# Oligodendrocytes Category: Metabolism Oligodendrocytes are one of the kinds of glial (or neuroglial) cells, and structurally they are unusual in having sheet-like, rather than just thread-like processes; they have a sensitivity ("receptors") to stress and valium, and produce pregnenolone when activated. Under the… 6 passages · 1 author · 2013–2014 · Most-cited: [Ray Peat](https://bioenergeticoracle.com/md/voices/ray-peat/index.md) Canonical page: https://bioenergeticoracle.com/concepts/oligodendrocytes ## Synthesis **Oligodendrocytes** are a type of glial cell that function as the brain's primary site of *steroidogenesis*, producing **pregnenolone** locally rather than merely storing hormones from the adrenals and gonads. [Source 1, 2] Peat argued that these cells have receptors for stress and valium, and they synthesize pregnenolone when activated, challenging the textbook view that their main role is electrical insulation for saltatory conduction. [Source 2, 4] He considered the "insulating" myelin dogma a fetish that obstructed progress, proposing instead that the steroid hormones produced by oligodendrocytes are directly relevant to the nerve conduction processes of the cells they surround. [Source 4] Structurally, oligodendrocytes are unusual among glial cells because they possess *sheet-like processes* rather than just thread-like ones. [Source 2] Under the influence of **thyroid hormone**, these cells wrap themselves in thin layers around the conductive axons of nerve cells, leaving a multilayered **myelin** coating composed of proteins, complex lipids, and a high concentration of cholesterol. [Source 2, 5] The absorption of thyroid hormone by these glial cells is promoted by **butyrate**, an anti-stress substance found in butter and coconut oil, which Peat noted increases T3 uptake. [Source 2, 3] The synthesis of myelin itself depends on adequate energy, with sugar, thyroid, and progesterone acting as limiting factors for its rapid formation. [Source 6] Peat drew a sharp distinction between the pathologies of oligodendrocytes in different degenerative conditions. In multiple sclerosis, the problem is specifically a failure of myelination, without defects in the nerve cells themselves or the formation of senile plaques. [Source 1] In contrast, he cited early research by Hiroisi and Lee showing that degenerating oligodendrocytes were the source of the **senile plaques** or amyloid deposits characteristic of Alzheimer's disease, ending as translucent "mucoid" spots. [Source 1] This led him to suggest that Alzheimer's might involve a specific premature loss of brain pregnenolone production by these cells, while thyroid function remains intact, whereas multiple sclerosis reflects a broader hypothyroid problem impairing the myelination process. [Source 1, 4] The decline of oligodendrocyte function is central to Peat's view of brain aging. He observed that brain steroid levels fall to about 5% of their youthful concentration in old age, correlating with the degeneration of these cells into amyloid-producing forms. [Source 1] He speculated that the halo of oligodendrocytes sometimes seen surrounding degenerating nerve cells might represent a *protective reaction* to supply the neuron with any pregnenolone the glial cells are still able to synthesize. [Source 1] The maintenance of mental clarity into advanced age through supplementation with **pregnenolone**, DHEA, progesterone, and thyroid underscores the functional importance of restoring the steroidogenic activity that normally originates with these glial cells. [Source 1] ## People also ask ### What do oligodendrocytes produce besides myelin? Peat argued that oligodendrocytes are the brain's primary site of steroidogenesis, synthesizing pregnenolone locally rather than just storing hormones from elsewhere. ### How does thyroid hormone affect oligodendrocyte function? The entry describes thyroid hormone causing oligodendrocytes to wrap around axons and deposit a multilayered myelin coating, with butyrate promoting T3 uptake to support this process. ### How are oligodendrocytes involved in Alzheimer's disease? Peat cited research showing degenerating oligodendrocytes are the source of senile plaques in Alzheimer's, suggesting the disease involves a premature loss of brain pregnenolone production by these cells. ## Related concepts - [Myelination](https://bioenergeticoracle.com/md/concepts/myelination/index.md) - [Cytochrome P450scc.](https://bioenergeticoracle.com/md/concepts/cytochrome-p450scc/index.md) - [Glial](https://bioenergeticoracle.com/md/concepts/glial/index.md) - [Thymus Gland](https://bioenergeticoracle.com/md/concepts/thymus-gland/index.md) - [Adrenaline](https://bioenergeticoracle.com/md/concepts/adrenaline/index.md) - [Age Pigment (Lipofuscin)](https://bioenergeticoracle.com/md/concepts/age-pigment-lipofuscin/index.md) ## Cited passages Passage numbers match the `[Source N]` markers in the synthesis above. ### Source 1 — Multiple Sclerosis and Other Hormone-Related Brain Syndromes Ray Peat · Article · 2013 · https://raypeat.com/articles/articles/multiple-sclerosis-hormone-related-brain-syndromes.shtml > ## OLD AGE > > A biologist friend of mine who was about 85 became very senile. His wife started giving him thyroid, progesterone, DHEA and pregnenolone, and within a few days his mental clarity had returned. He continued to be mentally active until he was 89, when his wife interfered with his access to the hormones. > > In old age the brain steroids fall to about 5% of their level in youth. Pregnenolone and DHEA improve memory in old rats, and improve mood stability and mental clarity of old people. Pregnenolone's action in improving the sense of being able to cope with challenges probably reflects a quieting and coordinating of the \"sequencing\" apparatus of the forebrain, which is the area most sensitive to energy deprivation. This is the area that malfunctions in hyperactive and \"dyslexic\" children. Weakening of the sequencing and sorting processes probably explains the common old-age inability to extract important sounds from environmental noise, creating a kind of \"confusion deafness.\" Insomnia, worry and \"restless legs\" at bedtime are problems for many old people, and I think they are variations of the basic energy-depletion problem. > > The oligodendrocytes were reported (Hiroisi and Lee, 1936) to be the source of the senile plaques or amyloid deposits of Alzheimer's disease. (16) Hiroisi and Lee showed the cells in different stages of degeneration, ending with translucent \"mucoid\" spots that stained the same as amyloid, the material in the senile plaques. This type of cell also appears to form a halo or crown around degenerating nerve cells--possibly in a protective reaction to provide the nerve cell with any pregnenolone the oligodendrocytes are able to make. The oligodendrocytes, the source of the brain steroids (that people previously believed came from the adrenals and gonads, and were just stored in the brain), myelinate nerve fibers under the influence of thyroid hormone (17). 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. ### Source 2 — Glossary Ray Peat · Glossary > Oligodendrocytes > > Oligodendrocytes are one of the kinds of glial (or neuroglial) cells, and structurally they are unusual in having sheet-like, rather than just thread-like processes; they have a sensitivity ("receptors") to stress and valium, and produce pregnenolone when activated. Under the influence of thyroid hormone, they wrap themselves in thin layers around the conductive parts of nerve cells, leaving a multilayered "myelin" coating. Their absorption of thyroid hormone is promoted by butyrate, an anti-stress substance found in butter and coconut oil. ### Source 3 — Multiple Sclerosis and Other Hormone-Related Brain Syndromes Ray Peat · Article · 2013 · https://raypeat.com/articles/articles/multiple-sclerosis-hormone-related-brain-syndromes.shtml > 2. Cytochrome P450scc. The cytochromes are \"pigments,\" in the same sense that they contain the colored \"heme\" group that gives hemoglobin its color. P450 means \"protein that absorbs light at a wavelength of 450. The scc means \"side-chain cleaving,\" which refers to the removal of the 6 carbon atoms that distinguish cholesterol from pregnenolone. Other Cyt P450 enzymes are important for their detoxifying oxidizing action, and some of these are involved in brain metabolism. > 3. Glial means \"glue-like,\" and glial cells are mostly spidery-shaped cells that used to be thought of as just connective, supportive cells in the brain. > 4. Mitochondria (the \"thread-like bodies\") are the structures in cells which produce most of our metabolic energy by respiration, in response to the thyroid hormones. > 5. Mucoid--refers to a mucoprotein, a protein which contains some carbohydrate. A glycoprotein; usually not intended as a precise term. > 6. Myelination. Myelin is a multilayered enclosure of the axons (the long processes) of nerve cells, composed of proteins and complex lipids, including cholesterol. The layered material is a flat, thin extension of the cytoplasm of the oligodendroglial cells. > 7. Oligodendrocytes are one of the kinds of glial (or neuroglial) cells, and structurally they are unusual in having sheet-like, rather than just thread-like processes; they have a sensitivity (\"receptors\") to stress and valium, and produce pregnenolone when activated. Under the influence of thyroid hormone, they wrap themselves in thin layers around the conductive parts of nerve cells, leaving a multilayered \"myelin\" coating. Their absorption of thyroid hormone is promoted by butyrate, an anti-stress substance found in butter and coconut oil. > 8. Steroidogenesis is the creation of steroids, usually referring to the conversion of cholesterol to hormones. ### Source 4 — Multiple Sclerosis and Other Hormone-Related Brain Syndromes Ray Peat · Article · 2013 · https://raypeat.com/articles/articles/multiple-sclerosis-hormone-related-brain-syndromes.shtml > It is easier to study the myelin sheath in peripheral nerves, and the electrical activity of a nerve is the most easily studied aspect of its physiology. Certain experiments seemed to indicate a \"jumping\" (saltatory) kind of conduction along the nerve between Schwann cells, and it