# Estrogen

Category: Hormones

If we named hormones according to their place of origin, as Selye suggested, we could call estrogen folliculin (as Selye did because it is produced abundantly in the ovarian follicle), or adipin, because it is sometimes produced in fat cells. But it can be produced by many…

12 passages · 3 authors · 1997–2021 · Most-cited: [Ray Peat](https://bioenergeticoracle.com/md/voices/ray-peat/index.md)

Canonical page: https://bioenergeticoracle.com/concepts/estrogen

## Synthesis

**Estrogen** is a hormone whose central biological action, according to Ray Peat, is the *interference with oxidative metabolism*, reducing cellular energy to turn on a primitive type of growth. [Source 8] Peat argued that estrogen's effect mimics the shock phase of the stress reaction, acting to decrease tissue oxygenation and shift cells toward a more primitive, water-logged state conducive to division. [Source 2, 8] He emphasized that estrogen is not simply "the female hormone," as it is produced in both sexes, can be synthesized in fat cells and the testicles, and its excess can even produce **hirsutism** and other masculine traits by overstimulating the adrenal glands. [Source 1, 8, 9] Georgi Dinkov has extended this view, describing estrogen as a signal of environmental distress—starvation, stress, or cold—that turns on metabolic switches associated with disease, including the inhibition of glucose oxidation and the stimulation of fat synthesis. [Source 11]

The hormone's mechanism is rooted in a profound disruption of cellular energetics and structure. Peat proposed that estrogen's biological effects result from its direct action on **cell water**, causing it to become more like bulk, high-dielectric water, a state associated with fatigue and aging. [Source 12] This hydration shift is linked to the uptake of water and loss of potassium, which Peat considered the simplest reaction a cell is capable of, underlying the coherent activation of processes from chromosomes to the cytoskeleton. [Source 9] Estrogen *steals oxygen from mitochondria*, promoting **lactic acid** formation and a shift toward inefficient glycolysis, while also stimulating the synthesis of porphyrins and the enzyme heme oxygenase, which generates carbon monoxide. [Source 1, 6] This metabolic pattern, characterized by increased lactate and ammonia, is analogous to tumor metabolism and is opposed by thyroid hormone, which promotes oxygen delivery and cellular energy. [Source 8, 12]

Peat consistently framed estrogen as a central mediator of degeneration and disease, directly contradicting claims of its protective effects. He noted that estrogen structurally weakens joint tissues, aggravating **osteoarthritis**, and that it retards bone growth rather than preventing osteoporosis, with young women having thinner bones than men due to estrogen's early inhibition of bone formation. [Source 2, 5] In the cardiovascular system, estrogen increases the tendency for blood clot formation and vascular spasms, and the famous Framingham study found its use increased heart attacks by 50% and strokes by 100%. [Source 2] Peat argued that the belief in estrogen's heart protection is based on the isolated, out-of-context observation that it raises the HDL/LDL ratio, a change also associated with a higher incidence of cancer. [Source 2] He further identified estrogen as deeply involved in carcinogenesis, not primarily through direct DNA damage, but by disrupting the **mitotic apparatus** and causing defective cell division, while simultaneously protecting aberrant cells through the antioxidant functions of carbon dioxide and biliverdin. [Source 6]

The activity and toxicity of estrogen are amplified by dietary context and opposed by a network of protective substances. Peat highlighted that the accumulation of **polyunsaturated fatty acids** in tissues promotes estrogen's action in a cumulative, self-accelerating manner. [Source 7, 10] The body possesses multiple antiestrogenic systems, including thyroid, progesterone, testosterone, and various detoxification pathways like sulfation and glucuronidation. [Source 9] Danny Roddy has synthesized this by noting that **progesterone** supports oxidative energy and opposes all of estrogen's effects, while estrogen has an inverse relationship with this "real" feminizing hormone, and is itself increased by stress, low thyroid, and inflammation. [Source 3, 4] Peat maintained that the varied, specific outcomes of estrogenic stimulation—whether feminization or masculinization, growth or tumefaction—are determined not by estrogen itself, but by the organism's resources and the effectiveness of these defensive, neutralizing systems. [Source 9]

## People also ask

### How does estrogen disrupt cellular energy production?

Peat argued that estrogen interferes with oxidative metabolism by stealing oxygen from mitochondria, promoting lactic acid formation and a shift toward inefficient glycolysis, which reduces overall cellular energy.

