# Mitochondria

Category: Metabolism

The structure inside the cell in which energy is produced by respiration is called the mitochondria.

10 passages · 1 author · 2007–2016 · Most-cited: [Ray Peat](https://bioenergeticoracle.com/md/voices/ray-peat/index.md)

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

## Synthesis

**Mitochondria** are the intracellular structures where oxidative energy production occurs, a process fundamentally driven by thyroid hormones. [Source 1, 5] Peat described them as the site where oxygen receives electrons primarily from glucose, creating water and carbon dioxide in the most efficient use of oxygen. [Source 6] Beyond energy production, a very important function of the mitochondrion is **steroid synthesis**, where it converts cholesterol into **pregnenolone** and **progesterone**, which then serve as precursors for all other steroid hormones. [Source 5] This process is activated by thyroid hormone and vitamin A, which are delivered to the mitochondria together on a single transport protein. [Source 5]

The vitality and structural integrity of mitochondria are constantly influenced by the balance between oxidative and glycolytic metabolism. Peat argued that **free fatty acids**, particularly *polyunsaturated fatty acids* (PUFA), suppress mitochondrial respiration, forcing a shift toward inefficient glycolysis that produces lactic acid and damages the mitochondria through escaped electrons. [Source 2, 4, 6] This suppression, known as the Crabtree effect, involves a physical competition between the products of glycolysis and carbon dioxide for binding sites, leading to a phase change in the mitochondrion that degrades its structure and function. [Source 4, 7] In contrast, carbon dioxide acts as a stabilizing agent that recruits proteins to enlarge and maintain the mitochondrial structure, while lactic acid promotes its degradation. [Source 7] Peat noted that when mitochondria are functioning fully, either glucose or saturated fats can safely provide energy, and saturated fats are actually the preferred fuel for cells at rest. [Source 8, 10]

Mitochondrial health is hormonally protected and environmentally sensitive. Peat identified **progesterone**, **testosterone**, and **thyroid** (T3 and T2) as protective hormones that shield mitochondria from the disruptive, catabolic effects of estrogen and cortisol. [Source 1, 4] He also highlighted that *red light* penetrates cells and repairs the same key respiratory enzyme that thyroid hormone activates, meaning a light deficiency acts on the enzymes identically to a thyroid deficiency. [Source 6] This was illustrated by research showing mitochondria in rabbits swelling and breaking down toward dawn, then progressively repairing during the daytime, a cycle that fails during the long dark of winter. [Source 3] Therapeutically, Peat suggested that substances like palmitate, vitamin B1, biotin, lipoic acid, carbon dioxide, and thyroid can counteract the antirespiratory production of lactic acid and support mitochondrial maintenance. [Source 4]

The functional state of the mitochondria has profound implications for aging and disease. Peat observed that in energy-deficient states like diabetes, the number of mitochondria does not increase, unlike in adaptation to high altitude or increased thyroid hormone. [Source 7] The chronic effect of burning PUFA under stress is known to destroy the *genetic material inside the mitochondrion*, contributing to cancer and the progressive increase of PUFA concentration in tissues with age. [Source 8] Interestingly, Peat pointed to evidence that animals with "uncoupled" mitochondria, which produce more carbon dioxide and fewer free radicals, live longer, and that a high carbon dioxide environment is associated with the extreme longevity of species like bats, queen bees, and naked mole rats. [Source 9] In the normal course of aging, the polyunsaturated fats suppress energy production, and this suppression is aggravated by their excitatory and inflammatory effects, skewing development toward sickness. [Source 10]

## People also ask

### How do mitochondria produce steroid hormones?

Peat described that mitochondria convert cholesterol into pregnenolone and progesterone, a process activated by thyroid hormone and vitamin A delivered together on a single transport protein.

### Why do polyunsaturated fats damage mitochondrial function?

Peat argued that polyunsaturated fatty acids suppress mitochondrial respiration through the Crabtree effect, forcing a shift to inefficient glycolysis that produces lactic acid and damages mitochondrial structure via escaped electrons.

### What role does carbon dioxide play in mitochondrial health?

The corpus describes carbon dioxide as a stabilizing agent that recruits proteins to enlarge and maintain mitochondrial structure, contrasting with lactic acid which promotes degradation.

