# Multiple Sclerosis

Category: Conditions

Also known as: MS, demyelination

Multiple sclerosis is a demyelinating condition that Ray Peat framed not as a primary autoimmune attack, but as a metabolic and energetic failure of the oligodendrocytes—the steroid-forming cells responsible for myelination. He argued that these cells require adequate thyroid…

10 passages · 2 authors · 2009–2020 · Most-cited: [Ray Peat](https://bioenergeticoracle.com/md/voices/ray-peat/index.md)

Canonical page: https://bioenergeticoracle.com/concepts/multiple-sclerosis

## Synthesis

**Multiple sclerosis** is a demyelinating condition that Ray Peat framed not as a primary autoimmune attack, but as a *metabolic and energetic failure* of the **oligodendrocytes**—the steroid-forming cells responsible for myelination. [Source 2, 7] He argued that these cells require adequate thyroid hormone (specifically T3) to produce **pregnenolone** locally, and that a deficiency of thyroid or a block in the conversion of T4 to T3 leaves the myelin sheath vulnerable to degeneration. [Source 2] Georgi Dinkov has cited direct evidence that demyelination is driven by low T3 levels and that T3 administration can restore the myelin sheath, positioning MS as a condition of clear metabolic origin. [Source 10]

Peat identified a characteristic physiological profile in people with MS: chronically elevated **cortisol**, hypoglycemia despite that cortisol excess, high **prolactin**, and a tendency toward hyponatremia and increased blood viscosity with platelet clumping. [Source 1] He saw this pattern as a vicious circle initiated by energy deficiency. When hypoglycemia occurs, adrenaline liberates free fatty acids; if those fatty acids are unsaturated, they trigger serotonin release, and both serotonin and the unsaturated fats suppress mitochondrial respiration, worsening the energy deficit. [Source 5] This cascade stimulates cortisol to mobilize amino acids from skeletal muscle, which are rich in tryptophan and cysteine—precursors for serotonin and excitotoxic agents that further suppress thyroid function. [Source 1, 5] The resulting *excess serotonin* promotes excessive water drinking, which can directly damage myelin enclosures through osmotic disruption. [Source 1]

Estrogen is a central aggravating factor in Peat's analysis. He documented that estrogen causes **mast cells** to release inflammatory mediators like histamine and serotonin, makes blood vessels leaky, and promotes platelet aggregation. [Source 1] These mast cells are more numerous in MS brains, and the serotonin they release contributes to the inflammatory destruction. [Source 1] Estrogen also disturbs the blood osmotically, causing water retention relative to solutes, and Peat emphasized that simple osmotic variations can damage myelin structures, suggesting this mechanism should be investigated before assuming immunological events are primary. [Source 1] He noted that the strong epidemiological association of MS with estrogen had been perversely interpreted by mainstream medicine as evidence that estrogen is protective, a logic he compared to claiming a stove burns you because it is not hot enough. [Source 4, 5]

Therapeutically, Peat reported that several people diagnosed with MS recovered completely when given **thyroid** supplementation, as their symptoms were manifestations of unrecognized hypothyroidism. [Source 7, 9] He also described a woman with an MS-like illness who achieved full motor and sensory recovery using **progesterone**, which counteracts estrogen's effects on mast cells and platelets. [Source 1, 7] Other stabilizing interventions he cited include maintaining high blood glucose to suppress the inflammatory cascade, ensuring adequate dietary protein to prevent the catabolic mobilization of amino acids, and using anti-inflammatory agents like aspirin. [Source 1, 3, 5] He noted that serotonin antagonists such as ondansetron and ketanserin have been used therapeutically with success, and that naloxone or naltrexone can sometimes break the pathological endorphin patterns established by prolonged stress. [Source 1, 6] Peat also observed that some MS diagnoses were simply cases of *protein deficiency*, with symptoms disappearing after a protein-rich meal. [Source 8] He cautioned that even the presence of brain plaques does not confirm an MS diagnosis, as studies found plaques in healthy medical students at the same rate. [Source 9]

## People also ask

### How does low thyroid hormone contribute to multiple sclerosis?

Peat argued that oligodendrocytes need T3 to produce protective pregnenolone locally, and that a deficiency or conversion block leaves the myelin sheath vulnerable to degeneration.

