# Alzheimer's and Dementia

Category: Conditions

Also known as: Alzheimer's, dementia, neurodegeneration, cognitive decline

Alzheimer's disease and related dementias are fundamentally disorders of defective energy metabolism, driven by the accumulation of polyunsaturated fatty acids (PUFAs) and the systemic dysregulation of hormones. Peat argued that the brain's greatly reduced ability to use…

11 passages · 2 authors · 1992–2025 · Most-cited: [Ray Peat](https://bioenergeticoracle.com/md/voices/ray-peat/index.md)

Canonical page: https://bioenergeticoracle.com/concepts/alzheimer-s-and-dementia

## Synthesis

**Alzheimer's disease** and related dementias are fundamentally disorders of *defective energy metabolism*, driven by the accumulation of **polyunsaturated fatty acids (PUFAs)** and the systemic dysregulation of hormones. [Source 1, 8] Peat argued that the brain's greatly reduced ability to use glucose is a central feature, a condition exacerbated by estrogen's effect of shifting metabolism away from glucose oxidation and decreasing **carbon dioxide** production. [Source 1] This metabolic suppression creates a state of physiological hibernation, where serotonin reduces energy expenditure, eliminating all brain functions except those needed for simple survival. [Source 3] The structural hallmarks of the disease—amyloid plaques and fibrillary tangles—are downstream consequences of this energetic failure, with the "beta pleated sheet" structure of amyloids being directly related to binding bacterial endotoxin (LPS), linking the pathology to an out-of-control innate immune response. [Source 1, 4]

The hormonal profile of Alzheimer's is characterized by a deficiency of protective steroids and an excess of catabolic ones. Peat consistently identified that when **pregnenolone** is inadequate, **cortisol** is over-produced, and when **progesterone** is deficient, estrogen's neurotoxic effects are largely unopposed. [Source 4, 11] This imbalance is compounded by hypothyroidism, which itself promotes estrogen synthesis even in fat cells. [Source 4] The enzyme *beta-glucuronidase* is activated in inflamed tissue, releasing estrogen within cells and activating further neurotoxic processes. [Source 10, 11] Estrogen exposure exacerbates all the changes leading to dementia, including increased vascular leakiness and the production of acute phase proteins, which Peat cited as the reason for the much higher incidence of Alzheimer's disease in women. [Source 1] Observational data showed that demented women had a much higher incidence of hysterectomy and a lower rate of progestogen use, while former estrogen users had 155% the rate of dementia compared to controls. [Source 5, 7]

The accumulation of specific toxins and the loss of protective factors drive the physical degeneration. Peat pointed to the accumulation of **iron** and **calcium** with aging, both of which promote excitatory damage and mitochondrial calcification. [Source 10] Roddy noted that neuroprostanes and isoprostanes—breakdown products from omega-3 fats—and acrolein are found in higher levels in Alzheimer's brains, alongside iron accumulation. [Source 6] The structural protein *transthyretin*, which normally carries vitamin A and thyroid hormone, becomes glycosylated and forms amyloid deposits when there is a deficiency of protective carbon dioxide. [Source 10] This glycosylation is a spontaneous process that occurs when the protein's amino groups are not protected by carbamino groups formed from carbon dioxide, directly linking the respiratory defect to the formation of plaques. [Source 10] The variant form of apolipoprotein E (epsilon 4 allele), associated with Alzheimer's risk, is involved in cholesterol delivery for pregnenolone synthesis, a process regulated by thyroid. [Source 4, 11]

Therapeutic intervention, in Peat's framework, centers on restoring oxidative energy metabolism and blocking inflammatory cascades. He suggested that improving energy production, for example by providing ketones as an alternative fuel, while reducing stress hormones, could replace defensive reactions with restorative nerve processes. [Source 3] Substances like **aspirin**, by blocking prostaglandin production, help retard or prevent neurodegenerative diseases. [Source 2] **Methylene blue** and **thyroid** were described as working similarly to help cells function properly by restoring their metabolic capacity. [Source 2] A comprehensive protective program would include the supplementation of pregnenolone and progesterone to oppose cortisol and estrogen, the use of vitamin E and magnesium for their protective effects, and the provision of short and medium-chain saturated fatty acids as a safe energy source that also has hormone-like effects. [Source 9] Since the innate immune system should be able to inactivate the prion-like proteins if the conditions amplifying inflammation are removed, Peat held that these conditions can be avoided and even reversed by systematically reversing the processes that amplify inflammation. [Source 1]

## People also ask

### How does estrogen contribute to Alzheimer's disease according to Peat?

Peat argued that estrogen shifts brain metabolism away from glucose oxidation, reduces protective carbon dioxide, and promotes vascular leakiness and inflammatory proteins, which he cited as the reason for the higher incidence of Alzheimer's in women.