## Related concepts

- [Crabtree effect](https://bioenergeticoracle.com/md/concepts/crabtree-effect/index.md)
- [Glycolysis](https://bioenergeticoracle.com/md/concepts/glycolysis/index.md)
- [Melatonin](https://bioenergeticoracle.com/md/concepts/melatonin/index.md)
- [Oxidation](https://bioenergeticoracle.com/md/concepts/oxidation/index.md)
- [Sugar (sucrose)](https://bioenergeticoracle.com/md/concepts/sugar-sucrose/index.md)
- [Uncoupling](https://bioenergeticoracle.com/md/concepts/uncoupling/index.md)

## Cited passages

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

### Source 1 — Glossary

Ray Peat · Glossary

> Mitochondria
>
> The structure inside the cell in which energy is produced by respiration is called the mitochondria.
>
> The vitality of the mitochondria, their capacity for oxidative energy production, is influenced by nutrition and hormones. In healthy people, mitochondria work efficiently at almost any altitude, but people with damaged or poorly regulated mitochondria are extremely susceptible to stress and hyperventilation. Progesterone, testosterone, and thyroid (T3 and T2) are protective of normal mitochondrial function, by both local and systemic effects.
>
> 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.

### Source 2 — Glucose and sucrose for diabetes.

Ray Peat · Article · 2012 · https://raypeat.com/articles/articles/glucose-sucrose-diabetes.shtml

> Mitochondria are the main source of ROS and are also the primary target of oxidative attacks."
>
> But much earlier (Wright, et al., 1988) it had been demonstrated that a deficiency of the "essential fatty acids" prevents toxin-induced diabetes and greatly increases resistance to inflammation (Lefkowith, et al., 1990). The lack of those so-called "essential fatty acids" also prevents autoimmune diabetes in a strain of diabetic mice (Benhamou, et al., 1995).
>
> Suppressing fatty acid oxidation improves the contraction of the heart muscle and increases the efficiency of oxygen use (Chandler, et al., 2003). Various drugs are being considered for that purpose, but niacinamide is already being used to improve heart function, since it lowers the concentration of free fatty acids.
>
> The antimetabolic and toxic effects of the polyunsaturated fatty acids can account for the "insulin resistance" that characterizes type-2 diabetes, but similar actions in the pancreatic beta-cells can impair or kill those cells, creating a deficiency of insulin, resembling type-1 diabetes.
>
> The suppression of mitochondrial respiration causes increased free radical damage, and the presence of polyunsaturated fatty acids in the suppressed cell increases the rate of fat decomposition and production of toxins.
>
> Increasing the rate of respiration by replacing the fats with glucose reduces the availability of electrons that can trigger lipid peroxidation and produce toxic free radicals, and the shift of fuel also increases the amount of carbon dioxide produced, which can protect the protein amino groups such as lysine from glycation and lipoxidation.
>
> While it's clear that it is the excessive oxidation of fat that damages cells in the "diabetic" state in which cells aren't able to use glucose, it's important to look at some of the situations in which so many researchers are blaming problems on hyperglycemia.
>
> Important problems in diabetes are slow wound healing, excessive permeability or leakiness of blood vessels which allows molecules such as albumin to be extravasated, and the impaired function and survival of pancreatic beta-cells.
>
> During the healing of a wound in a diabetic individual, the local concentration of glucose decreases and then entirely disappears, as healing stops. Applying glucose and insulin topically to the wound, it heals quickly. The very old practice of treating deep wounds with honey or granulated sugar has been studied in controlled situations, including the treatment of diabetic ulcers, infected deep wounds following heart surgery, and wounds of lepers.

### Source 3 — Politics And Science: Diabetes 2000-2001

Ray Peat · Interview · Jul 26, 2013

> **John Barkhausen:** So the red light at those heat lamps you can get at the hardware store, I believe?
>
> **Ray Peat:** Yeah, that's red enough. Those clear-fronted... so-called infrared lights. They're just designed to run on a high voltage, so when you run them on 120 volts, the filament doesn't get as hot as in a regular light bulb. That means that the light is biased away from blue and towards yellow and red. And so that's the penetrating beneficial light.
>
> **John Barkhausen:** We have a caller, and I'm going to ask them to whisper, basically, because we have a sound level problem where Ray is very low, and the callers are always about three times the level. So if you could talk very softly
>
> **Caller:** or... All right. This is Jim. You can tell me if I get too loud.
>
> **John Barkhausen:** Yeah, maybe just hold the phone farther away from you.
>
> **Caller:** All right. Is this okay?
>
> **John Barkhausen:** That's tolerable, but you could even do better.
>
> **Caller:** Wow. Yeah. I feel like I'm whispering.
>
> **John Barkhausen:** Yeah, it's fine. We can hear you.
>
> **Caller:** If I understood more, I would have a lot of questions, but... Could you explain a little bit more what cortisol is? If you want to write these questions down, I've got a couple. What is cortisol? And could you explain a little bit more about the nature of the mitochondria and what they actually do? I understand what happens to them when they don't get enough light, but what their real function is.