### Why did Peat consider estrogen a key aggravating factor in MS?

He documented that estrogen activates mast cells to release inflammatory mediators, makes blood vessels leaky, promotes platelet aggregation, and causes osmotic disturbances that can directly damage myelin structures.

### What dietary factor did Peat say could resolve symptoms mistaken for MS?

He observed that some MS diagnoses were simply cases of protein deficiency, with symptoms disappearing after a protein-rich meal.

## Related concepts

- [Glucose](https://bioenergeticoracle.com/md/concepts/glucose/index.md)
- [Myelination](https://bioenergeticoracle.com/md/concepts/myelination/index.md)
- [Adrenaline](https://bioenergeticoracle.com/md/concepts/adrenaline/index.md)
- [Albumin](https://bioenergeticoracle.com/md/concepts/albumin/index.md)
- [Bromocriptine](https://bioenergeticoracle.com/md/concepts/bromocriptine/index.md)
- [Cytochrome P450scc.](https://bioenergeticoracle.com/md/concepts/cytochrome-p450scc/index.md)

## Cited passages

Passage numbers match the `[Source N]` markers in the synthesis above.

### Source 1 — Multiple sclerosis, protein, fats, and progesterone

Ray Peat · Article · 2009 · https://raypeat.com/articles/articles/ms.shtml

> In people with MS, the blood is more viscous, and the platelets tend to clump together more easily.
>
> Their cortisol level is higher than normal, and their pituitary adrenal-cortex-stimulating hormone is harder to suppress. This is a condition that is also seen in depression and old age.
>
> Despite the chronically elevated cortisol, people with MS typically have hypoglycemia.
>
> They are occasionally found to have low blood sodium, hyponatremia, but this is hard to determine when the blood's water content is variable.
>
> Their prolactin is likely to be high, and this can result from high estrogen, high serotonin, low sodium, or low thyroid.
>
> Drinking too much water can increase prolactin, and can damage the nerves' myelin enclosures; too much serotonin tends to cause excessive drinking.
>
> Disturbances of blood glucose, sodium, and water content can disrupt the brain's myelin structure.
>
> High estrogen disturbs the blood osmotically, making it retain too much water in relation to the solutes, and this relates to many of estrogen's effects; since simple osmotic variations can damage the myelin structures, it seems that this mechanism should be investigated thoroughly before it is assumed that the immunological events are primary.
>
> Mast cells, which promote inflammation by releasing substances such as histamine and serotonin (and make blood vessels leaky), are more numerous in the brain in multiple sclerosis than in normal brains.
>
> Since platelet clumping releases serotonin, and also because serotonin excess is suggested by so many other features of MS, serotonin antagonists (ondansetron and ketanserin, for example) have been used therapeutically with success.
>
> Estrogen causes mast cells to release their inflammatory mediators, and it causes platelets to aggregate, releasing their serotonin.
>
> Since estrogen dominance is closely associated with the presence of active brain lesions, antiestrogen therapy would seem obvious in MS.
>
> Progesterone counteracts estrogen's effects on both mast cells and platelets.
>
> Aspirin protects against a variety of inflammatory processes, but it's most famous for the inhibition of prostaglandins.
>
> While aspirin is often used to relieve pain in MS, and another inhibitor of prostaglandin synthesis, indomethacin, has been used therapeutically in MS, it would seem appropriate to investigate more carefully aspirin's possible role in preventing or relieving MS.
>
> A simple protein deficiency has many surprising effects.