### Why did Peat consider carbon dioxide deficiency central to plaque formation?

The entry describes that without sufficient carbon dioxide, the protein transthyretin becomes glycosylated and forms amyloid deposits because its amino groups are not protected by carbamino groups, directly linking the respiratory defect to plaque development.

### What substances did Peat suggest for restoring brain energy metabolism in dementia?

The corpus notes that Peat proposed using ketones as an alternative fuel, along with aspirin, methylene blue, thyroid, pregnenolone, progesterone, vitamin E, magnesium, and short-chain saturated fats to restore oxidative metabolism and block inflammation.

## Related concepts

- [Pregnenolone](https://bioenergeticoracle.com/md/concepts/pregnenolone/index.md)
- [Raw carrot salad](https://bioenergeticoracle.com/md/concepts/raw-carrot-salad/index.md)
- [Age Pigment (Lipofuscin)](https://bioenergeticoracle.com/md/concepts/age-pigment-lipofuscin/index.md)
- [Albumin](https://bioenergeticoracle.com/md/concepts/albumin/index.md)
- [Amyloid](https://bioenergeticoracle.com/md/concepts/amyloid/index.md)
- [Anemia](https://bioenergeticoracle.com/md/concepts/anemia/index.md)

## Cited passages

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

### Source 1 — BSE - mad cow - scrapie, etc.: Stimulated amyloid degeneration and the toxic fats

Ray Peat · Article · 2007 · https://raypeat.com/articles/aging/madcow.shtml

> According to a 1989 study (Laura Manuelidis, neuropathology department at Yale), 13% of the people who had died from “Alzheimer’s disease” actually had CJD. Between 1979 and 2000, the number of people dying annually from Alzheimer’s disease increased 50-fold. Very competent neuropathologists differ radically in their descriptions of the dementia epidemic.
>
> By some tests, the “prion” resembles the LPS endotoxin. One of the interesting developments of the prion theory is that a particular structure that appears when the prion becomes toxic, the “beta pleated sheet,” is also a feature of most of the normal proteins that can form amyloid, and that this structure is directly related to binding and eliminating the bacterial LPS. If the prion theory is correct about the conversion of a normal protein into the pleated sheet, it isn’t necessarily correct about the incurability of the condition. The innate immune system should be able to inactivate the prion just as it does the bacterial endotoxin, if we remove the conditions that cause the innate immune reaction to amplify the inflammation beyond control.
>
> In the prion diseases, the severely damaged brain appears to have a “pathological overactivity” of the serotonergic systems (Fraser, et al., 2003). This is an interesting parallel to Alzheimer’s disease, since it has been known for several years that the blood platelets have an increased tendency to release serotonin in that more common form of dementia. Serotonin itself is toxic to nerves, and is part of the adaptive system that gets out of control during prolonged inflammation. Serotonin is an important activator of the phospholipases.
>
> The modification of proteins’ structure by glycosylation is involved in the development of the toxic form of the “prionic” protein, as well as in all the degenerative processes of aging. Until the ability to use sugar is impaired, cells produce enough carbon dioxide to protect proteins against random glycation, but with each exposure to free polyunsaturated fatty acids, the ability to use glucose is damaged. In the dementias, the brain has a greatly reduced ability to use glucose.
>
> One of estrogen’s central effects is to shift metabolism away from the oxidation of glucose, decreasing carbon dioxide production.

### Source 2 — Dr. Ray Peat | DNA, OBE & Dejavu, Vision, Liver, Ions, Cancer, Ray's parents and much more

Ray Peat · Interview · Jun 3, 2024 · https://open.spotify.com/episode/1V7nHSyImpegsLdJ9xJIiW

> **Ray Peat:** defense. The cholesterol is combined in an ester with the polyunsaturated fats. And so the medical industry has tried to put the blame on cholesterol. That whole attempt of the body to
>
> **Primitive Initiative:** Okay, so then consuming more cholesterol for somebody who's demented or has Alzheimer's would be beneficial, right?
>
> **Ray Peat:** So aspirin, for example, by blocking prostaglandin production, helps to retard or prevent neurodegenerative diseases like
>
> **Primitive Initiative:** dementia and Parkinson's. I see. And so you would use vitamin E then to kind of help stabilize the damage you've done in the past, but vitamin E doesn't necessarily make it safe to keep eating PUFA, right? No. Wow. Okay, so I see that marketed a lot. It's like, oh, you can have your french fries at whatever restaurant you want as long as you got your bottle of vitamin E. Doesn't sound like an option. Well, it's an option, but not one you might want to go with. So, I don't remember, I don't want to put words in your mouth, but... And methylene blue seemed to have some positive effects on people with dementia and Alzheimer's. So how is that exactly working? Is that just helping their metabolism and their cells function, almost forcing their cells to function the way that they should?