was argued that the insulating function of the myelin sheath made this kind of conduction possible. This idea has become a standard item in physiology textbooks, and its familiarity leads many people to assume that the presence of myelin sheaths in the brain serves the same \"insulating\" function. > > For a long time it has been known that heat production during nerve conduction reveals a more continuous mode of conduction, that doesn't conform to the idea of an electrical current jumping around an insulator. Even if the myelin functioned primarily to produce \"saltatory conduction\" in peripheral nerves, it isn't clear how this process could function in the brain. I think of the issue of \"saltatory conduction at the nodes of Ranvier\" as another of the fetish ideas that have served to obstruct progress in biology in the United States. A more realistic approach to nerve function can be found in Gilbert Ling's work. Ling has demonstrated in many ways that the ruling dogma of \"cell membrane\" function isn't coherently based on fact. He found that hormones such as progesterone regulate the energetic and structural stability of cells. Many people, unaware of his work, have felt that it was necessary to argue against the idea that there are anesthetic steroids with generalized protective functions, because of their commitment to a textbook dogma of \"cell membrane\" physiology. > > I think the myelinating cells do have relevance to nerve conduction, but I don't think they serve primarily as electrical insulators. If the adrenal cortex were inside the heart, it would be obvious to ask whether its hormones aren't important for the heart's function. Since the oligodendrocytes are steroid-synthesizers, it seems obvious to ask whether their production of pregnenolone in response to stress or fatigue isn't relevant to the conduction processes of the nerves they surround. > > ## OLD AGE > > A biologist friend of mine who was about 85 became very senile. His wife started giving him thyroid, progesterone, DHEA and pregnenolone, and within a few days his mental clarity had returned. ### Source 5 — Glossary Ray Peat · Glossary > Myelination > > Myelin is a multilayered enclosure of the axons (the long processes) of nerve cells, composed of proteins and complex lipids, including cholesterol. The layered material is a flat, thin extension of the cytoplasm of the oligodendroglial cells. ### Source 6 — KMUD Herb Doctors — April 18, 2014 (partial recording) Ray Peat · Interview · Apr 18, 2014 > **Caller:** Okay. Thank you so much. > > **Andrew Murray:** You're very welcome. Okay, I think there was another caller on the air. No, okay. The caller's gone. Okay, Dr. Peat, I've got another question for you, and it's about cholesterol. I know you've mentioned in the past that the free, the free, Not three, but a free form of cholesterol is good. And the esterified form is destructive, particularly with reference to Alzheimer's and what goes on in the brain of the Alzheimer's patient. But what causes this cholesterol to become esterified? And how is myelin, which comprises the nerve sheath, and so important to proper nerve signaling, made? > > **Ray Peat:** Sugar and thyroid and progesterone are... And often the limiting factors in making myelin fast enough and sugar in the system in general helps you make cholesterol. Keeping the energy up is necessary to make enough cholesterol. And the cholesterol is a stabilizing factor for every aspect of the cell, cell division. multiplication, ion regulation, and so on. And it happens that the myelin is especially rich in cholesterol. But apparently stress activates enzymes that attach fatty acids to the cholesterol as possibly some kind of adaptive reaction for changing the rate of cholesterol synthesis maybe. Anyway, estrogen is one of the factors that promotes the combination with fatty acids. The fact that so few animals are given a diet low in unsaturated fats, that has influenced the research on trying to explain what the ester form of the cholesterol means. Because when we find that, for example, if you look at an atheroma in a hardening artery, as it begins to form, there's only a little of the ester form of cholesterol. But as it ages and advances and becomes more destructive to the artery, the concentration of linoleic acid attached to the cholesterol increases progressively with deterioration and aging. And the research just hasn't been interested in looking at animals that are deprived of unsaturated fats to see if they would even form the atherosclerotic plaque at all. Many of the degenerative changes are extremely delayed when animals are made deficient in the so-called essential fatty acids. For example, in relation to diabetes, several experimenters have created... a technical deficiency of essential fatty acids by giving them a diet containing almost no linoleic or arachidonic acid. And then they poison them with the standard chemicals for creating diabetes and they're essentially impervious. They just refuse to get diabetes in the usual conditions. Their pancreas is so resistant. _Generated 2026-07-20 from the Bioenergetic Oracle corpus._