### Why did Peat believe estrogen is not protective for bones and joints?

Peat noted that estrogen structurally weakens joint tissues and retards bone growth, with young women having thinner bones than men due to estrogen's early inhibition of bone formation, contradicting claims of protection against osteoporosis.

### What substances oppose estrogen's effects in the body?

The corpus describes multiple antiestrogenic systems including thyroid, progesterone, and testosterone, with progesterone specifically supporting oxidative energy and opposing all of estrogen's effects.

## Related concepts

- [Adrenaline](https://bioenergeticoracle.com/md/concepts/adrenaline/index.md)
- [Albumin](https://bioenergeticoracle.com/md/concepts/albumin/index.md)
- [Aldosterone](https://bioenergeticoracle.com/md/concepts/aldosterone/index.md)
- [Anemia](https://bioenergeticoracle.com/md/concepts/anemia/index.md)
- [Dehydroepiandrosterone (DHEA)](https://bioenergeticoracle.com/md/concepts/dehydroepiandrosterone-dhea/index.md)
- [Endotoxin (Lipopolysaccharide, LPS)](https://bioenergeticoracle.com/md/concepts/endotoxin-lipopolysaccharide-lps/index.md)

## Cited passages

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

### Source 1 — Glossary

Ray Peat · Glossary

> Estrogen
>
> If we named hormones according to their place of origin, as Selye suggested, we could call estrogen folliculin (as Selye did because it is produced abundantly in the ovarian follicle), or adipin, because it is sometimes produced in fat cells. But it can be produced by many cells when they are under stress, and it seems to be normal for some to be produced in the testicle.
>
> Estrogen is the hormone for beginnings, a sort of biochemical eraser which can eliminate recently recorded information, restoring the underlying primitive capacity for growth. When we are threatened, by injury or aging, we need the capacity for renewal of ce
>
> Estrogen steals oxygen from mitochondria, shifting patterns of growth and adaptation.
>
> It has recently been demonstrated that estrogen stimulates the adrenal glands, independently of the pituitary's ACTH. This can increase the production of androgens, leading to hirsutism, and other male traits, including anabolic effects.

### Source 2 — From PMS to Menopause: Female Hormones in Context

Ray Peat · Book · 1997

> **Ray Peat:** Studies of both animals and humans show that estrogen contributes to a variety of inflammatory degenerative diseases, and one condition known to be aggravated by estrogen is osteoarthritis. Osteoarthritis is sometimes referred to as a matter of "wear" of the joints, but estrogen's contribution seems to be that it structurally weakens the joint tissues, after binding to estrogen-sensitive receptors. This research should be kept in mind when listening to the claims about its "protecting the bones." Other studies have implicated estrogen in other types of arthritis. Several years ago it was noticed that estrogen treatment caused changes in the types and amounts of fat carried in the blood. Ordinarily, unexpected changes caused by drugs are treated as abnormalities, and bring the drug into question. But with estrogen, the situation is different: Recently, a reviewer noted that estrogen alters the triglyceride (simple fat) levels in the blood, but dismissed the change as "probably benign." In the case of cholesterol, the abnormality was interpreted as a virtue. Estrogen increased the ratio of HDL (high density lipoprotein--"good"-- cholesterol) to LDL (low density lipoprotein-"bad"--cholesterol). In other situations, a high ratio of HDL to LDL has been found to be associated with a lower incidence of heart attacks (but a higher incidence of cancer), and this single trait has been considered alone, out of context, to allow many people to claim that estrogen "protects against heart attacks," since it shifts that indicator in the direction associated with fewer heart attacks. But estrogen also does many things that are more directly associated with heart attacks: It increases the tendency to form blood clots, and it increases the tendency of blood vessels to go into spasm during stress (synergizing with adrenalin). When men were given estrogen following a heart attack, it was found to increase--rather than decrease--the risk of another heart attack.