### Source 3 — Serotonin: Effects in disease, aging and inflammation

Ray Peat · Article · 2015 · https://raypeat.com/articles/articles/serotonin-disease-aging-inflammation.shtml

> The brains of people with Alzheimer's disease have a decreased ability to metabolize glucose, and high cortisol contributes to the altered glucose metabolism, and to the destruction of nerve cells. People with Cloninger's "harm avoidance" personality trait, which is closely associated with serotonin (Hansenne, et al., 1999), are more likely to develop dementia (Clément, et al., 2010). These observations are consistent with the stress-susceptibility of people with high serotonin exposure, and to the effects of cortisol on nerves and glucose-derived energy production.
>
> Researchers in Brasil have suggested that the serotonergic system facilitates conditioned fear, while inhibiting the fight or flight reaction, and that this can protectively limit the stress response (Graeff, et al., 1996). "5HT systems reduce the impact of impending or actual aversive events. Anticipation of an aversive event is associated with anxiety and this motivates avoidance behaviour" (Deakin, 1990). In a stressful situation, the serotonergic nerves can prevent ulcers. In other contexts, though, increased serotonin can cause ulcers.
>
> The protective, defensive reactions involving serotonin's blocking of certain types of reaction to ordinary stresses, are similar to the effects of serotonin in hibernation and in Alzheimer's disease (Mamelak, 1997; Heininger, 2000; Perry, et al., 2002). In those extreme conditions, serotonin reduces energy expenditure, eliminating all brain functions except those needed for simple survival. These parallels suggest that improving energy production, for example by providing ketones as an alternative energy source, while reducing the stress hormones, might be able to replace the defensive reactions with restorative adaptive nerve processes, preventing or reversing Alzheimer's disease.
>
> One of the factors promoting excess cortisol production is intestinal irritation, causing absorption of endotoxin and serotonin. Fermentable fibers (including pectins and fructooligosaccharides) support the formation of bacterial toxins, and can cause animals to become anxious and aggressive. Fed to horses, some types of fiber increase the amount of serotonin circulating in the blood. Grains, beans, and other seeds contain fermentable fibers that can promote intestinal irritation.
>
> The liver has several ways to detoxify endotoxin and serotonin, but these can fail as a result of poor nutrition and hypothyroidism.
>
> The lung can bind and destroy any excess serotonin that reaches it.

### Source 4 — The problem of Alzheimer's disease as a clue to immortality Part 2

Ray Peat · Article · 2006 · https://raypeat.com/articles/articles/alzheimers2.shtml

> When pregnenolone is inadequate, cortisol is over-produced.
>
> When progesterone is deficient, estrogen's effect is largely unopposed.
>
> When both thyroid and progesterone are deficient, even fat cells synthesize estrogen.
>
> ## THE NATURE OF ALZHEIMER'S DISEASE
>
> Although Alzheimer's disease until recently referred to a certain type of organic dementia occurring in people in their thirties, forties and fifties (presenile dementia), structural similarities seen in senile dementia have caused the term to lose its original meaning. Alzheimer's sclerosis of blood vessels, and even the death of nerve cells, are sometimes neglected in favor of the more stylish ideas, emphasizing certain proteins that cause the tangles and plaques. Until recently, the "tangles" were commonly interpreted as the debris left after the death of a cell, rather than as one of the processes causing the death of the cell. Alzheimer-type dementia is different from other dementias, but it overlaps with them, and with age-related and stress-related changes in other organs.
>
> Physical signs (seen at autopsy) of AD:
>
> 1. Death of neurons (increase of glial cells)
> 2. Amyloid plaques (extracellular), associated with a particular variant of apolipoprotein E, the epsilon 4 allele
> 3. Fibrillary tangles (intracellular, or remaining after the rest of the cell has disappeared)
> 4. Amyloid in blood vessels.
>
> Functional and biochemical observations:
>
> 1. The mitochondrial energy problem, cytochrome oxidase and its regulation; body temperature/pulse-rate cycle disturbance; lipid peroxidation; respiratory defect; altered amino acid uptake; memory impairment; dominance of the excitatory systems vs. the inhibitory adenosine/GABA/progesterone /pregnenolone system. Increased calcium uptake, which is associated with lipid peroxidation and cell death. Increased cortisol and DHEA.
> 2. Deposit of abnormal proteins, such as transthyretin-amyloid; albumin binding of PUFA, vs. transport of thyroid and retinol. Beta-glucuronidase increases, depositing estrogen in cells. (A. J. Cross, et al., "Cortical neurochemistry in Alzheimer-type dementia," Chapter 10, pages 153-170 in Aging of the Brain and Alzheimer's Disease, Prog. in Brain Res.