### Source 2 — Multiple Sclerosis and Other Hormone-Related Brain Syndromes

Ray Peat · Article · 2013 · https://raypeat.com/articles/articles/multiple-sclerosis-hormone-related-brain-syndromes.shtml

> Thyroid is responsible for both myelination and hormone formation. In old age, glial cells become more numerous, and nerve cells become structurally and functionally abnormal, but usually there is no problem with the formation of myelin. In MS, the problem is just with myelination, and there are no senile plaques or defects in the nerve cells themselves.
>
> These differences suggest the possibility that Alzheimer's disease involves a specific premature loss of brain pregnenolone production, but not of thyroid. Recent work suggests a central role for pregnenolone and progesterone in the regulation of consciousness (18), and possibly in the brain's detoxifying system. Elsewhere, I have suggested that vitamin A deficiency might cause the excessive production of the \"amyloid\" protein. A vitamin A deficiency severely inhibits steroid synthesis. (It is used so massively in steroid synthesis that a progesterone supplement can prevent the symptoms of vitamin A deficiency.) I suspect that vitamin A is necessary for the side-chain cleavage that converts cholesterol to pregnenolone. Iron-stimulated lipid peroxidation is known to block steroid formation, and vitamin A is very susceptible to destruction by iron and oxidation. Iron tends to accumulate in tissues with aging. Gajdusek has demonstrated that brain deterioration is associated with the retention of whatever metal happens to be abundant in the person's environment, not just with aluminum. (One type of glial cell is known for its metal-binding function, causing them to be called \"metallophils.\"). According to Gajdusek, \"calcium and other di- and trivalent elements\" are \"deposited as hydroxyapatites in brain cells\" in brain degeneration of the Alzheimer's type. (19)
>
> Even early forms of Alzheimer's disease begin at an age when the youth-associated steroids have begun to decline. If MS involves a deficiency of thyroid (or of T3 within the oligodendrocytes, where T3 normally can be made from thyroxine; many things, including protein deficiency, can block the conversion of T4 to T3), those cells would necessarily be deficient in their ability to produce pregenolone, but in young people the brain would still be receiving a little pregnenolone, progesterone, and DHEA from the adrenals and gonads.

### Source 3 — Politics Science Autoimmune Diseases and Movement Disorders

Ray Peat · Interview · 2012

> **John Barkhausen:** MS?
>
> **Ray Peat:** Yeah, and the skeletal, nervous, inflammatory…diabetes even, involves inflammation and the failure to regenerate properly the beta cells. [Beta cells] are being killed in the same way as brain cells are being killed basically. Instead of making insulin as the cells are renewed, the cells are killed as fast as they are renewed so they stop making insulin. But if you stop killing them they can start making insulin again. The same with the brain, if you stop killing the brain it's always in a process of repair and regeneration. I might have mentioned a man with ALS that I talked to about 8 or 10 years ago; 70 years old and he'd had all the best neurologists examine him and he absolutely was convinced he had Lou Gehrig's disease. He was declining the same as other people he met in the neurology offices. He decided to start doing things to stop inflammation and support repair, and he did them consistently for a few months while still declining, but then he stopped declining and within a few months was repaired. It was less than a year of the whole process, and people he had met in the neurology offices when they had the same rate of decline were totally disabled by the time he was totally well.

### Source 4 — Multiple sclerosis, protein, fats, and progesterone

Ray Peat · Article · 2009 · https://raypeat.com/articles/articles/ms.shtml

> The strong association of MS with estrogen has led to an illogical, but popular and well-publicized medical conclusion that estrogen is protective against MS, and some have claimed that estrogen has beneficial therapeutic effects.
>
> This strange way of thinking has its equivalent in the idea that, since women are much more likely than men to develop Alzheimer's disease, estrogen is protective against it; or that, since women have more fragile bones than men do, and their progressive bone loss occurs during the times of their greatest exposure to estrogen, estrogen prevents osteoporosis.
>
> In this medical environment, close associations between estrogen and degenerative diseases are acknowledged, but they are given a meaning contrary to common sense by saying that the association occurs because there isn't enough estrogen. The stove burns you because it isn't hot enough. As Dave Barry would say, I'm not making this up.
>
> Recently well publicized articles have suggested that estrogen protects the brain (even against stroke!) because it increases serotonin and NO.
>
> There is something almost esthetically pleasing when so many major errors are concentrated into a single article.
>
> Nitric oxide and serotonin are both neurotoxic (Joseph, et al., 1991; Skaper, et al., 1996; Parkinson, et al., 1997; Santiago, et al., 1998; Barger, et al., 2000), as a result of suppressing mitochondrial respiration. NO plays a major role in lipid peroxidation and demyelination. It's interesting to see serotonin and NO openly associated with estrogen, whose mitochondrial toxicity has been carefully hidden from public view.
>
> There are several theories about the cause of MS, old theories about genes and viruses, and newer theories about bacteria, vitamin deficiencies, oil deficiencies, poisons, and reactions to vaccinations (especially for hepatitis B and influenza). The only theory that has been abandoned is the 19th century psychiatric theory about "hysterical paralysis," though occasionally someone does still talk about emotional causes of multiple sclerosis; the term "female hysteria" has evolved into "conversion disorder." Each of the main theories has a few facts that seem to support it, but neglects to account for many other facts.
>
> Everyone agrees that the immune system is involved in MS in some way, but that's really where the problem starts, because of the idea that inflammation is an intrinsic part of immunity.