### Source 3 — The Peat Whisperer

Danny Roddy · Book · 2012

> ### Estrogen
>
> **Danny Roddy:** - While often referred to as “the female hormone,” estrogen is found in both sexes and is increased in malnutrition and stress. Hans Selye called estrogen “the shock hormone” because of its ability to mimic the first stage of stress. Estrogen increases energy requirements, while at the same time inhibiting the cell’s ability to produce energy. Glycolysis - A deficiency of carbon dioxide (or damaged mitochondria) inhibits the cell’s utilization of oxygen and results in glycolysis; a drastically less efficient way to obtain energy producing less carbon dioxide and less energy. Metabolic Rate - The metabolic rate can be determined by the amount of water and calories disposed of in a day. Two other indicators are pulse rate and body temperature. Those with low metabolic rates often have cold extremities (hands, feet, nose, genitals) and a low pulse rate (~60s and 70s). The metabolic rate is heavily influenced by thyroid hormone, but paradoxically can be falsely elevated by numerous adaptive stress hormones. Mitochondria - Structure of the cell where energy is produced. Oxidative Metabolism - A highly efficient way of producing energy. Oxidation refers to the mitochondrial use of oxygen to produce energy (ATP) and carbon dioxide (CO2). Parathyroid Hormone (PTH) - Calcium in the body is monitored by the quadruple redundancy of the parathyroid glands. When calcium intake (or absorption) is inadequate, the parathyroid glands release parathyroid hormone (PTH) to mobilize calcium from bones. PTH is inflammatory, increases serotonin, and influences numerous other adaptive stress hormones. Pregnenolone - Pregnenolone is produced from active thyroid hormone (T3), cholesterol, and vitamin A in the mitochondria of the cell. It functions as a pre-hormone to which all other steroid hormones are broken down from. Progesterone - Progesterone is the prominent “female” hormone in the body, although it is found (and important) in both sexes.

### Source 4 — The Peat Whisperer

Danny Roddy · Book · 2012

> ### Estrogen
>
> **Danny Roddy:** Estrogen has been labeled “the female hormone,” yet its ability to increase adrenal androgens,28 mimic the first phase of the stress reaction, and promote numerous male characteristics, 29,30 suggest otherwise. While women normally have higher levels than males, malnutrition, stress, low thyroid, and inflammation can greatly influence estrogen levels in both sexes.31,32 When blood sugar runs low, adrenaline is released to mobilize additional glucose from the liver (glycogen). If glycogen is low or has been depleted, fuel requirements will be met by releasing free fatty acids as a backup fuel, while glucose will be provided by cortisol’s breakdown of protein. Along with a de-energized liver (glycogen deficient), which normally detoxifies all of the estrogen in the body, the release of free fatty acids can be broken down into proinflammatory prostaglandins activating the aromatase enzyme (creates new estrogen). 33 Estrogen has an inverse relationship with progesterone, which can be considered the “real” feminizing hormone. Whereas estrogen wastes nutrients,32 causes deranged glucose metabolism,35,36 inhibits the production of thyroid hormones (stimulates thyroglobulin, but inhibits its breakdown),37 increases serotonin,38 and can increase prolactin;39 progesterone has all of the opposite effects.40,41

### Source 5 — From PMS to Menopause: Female Hormones in Context

Ray Peat · Book · 1997

> **Ray Peat:** Poisoning by cyanide, or oxygen deprivation, can increase the retention of calcium by tissue, and since an immediate effect of estrogen is to decrease the oxygenation of tissue, I see estrogen's effect on calcium metabolism as analogous to its effect on iron: In stress,organisms absorb calcium and iron. In dying cells, both calcium and iron tend to be deposited together. Estrogen has its place in normal growth and development, but the people who advocate its use as a supplement seem to have no respect for the complexity of its relation to the developing organism. In young animals, estrogen retards the growth of cartilage. Physicians sometimes give estrogen to tall children, when their parents want their growth to stop, because it does stop bone growth. Estrogen is not an anabolic hormone, like testosterone, which builds up bone and muscle. In fact, it strongly opposes the effects of those hormones. In the polycystic ovary syndrome, an excess of estrogen stimulates the adrenal glands to produce a large amount of the androgenic steroids, probably to balance estrogen in the way progesterone does when the ovaries are functioning properly. These anabolic/androgenic hormones apparently have some of the good effects of progesterone, such as reducing the incidence of cancer, but many women are disturbed by the increased growth of body and facial hair; facial features also tend to be masculinized. In France, progesterone lotions have been in use for several years for reversing some of these effects of the adrenal hormones, and for balancing estrogen. Considering this sort of information, it is very unfortunate for women that the osteoporosis problem is so often seen simply as an opportunity for prescribing estrogen. In some countries, old women don't have a problem with osteoporosis. Shouldn't physicians pay more attention to emulating the factors that prevent osteoporosis, instead of thinking that it is a pharmacological problem?