### Source 5 — The problem of Alzheimer's disease as a clue to immortality Part 1

Ray Peat · Article · 2007 · https://raypeat.com/articles/articles/alzheimers.shtml

> Degenerative aging, rather than being "physically derived from the properties of time," seems to be produced situationally, by various types of contamination of our energy supply. Unsaturated fats, interacting with an excess of iron and a deficiency of oxygen or usable energy, redirect our developmental path. The saturated fats, in themselves, seem to have no "signalling" functions, and when they are naturally modified by our desaturating enzymes, the substances produced behave very differently from the plant-derived "eicosanoids." As far as their effects have been observed, it seems that they are adaptive, rather than dysadaptive.
>
> All of the factors that affect the brain of a fetus should be examined in relation to the aging brain. Besides estrogen and fats, I am thinking of oxygen and carbon dioxide, glucose, iron and calcium, cholesterol, progesterone, pregnenolone, DHEA, the endorphins, GABA, thyroid, and vitamin A. An additional factor, endotoxin poisoning, eventually tends to intervene during stress and aging, exacerbating the trend begun under the influence of the other factors.
>
> ## IV. FALSE SIGNALS FROM THE ENVIRONMENT
>
> The environment can be supportive, but it can also divert development from an optimal course. Passively taking whatever you are given, by history and nature, is entropic; choosing intelligently from possible diets, selecting courses of action, will create pattern and reduce entropy. If education contains an element of choice and self-actualization, then the results seen in several Alzheimer's studies could have a significance larger than what has been suggested by the investigators.
>
> A diagnostic bias has been reported to result from the use of standardized tests based on vocabulary, because education increases vocabulary, and tends to cover up the loss of vocabulary that occurs in dementia. In the Framingham study, it was concluded that there was a real association of lower educational level with dementia, but the suggestion was made that self-destructive practices such as smoking were more common among the less educated. The Seattle study of the patients in a health maintenance organization showed a very distinct difference in educational level between the demented and the non-demented, both of whom had roughly similar frequency of prescriptions for estrogen.

### Source 6 — Danny Roddy – Sugar Feeds Our Cells, PUFAs Are Poison, Hormones & A Bioenergetic Concept of Health!

Danny Roddy · Interview · Aug 11, 2025

> **Justin:** This is a good one. And if you don't know, it's no big deal, but it's not about, you know, obviously this, but it kind of ties back into what I think when we talked about PUFAs. But they wanted to know what your thoughts were on the cause of Alzheimer's and dementia. Have you looked much into that?
>
> **Danny Roddy:** Not really, to be honest. Ray has a couple fantastic articles about it and identifying that the neuroprosthenes and isoprosthenes accumulate in the brain, and those are from the omega-3s, and things like acrolein, I think, are repeatedly found to be in higher levels in Alzheimer's brain. And also, there are a few articles that I have in my notes about just generalized hypothyroidism being involved as well. So I think a series of things are happening there, but... I couldn't speak intelligently about them. It's not something I've learned a lot about in this whole process.
>
> **Justin:** Yeah, I wonder if there's an accumulation of iron and PUFA in someone's brain who has Alzheimer's. I wonder if that oxidation is somehow getting into their brain.
>
> **Danny Roddy:** I think there was a lecture I watched. It was some like mainstream institution. It was like UCLA or something. And their finding through some type of imaging was that the Alzheimer's brain had a lot of iron in it. So I don't think that that doesn't sound unreasonable to me.