### Source 5 — Multiple sclerosis, protein, fats, and progesterone

Ray Peat · Article · 2009 · https://raypeat.com/articles/articles/ms.shtml

> Each of the main theories has a few facts that seem to support it, but neglects to account for many other facts.
>
> Everyone agrees that the immune system is involved in MS in some way, but that's really where the problem starts, because of the idea that inflammation is an intrinsic part of immunity. If "inflammation is necessary and good," then it becomes a problem to define exactly where the boundary is between an appropriate reaction and a degenerative process. Edema, reduced cellular respiration, loss of normal functions, fibrosis in its various degrees, each component of inflammation can be seen in a good light, as part of a "defensive immune reaction."
>
> When tissue injury leads to repair, it "must" be seen as beneficial, even if it leads to the formation of a scar in place of functional tissue, because the comparison is between an imagined worst possible outcome, and an imperfect recovery, rather than comparing the inflammatory process with the possibility that a potentially noxious agent might have done no harm at all.
>
> The simplest illustration of how inflammation relates to the organism's resources was an experiment in which blood glucose was varied, while an animal was exposed to chemicals that varied from mildly irritating to potentially deadly. When the animal had very low blood sugar, the mildest irritant could be deadly, but when its blood glucose was kept very high, even the deadly antigens were only mildly irritating. Varying the blood sodium concentration had similar, but weaker, effects.
>
> There is a tendency to see inflammation not only as a normal part of immunity, but to see it as being proportional to the nature of the antigen, except when the immune system has been primed for it by previous contact, in which case the organism will either not react at all (because it has become immune), or it will react much more violently than it did on the first exposure, because it has become allergic.
>
> But, in reality, the mere concentration of glucose and sodium in the blood (and of thyroid, and many other substances that aren't considered to be part of the immune system) can make a tremendous difference in the degree of "immunological" reaction.
>
> In the excessively sensitive condition produced by hypoglycemia, several things happen that contribute to the maladaptive exaggerated inflammatory response.
>
> Adrenaline increases in hypoglycemia, and, if the adrenaline fails to convert glycogen into glucose, it will provide an alternative fuel by liberating free fatty acids from fat cells.

### Source 6 — Politics & Science: Two Hour Fundraiser II

Ray Peat · Interview · Feb 22, 2012 · http://l-i-g-h-t.com/files/politics-science-two-hour-fundraiser-2.mp4

> ## MS Drugs: Naloxone and Naltrexone
>
> **John Barkhausen:** If you wanted to keep the inflammation low, could you just use some other anti-inflammatory?
>
> **Ray Peat:** Oh, yeah. All kinds of stabilizing anti-inflammatory things. Thyroid, progesterone, short-chain fatty acids, and sugars are all things that help restore injured, demyelinated nerves.