### Source 6 — Townsend Letter — April 1999

Ray Peat · Newsletter · Apr 1, 1999

> Estrogen promotes lactic acid formation, and promotes porphyrin synthesis, providing the material for forming heme and carbon monoxide. Besides causing porphyria, estrogen causes many other liver diseases, including cholestasis, the failure to release bile; the inhibition of carbon monoxide formation has been found to promote bile flow. Estrogen promotes the formation of the enzyme heme oxygenase, which forms carbon monoxide from heme. Carbon monoxide increases the formation of cortisol, by stimulating ACTH release from the pituitary.
>
> The stress response is self-sustaining on several levels. For example, stress increases the absorption of bacterial endotoxin from the intestine, which increases the estrogen level and synergizes with biliverdin and cortisol. While estrogen does cause direct DNA damage, its clearest effect in carcinogenesis is on the cytoskeleton which regulates cell division, and defective cell division, rather than "gene mutation," is one of the important steps in the progression of cancer (Rubin, Duesberg). Cancer cells are protected against the body's ability to destroy them, by the antioxidant functions of carbon dioxide and biliverdin and simultaneously destabilizing normal cellular phenotypes.
>
> The multilevel physiological nature of cancer calls for a multilevel physiological approach to its prevention and cure. This would include antiestrogen regimes, antiinflammatory and antihistamine factors (histamine interacts closely with nitric oxide and carbon monoxide), adequate nutrition, carbon dioxide, and specific anti-carbon monoxide therapies (such as light, alcohol, and possibly the minerals which convert porphyrin into compounds that inhibit the production of carbon monoxide), and methods to decrease nitric oxide formation and to restrain cortisol production, since these promote the formation of carbon monoxide. One of the most interesting approaches to inhibiting carbon monoxide production is to use vitamin B12, as hydroxocobalamin, as an antidote to nitric oxide, preventing the nitric oxide from stimulating the formation of heme oxygenase. Wherever carbon monoxide mediates a biological malfunction, as in acquired immunodeficiency, Alzheimer's disease, and cancer, vitamin B12 seems to have a place as a detoxicant. Progesterone and thyroid have several desirable properties that make them generally useful in cancer prevention and therapy. The shorter-chain saturated fatty acids contained in coconut oil have several beneficial effects.

### Source 7 — Natural Estrogens

Ray Peat · Article · 2008 · https://raypeat.com/articles/articles/natural-estrogens.shtml

> The accumulation of the “essential fatty acids,” the polyunsaturated oils, in the tissues promotes the action of estrogen in a variety of ways, and this effect of diet tends to be cumulative, and to be self-accelerating.
>
> Science is a method that helps us to avoid believing things that are wrong, but there is a distinct herd instinct among people who “work in science,” which makes it easy to believe whatever sounds plausible, if a lot of other people are saying it is true. This is just as evident in physics as it is in medicine. Sometimes powerful economic interests help people to change their beliefs, for example as the insurance industry helped to convince the public of the dangers of smoking. Two of the biggest industries in the world, the estrogen industry and the soy bean industry, spend vast amounts of money helping people to believe certain plausible-sounding things that help them sell their products. Sometimes they can achieve great things just by naming the substance.
>
> Estrogenicity can be defined most simply as “acting the way estrogen does,” (originally, the term “estrogen” meant “producing estrus,” the female readiness to mate) and since our natural estrogen does many things, the definition is often, for practicality, based on the rapid changes produced in certain female organs by estradiol, specifically, the enlargement of the uterus by first taking up a large amount of water, and secondarily by the multiplication of cells and the production of specific proteins. A similar process occurring in the breast is also recognized as an important feature of the estrogen reaction, but as we try to define just what “estrogenicity” is, we see that there is something deeply wrong with this method of defining a hormone, because we are constantly learning more about the actions of estrogen, or of a specific form of the molecule. Calling it “the female hormone” distracted attention from its many functions in the male, and led to great confusion about its antifertility actions and its other toxicities.