### Source 7 — From PMS to Menopause: Female Hormones in Context

Ray Peat · Book · 1997

> ### 23. ALZHEIMER'S DISEASE
>
> **Ray Peat:** The results seen in several Alzheimer's studies could have a significance larger than what has been suggested by the investigators. A diagnostic bias has been reported to result from the use of standardized tests based on vocabulary, because education increases vocabulary, and tends to cover up the loss of vocabulary that occurs in dementia. In the Framingham study, it was concluded that there was a real association of lower educational level with dementia, but the suggestion was made that self-destructive practices such as smoking were more common among the less educated. The Seattle study of the patients in a health maintenance organization showed a very distinct difference in educational level between the demented and the non-demented, both of whom had roughly similar frequency of prescriptions for estrogen. The features that seemed important to me, that weren't discussed by the authors, were that the demented women had a much lower rate of progestogen use, and a much higher incidence of hysterectomy, which interferes with natural progesterone production. Although Brenner, et al., in the Seattle study concluded that "this study provides no evidence that estrogen replacement therapy has an effect on the risk of Alzheimer's disease in postmenopausal women," they reported that "Current estrogen use of both the oral and the vaginal routes had odds ratios below 1, while former use of both types yielded odds ratios above1...."(They seem to neglect the fact that Alzheimer's-type disease in old people has a long developmental history, so it is precisely the "former" use that is relevant. 31% of the demented women had formerly used estrogen, and only 20% of the control group. Since estrogen is a brain excitant, present use creates exactly the same sort of effect on verbal fluency and other signs of awareness of the environment that a little cocaine does.

### Source 8 — Life Supporting Substances Its Rain Making Time 2011 07 04

Ray Peat · Interview · Jul 4, 2011 · http://l-i-g-h-t.com/files/rarinmaking-time-life-supporting-substances.mp4

> **Kim Greenhouse:** My mom died in 2008 of Alzheimer's, and I wish I had put it together about the coconut oil and some of the other things that you write about with that. At least the information is out there now for others who have family, friends or associates who are stricken with disease.
>
> **Ray Peat:** My website has two articles on Alzheimer's; and it gives a lot of attention to the role of polyunsaturated fats in causing the brain degeneration. There is another article that covers the role of polyunsaturated fats in scrapie and bovine spongiform encephalitis (mad cow disease). The polyunsaturated fats, I think, have a major role in all of the degenerative brain diseases, including Huntington's, Lou Gehrig's disease and other special types of degeneration.
>
> **Kim Greenhouse:** I know that you have a very different view about taking flax seed oil and DHA. And I'd like you to talk about it, because in the anti-aging industry, it is heavily touted and also by doctors, and even Suzanne Somers in her book "Knock out"; in a lot of her investigative work, she talked to people in the orthomolecular field that are proposing flax seed oil, and fish oils. I want you to share your perspective about them for the public to have a rethinking about it.

### Source 9 — Townsend Letter — August / September 1992

Ray Peat · Article · 1992 · with Richard L. Farr, Ray Peat

> **Ray Peat:** I suspect that the plaques in Alzheimer's disease are the brain's equivalent to the plaques of leucoplakia, or of dandruff, and that the overgrowth of the glial cells is the result of the same tendency of cells to divide rapidly, while the non-dividing neurons accumulate an excess of fibrous proteins that can’t be degraded. In degenerative diseases, the stress- and age-induced accumulation of iron and other mitochondria-toxic material (e.g., calcium, aluminum, and lipid peroxidation products including age pigment) and the failure of detoxifying systems make therapy with ordinary nutritional supplements fairly ineffective. Direct supplementation of the various natural protective substances (or their analogues) in addition to the protective vitamins (especially E) and minerals (especially magnesium) is more appropriate. The supplementation of pregnenolone, etc., will allow dietary vitamin A to be spared for other purposes, including regulation of mitosis, differentiation, and oxidation. GABA-related metabolites, such as GHB, butyric acid, succinic acid, and the butyrobetaines, have multiple protective functions, including promotion of respiration and pregnenolone synthesis, regulating gene expression, and reducing damage from glucocorticoids. DHEA seems to be involved in various regenerative processes, and a deficiency of it is prognostic of increased probability of death from various causes, including cancer, heart disease, and AIDS. Progesterone has the special status of being an essential nerve growth factor, and generally blocks the catabolic actions of the glucocorticoids and estrogen, thereby protecting all tissues, from brain cells to white blood cells. Thyroid hormone protects against stress and supports normal differentiation. Short and medium-chain saturated fatty acids provide a safe source of energy, as well as having hormone-like and adaptogenic effects. The short-chain saturated fatty acids are important in regulating bowel flora.