### Source 7 — Multiple Sclerosis and Other Hormone-Related Brain Syndromes

Ray Peat · Article · 2013 · https://raypeat.com/articles/articles/multiple-sclerosis-hormone-related-brain-syndromes.shtml

> In experimental poisoning of animals with carbon monoxide or cyanide, the brain lesions resembling MS include blood clots. The patchy distribution of these spots in the brain suggests that the clotting is secondary to metabolic damage in the brain. Presumably, the same would be true in ordinary MS, with clots and spasms being induced in certain areas by metabolic abnormalities in brain cells. The injured cells that are responsible for myelination of nerve fibers are steroid-forming cells. A failure to secrete their protective pregnenolone could cause a local spasm of a blood vessel. The circulatory problem would exacerbate the respiratory problem. Steroid production is dependent on NADH and NADPH, and so requires adequate energy supplies and energy metabolism. The phenomenon of blood-sludging, studied by M. Knisely at the University of Chicago in the 1930s and 1940s, is apparently a general result of decreased energy metabolism, and is likely to be a factor in energy-and-circulatory vicious circles.
>
> ## SYMPTOMS AND THERAPIES
>
> Around 1976 I met a woman in her mid-thirties who heard about my work with progesterone in animals. She had been disabled by a brain disease that resembled MS or Devic's disease, inflammation of the optic nerves. It would sometimes cause blindness and paralysis that persisted for weeks at a time. During remissions, sometimes using a wheelchair, she would go to the medical school library to try to understand her condition. She came across Katherina Dalton's work with progesterone, and convinced a physician to give her a trial injection. Although she had trouble finding people who were willing to give her progesterone, her recovery was so complete that she was able to climb stairs and drive her car, and she came to my endocrinology class and gave a very good (and long) lecture on progesterone therapy. Although her sensory and motor functions became normal, she remained very fat, and chronically suffered from sore areas on her arms and legs that seemed to be abnormal blood vessels, possibly with phlebitis. She appeared to need thyroid hormone as well as larger amounts of progesterone, but never found a physician who would cooperate, as far as I know.
>
> In the late 1970s I was seeing a lot of people who had puzzling health problems.

### Source 8 — Weight Loss, Macros, Prolactin, Cancer, Cold Therapy & More, Q&A

Ray Peat · Interview · Oct 11, 2020 · https://www.youtube.com/watch?v=EK8qhzo4w9s

> **Jodelle Fitzwater:** I know that the experiments with isolated intestine
>
> **Ray Peat:** tested what happens to the intestine when it's given a pure protein or pure fat or pure carbohydrates or a mixture and the intestine responds good balance of proteins, fat, and carbohydrates all at the same time.
>
> **Jodelle Fitzwater:** Awesome. Okay, so we're on to Craig Doe asks, Dr. Peat, the significance of vitamin D for multiple sclerosis. Is there anything else one could do to help with the symptoms? Because the problem is...
>
> **Ray Peat:** are the other main protective things. Several people who told me that they had a diagnosis of MS, when I looked at their diet and their symptoms, a couple of them were simply protein deficient. And eating a big fish dinner, for example, sometimes disappeared and they discovered it was a mistaken diagnosis.
>
> **Jodelle Fitzwater:** I would agree with that. Okay, Mitchell Lester asks, I have had allergies to dogs and cats and tree nuts and shellfish my entire life. Luckily grew out of an egg allergy. Any recommendation on how to mitigate, overcome these allergies? I've tried antihistamines, elevating blood sugar, and aspirin, which do reduce symptoms but not completely. Thanks.

### Source 9 — EastWest Healing: Questions and Answers I

Ray Peat · Interview · Jul 12, 2011 · http://l-i-g-h-t.com/files/east-west-questions-and-answers-I.mp4

> **Ray Peat:** I think it's good to keep investigating because so many things are called MS that aren’t really. There was a study in which people had their heads x-rayed and many of the people diagnosed as MS had visible plaques in their brains but when they used a group of healthy medical students as controls, just as many had plaques in their heads. So even finding the plaques doesn't absolutely confirm the diagnosis. So it's good to keep your eyes open for other explanations.

### Source 10 — Thyroid hormone (T3) therapy may treat multiple sclerosis (MS)

Georgi Dinkov · Article · Apr 21, 2020 · https://haidut.me/?p=1021

> A great study, which directly demonstrates that the demyelination seen in this “autoimmune” condition targeting the nervous system is driven by low levels of T3. Conversely, the study also found that administration of either plain T3 or a synthetic analog was able to restore the myelin sheet and ameliorate the disease. As such, MS is likely yet another condition of clear metabolic origin, and in which metabolic therapies may be curative.
>
> [references]

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