### Source 8 — From PMS to Menopause: Female Hormones in Context

Ray Peat · Book · 1997

> **Ray Peat:** I considered many ways in which estrogen might be a cancer hormone, including its promotion of the oxygen-wasting age pigment, and its stimulation of porphyrin metabolism, since some researchers had seen an association between cancer and porphyrins. At that time, it wasn't known that the breakdown of the porphyrin, heme, produced carbon monoxide. But beyond the possibility that estrogen was deeply involved in the nature of cancer, I felt that its biological role had to do with its interference with oxidative metabolism. Selye had characterized estrogen's effect as "like the shock phase of the stress reaction." Estrogen does act in conjunction with histamine, and histamine alone tends to cause circulatory collapse by allowing fluid to leak out of blood vessels. Lack of oxygen probably relates more generally to the shock reaction than does histamine. The reduction of cellular energy is probably estrogen's central action, and in Warburg's scheme, this would be t he way to turn on cell division and growth. In the absence of oxygen, cells take up water, and when water-logged (even from being placed in a hypotonic fluid), they begin to divide. Since some pituitary hormones (including prolactin, ACTH, and the gonadotropins) cause cell division in their "target organs," I suspect that they function much the way estrogen does, except that they have different affinities and so act on different types of cell. The thyroid hormone is opposed to estrogen in many ways, promoting the delivery of oxygen to tissues, reducing tissue edema, etc. It is also antagonistic to some of the pituitary hormones, especially prolactin. In bones, prolactin causes osteoporosis, estrogen blocks bone forming processes as well as bone destroying processes, while thyroid increases bone turnover, activating both formation and removal.

### Source 9 — Townsend Letter — March 2000

Ray Peat · Newsletter · Mar 1, 2000

> Estrogen, as an easy derivative of testosterone, is deeply involved in the establishment of masculine features; even in mature women, estrogen excess (progesterone deficiency) can produce hirsutism and other masculine traits when it overstimulates the adrenal glands. As a goad (the term estrogen is based on estrus, gadfly, intense stimulus, goad), estrogen initiates activity in cells and systems; depending on the organism’s resources, that stimulus will be restrained before it gets out of control.
>
> Does the specific outcome of stimulation take its direction from estrogen, or rather from the ways in which estrogen is neutralized and detoxified? There are many antiestrogenic systems—thyroid, progesterone, testosterone, sulfation, methylation, glucuronidation, antiinflammatory factors, etc.—and the varied, specific nature of the organism’s response to stimulation is probably sufficient to account for the different outcomes, such as masculinity or femininity, tumefaction or growth, alertness or mania.
>
> How specific is estrogenic stimulation itself? Asphyxia, radiation injury, vitamin deficiencies, and other harmful stimuli, closely mimic the estrogenic excitation/shock response (Boling, et al., 1939; Mandl and Zuckerman, 1956; Biskind, 1946). Estrogenic activation, with the uptake of water and the loss of potassium (relative to intracellular sodium), is probably the simplest reaction a cell is capable of, and any specificity that can be found in the process is the result of pre-existing cellular conditions, or of defensive reactions of the organism. Depending on its place in the life of an individual, estrogen can either masculinize or feminize, produce breasts or whiskers.
>
> The similarity of radiation injury to estrogenic stimulation has led to studies showing some radiation protection from progesterone; similar protective actions of progesterone can be seen for other types of injury. Thyroid, and other antiestrogens, also have a wide spectrum of protective actions, against radiation, asphyxia, carcinogens, etc.
>
> I think the only way to approach the general nature of cellular excitation is to see it in terms of the basic properties of the living material.

### Source 10 — Natural Estrogens

Ray Peat · Article · 2008 · https://raypeat.com/articles/articles/natural-estrogens.shtml

> Calling it “the female hormone” distracted attention from its many functions in the male, and led to great confusion about its antifertility actions and its other toxicities. Many biologists called it “folliculin,” because of the ovarian follicle's significant role in its production, but the pharmaceutical industry succeeded in naming it in relation to one of its functions, and then in extending that idea of it as “the producer of female receptivity” to the even more misleading idea that it is “the female hormone.” But when people speak about the “estrogenicity” of a substance, they mean that it has properties that parallel those of “folliculin,” the particular group of ovarian hormones that includes estradiol, estrone, and estriol.
>
> Over the last 100 years, thousands of publications about estrogen's toxicity have created a slight resistance to the consumption of the major estrogen products. One ploy to overcoming this resistance is to call certain products “natural estrogen,” as distinguished from “synthetic estrogens.” The three main estrogens in our bodies are estradiol, estrone, and estriol, though there are many other minor variants on the basic molecule. These three estrogens, singly or in combinations, are being sold as natural estrogens, with their virtues explained in various ways. Implicit in many of these explanations, is the idea that these are safer than synthetics. They are sometimes contrasted to the “horse estrogen” in Premarin, as if they are better because they are like the estrogens that people produce. But it was exactly the normal human estrogens, produced by the ovaries, that led to the basic discoveries about the toxicity of estrogen, its ability to produce cancer in any organ, to cause seizures, blood clots, birth defects, accelerated aging, etc. Although I would suppose that a hormone from a horse might be “more natural” for a person's body than a hormone from a plant, the word “natural” as used in the phrases “natural food store,” or “natural medicine,” has come to be associated strongly with things derived from plants. The health food industry, now largely taken over by giant corporations to sell products that weren't producing as much revenue when sold in supermarkets and drugstores, has helped to create a culture in which botanical products are thought to be especially good and safe.

