluid intake daily, hypercalcemia was not found to be a first-line risk. The authors concluded the protocol is safe under experienced physician supervision.

Feige J, Moser T, Bieler L, Schwenker K, Hauer L, Sellner J. Vitamin D Supplementation in Multiple Sclerosis: A Critical Analysis of Potentials and Threats. Nutrients. 2020;12(3):783. doi:10.3390/nu12030783.
Link: https://pmc.ncbi.nlm.nih.gov/articles/PMC7146466/  
Key finding: Sustained doses of vitamin D at or above 50,000 IU/day for weeks or months are frequently associated with toxic effects, including renal failure, cardiac arrhythmia, and calcification of coronary vessels and heart valves.

Alharbi FM. Update in vitamin D and multiple sclerosis. Neurosciences (Riyadh). 2015;20(4):329-335. doi:10.17712/nsj.2015.4.20150357. Link: https://pubmed.ncbi.nlm.nih.gov/26492110/
Key finding: Review of the literature on MS and vitamin D concludes there is clear evidence that vitamin D deficiency is a risk factor for MS, though direct evidence for vitamin D’s effect on MS progression is still lacking.

Ayele BA, Wuhib MZ, Zenebe BG, Metaferia GZ. Serum Vitamin D Level among Multiple Sclerosis Patients in the Tropics: Experience from a Private Clinic in Addis Ababa, Ethiopia. Ethiop J Health Sci. 2021;31(3):611-618. doi:10.4314/ejhs.v31i3.18. Link: https://pmc.ncbi.nlm.nih.gov/articles/PMC8365493/  
Key finding: 96% of MS patients (24 of 25) at a private clinic in Addis Ababa had vitamin D deficiency, with an average serum vitamin D level of 14.8 ± 10.4 ng/mL.

Sintzel MB, Rametta M, Reder AT. Vitamin D and multiple sclerosis: a comprehensive review. Neurol Ther. 2018;7(1):59-85. doi:10.1007/s40120-017-0086-4.
Link: https://pmc.ncbi.nlm.nih.gov/articles/PMC5990512/
Key finding: Comprehensive review of epidemiological and Mendelian-randomization evidence supporting vitamin D deficiency as a modifiable risk factor in MS.

Bikle DD. Vitamin D and the immune system: role in protection against bacterial infection. Curr Opin Nephrol Hypertens. 2008;17(4):348-352. doi:10.1097/MNH.0b013e3282ff64a3. Link: https://pubmed.ncbi.nlm.nih.gov/18660668/
Key finding: Describes vitamin D signaling’s role in innate immunity, specifically how it enables macrophages to respond to and kill Mycobacterium tuberculosis, and how it helps keratinocytes respond to disruption of the skin’s barrier function.

Cuna WR, Passera R, Rodriguez C. Interplay of Gastrointestinal Parasites, Micronutrient Deficiencies, and Anemia in Children from the Bolivian Highlands. Microorganisms. 2026;14(2):511. doi:10.3390/microorganisms14020511.
Link: https://www.mdpi.com/2076-2607/14/2/511
Key finding: In a cross-sectional study of 212 schoolchildren (ages 5–13) in the La Paz highlands of Bolivia, overall vitamin D deficiency was 18%, but was significantly higher among children infected with specific parasites: 78.9% with Giardia lamblia (p=0.001), 69.7% with Blastocystis spp. (p=0.004), and 37% with Ascaris lumbricoides (p=0.018). Entamoeba coli infection was also significantly associated with vitamin D deficiency (p=0.021).

Autoimmunity Research Foundation. Metabolism of vitamin D and the Vitamin D Receptor. Marshall Protocol Knowledge Base. Updated September 14, 2022. Accessed August 7, 2026. Link: https://mpkb.org/home/pathogenesis/vitamind/metabolism

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.
Link: https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2021.655739/full
Key finding: Proposes that acquired vitamin D resistance is a plausible mechanism behind autoimmune disease development, supported by clinical response to a high-dose vitamin D3 therapeutic protocol. Citing a whole-genome microarray study of monocytes, the authors report: “This technique revealed a 60-fold downregulation of the VDR by live Borrelia [burgdorferi].”