### Source 10 — Townsend Letter — December 1999

Ray Peat · Newsletter · Dec 1, 1999

> Similarly, when serum bicarbonate decreases, the calcium escapes from its soluble complex, and in effect the available calcium—the forms of calcium which are not bound to bicarbonate—has increased, exactly the opposite of what the Carlson school has argued.
>
> Calcium, which is released into the cytoplasm by the excitotoxins, triggers the release of fatty acids, the activation of nerve and muscle, and the release of a variety of transmitter substances, in a cascade of excitatory processes, but at the same time, it tends to impair mitochondrial metabolism, and progressively tends to accumulate in mitochondria, leading to their calcification death, which is also promoted by the antirespiratory effects of the unsaturated fatty acids and the lipid peroxidation they promote. Iron and calcium both tend to accumulate with aging or stress, and both promote excitatory damage; bicarbonate contributes to keeping iron in its inactive state, and probably has a similar effect against a broad spectrum of excitatory substances. Histamine release, nitric oxide, and carbon monoxide are broadly involved in excitotoxic damage, and carbon dioxide tends to be protective against these, too.
>
> Besides the simple excitotoxic killing of nerve cells, the processes which impair carbon dioxide production set in motion the long degenerative process that ranges from diabetic lacticacidemia to dementia. In Alzheimer’s disease, brain respiratory metabolism is inhibited, creating a carbon dioxide deficiency with an excess of lactic acid and ammonia. Both Alzheimer’s disease and multiple sclerosis involve depressed brain metabolism combined with an inflammatory process. In any inflamed tissue, the enzyme betaglucuronidase is activated, and this enzyme releases estrogen within the irritated cell, activating another sequence of neurotoxic processes.
>
> In Alzheimer’s disease, two other outstanding features are the tangles of microtubular material left where cells have disintegrated, and the amyloid plaques, which often form in extracellular spaces and around blood vessels.
>
> One of the forms of amyloid (amyloid is named for its “starchy” appearance in stained slides) is produced from the normal protein, transthyretin, which carries vitamin A and thyroid hormone, when this protein is “glycosylated,” by the addition of sugar molecules. In this glycosylated form, it resembles a mutant protein, and binds to the extracellular matrix.

### Source 11 — The problem of Alzheimer's disease as a clue to immortality Part 2

Ray Peat · Article · 2006 · https://raypeat.com/articles/articles/alzheimers2.shtml

> Beta-glucuronidase increases, depositing estrogen in cells. (A. J. Cross, et al., "Cortical neurochemistry in Alzheimer-type dementia," Chapter 10, pages 153-170 in Aging of the Brain and Alzheimer's Disease, Prog. in Brain Res. 70, edited by D. F. Swaab, et al., Elsevier, N.Y., 1986. )
> 3. Abnormally phosphorylated (tau) proteins; association with the variant form of Apo E; tau microtubule organizing proteins, microtubules are involved in transporting cholesterol; phosphorylation, by the kinase systems, regulated by PUFA; the intermediate filaments are generally stress-associated.
> 4. ApoE, in cytoplasm, involved in cholesterol delivery for pregnenolone synthesis, as in the adrenal; its expression regulated by thyroid. Regulation of the side-chain cleaving enzymes; regulation of the cholesterol intake and conversion to pregnenolone by the endozepine receptor/GABA receptor, modified by progesterone.
>
> ## AN EXAMPLE OF A REGULATORY PROBLEM
>
> Vegetable oil suppresses the thyroid, increasing estrogen. Estrogen and calcium depolymerize microtubules. Microtubule transport for Apo E, transthyretin, thyroid, and cholesterol for pregnenolone synthesis is disrupted. Transthyretin and Apo E accumulate unused, and deposit in blood vessels, around nerves, and in cytoplasm. Pregnenolone and progesterone deficiency (aggravating thyroid deficiency) causes memory loss, destabilization of nerve cells, failure of myelin formation, and excess cortisol synthesis. Free radicals and calcium cause multiple cell injuries including nerve-death. Estrogen is released by elevated beta-glucuronidase. Imbalances of other steroids, including cortisol and DHEA, develop as cells compensate for pregnenolone deficiency, causing shifts in balance of glial cells. Hypothyroidism, estrogen excess, free unsaturated fats cause increased vascular permeability and brain edema, protein leakage, and alteration of the matrix..
>
> ## VIII: STRUCTURE AS A REGULATORY SYSTEM--AN EMERGING VISION OF PERVASIVE EPIGENESIS
>
> In the introduction I mentioned that membranous regulation and genetic determination should be considered as defunct theories.

_Generated 2026-07-20 from the Bioenergetic Oracle corpus._