### Source 11 — 001 Pro-Metabolic Hormones with Georgi Dinkov

Georgi Dinkov · Interview · Feb 27, 2021 · https://open.spotify.com/episode/55VW3kJaaOjlJrxlkh7XFF

> **Georgi Dinkov:** And if you look at some of the older publications, they were pretty open about the fact that estrogen stimulates cellular proliferation, estrogen stimulates the oxidation of fat, estrogen inhibits the oxidation of glucose, estrogen stimulates the synthesis of fat, even from glucose, right? So all of these things that are essentially the characteristics of the deranged metabolic state that the first state is diabetic, right? And then eventually proceeds to fibrosis and into cancer. It looks like estrogen is capable of starting, or at least turning on all of these light switches that are associated with a disease state, with a sickness state. And if you look, so if you start looking at some publications that talk about estrogen, especially the older ones, they're actually not shy about drawing parallels between estrogen and other hormones. In other words, what works like estrogen and what works unlike estrogen. In other words, in an opposite fashion. And it has been known to mainstream medicine since the 1950s that androgenic hormones work in ways opposite to estrogen. Progesterone works in pathways opposite to estrogen. However, cortisol... aldosterone, prolactin, serotonin, a number of other, you can call mediators and or, I'm sorry, hormones or neurotransmitters because prolactin and serotonin are technically, serotonin is a neurotransmitter, not necessarily a hormone. But if we think of hormone as a messenger substance, then all of them are hormones. And then all the publications said, look, estrogen is really a mediator, a signal from the environment that things are not going well, that you're either starving, you're under stress, food is not abundant, You know, temperature is low. You're living in some kind of a, I don't know, you know, a very cold climate with a lot of snow. There's no there's no easy availability of food. There's no easy availability really of sugar.

### Source 12 — Fatigue, Aging, and Recuperation

Ray Peat · Article · 2013

> Estrogen lowers stimulation threshold in the gallbladder, as it does in the brain. Part of its excitatory action might be the result of increased hypotonic tissue water, but its effects on nerve thresholds are practically instantaneous.
>
> In 1971 and '72, I gave some of the reasons for thinking that estrogen's biological effects result from its direct effects on cell water, causing it to become more like bulk (high dielectric) water. For example, NMR (spin echo) of estrogen treated uterus and of the uterus from an old animal were closer to bulk water than that of a young animal. Estrogen, like fatigue or excessive oxygen, slows nerve conduction.
>
> Lactic acid production increases with fatigue, aging, hypothyroidism, estrogen excess, and other inefficient biological states. Its presence, when oxygen is available, indicates that something is interfering with efficient oxidative energy metabolism. Ammonia, free fatty acids, and various inflammatory cytokines are also likely to increase in those stress states.
>
> A dangerously high level of ammonia in the blood (hyperammonemia) can be produced by exhaustive exercise, but also by hyperbaric oxygen (or a high concentration of oxygen), by high estrogen, and by hypothyroidism. It tends to be associated with an excess of lactic acid, probably because ammonia stimulates glycolysis. Excess oxygen, like hypothyroidism, is equivalent to hyperventilation, in producing an abnormally low level of carbon dioxide in the blood. The Krebs cycle, during stress, is limited by the unavailability of carbon dioxide. These factors result in the waste of glucose, turning it into lactic acid, rather than carbon dioxide and energy. In these ways, the metabolism of fatigued muscle (or any cell under stress) is similar to tumor metabolism.
>
> Hyperammonemia disturbs excitatory processes, and can cause seizures, as well as stupor, and is probably involved in mania and depression. Lithium happens to complex electronically with ammonia, and I think that accounts for some of its therapeutic effects, but carbon dioxide is the main physiological factor in the elimination of ammonia, since it combines with it to form urea. The changes in cell water in the excited/fatigued state represent an increase in the water's structural temperature, and that would imply that less carbon dioxide could remain dissolved during excitation.

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