### Source 4 — Mitochondria and mortality

Ray Peat · Article · 2016 · https://raypeat.com/articles/articles/mitochondria-mortality.shtml

> Avoiding the stress-promoting antithyroid unsaturated oils is extremely important. Their role in diabetes, cancer, and other age-related and degenerative diseases (and I think this includes the estrogen-promoted autoimmune diseases) is well established. Avoiding phytoestrogens and other things that increase estrogen exposure, such as protein deficiency, is important, because estrogen causes increased levels of free fatty acids, increases the tendency to metabolize them at the expense of glucose metabolism, increases the tissue content of unsaturated fatty acids, and inhibits thyroid functions.
>
> Light promotes glucose oxidation, and is known to activate the key respiratory enzyme. Winter sickness (including lethargy and weight gain), and night stress, have to be included within the idea of the "respiratory defect," shifting to the antirespiratory production of lactic acid, and damaging the mitochondria.
>
> Therapeutically, even powerful toxins that block the glycolytic enzymes can improve functions in a variety of organic disturbances "associated with" (caused by) excessive production of lactic acid. Unfortunately, the toxin that has become standard treatment for lactic acidosis—dichloroacetic acid—is a carcinogen, and eventually produces liver damage and acidosis. But several nontoxic therapies can do the same things: Palmitate (formed from sugar under the influence of thyroid hormone, and found in coconut oil), vitamin B1, biotin, lipoic acid, carbon dioxide, thyroid, naloxone, acetazolamide, for example.
>
> Progesterone, by blocking estrogen's disruptive effects on the mitochondria, ranks along with thyroid and a diet free of polyunsaturate fats, for importance in mitochondrial maintenance.
>
> [references]

### Source 5 — Ask the Herb Doctor: Mitochondria, GABA, Herbs, and More

Ray Peat · Interview · Apr 15, 2016 · http://l-i-g-h-t.com/files/herb-doctors-mitochondria-gaba-and-more.mp4

> ## Mitochondria and Hormones
>
> **Andrew Murray:** We’ve heard a lot from you in the past regarding thyroid hormone physiology, progesterone, pregnenolone, and aging. Tonight we are discussing mitochondria: what they do, how they operate, and what substances deactivate them over time.
>
> **Sarah Murray:** Dr. Peat, can you explain simply what the mitochondria is? I've been told it's the "powerhouse of the cell." Can you explain that to our listeners?
>
> **Ray Peat:** That's a good enough definition, but there is a very stereotyped, textbook definition of it consisting of a certain kind of membrane, special enzymes, and some DNA separate from the nucleus. It handles various functions other than energy production. Steroid synthesis is one of its very important functions. It converts cholesterol into pregnenolone and progesterone, and those turn into all of the steroid hormones.
>
> **Sarah Murray:** Is that why when people age, their cholesterol goes up? Because their mitochondria aren't as efficient in converting the cholesterol into those hormones?
>
> **Ray Peat:** Yeah. Thyroid is the main hormone that activates the oxidative metabolism of the mitochondrion. If your thyroid is low, the mitochondria don't pull in the cholesterol and turn it into pregnenolone. The other cofactor working with thyroid happens to be Vitamin A. A protein in the blood carries thyroid and Vitamin A on a single protein and delivers it to the mitochondria, where they act like a factory with a conveyor belt bringing in the raw materials and the catalysts.

### Source 6 — Politics And Science: Diabetes 2000-2001

Ray Peat · Interview · Jul 26, 2013

> **John Barkhausen:** So I think that's what Jim wants to know is, you know, what does the mitochondria actually do?
>
> **Ray Peat:** Yeah, the essential function as far as the whole energy balance goes of the mitochondrion is that it is where oxygen receives the electrons from glucose primarily. The most efficient thing is for glucose to be oxidized, giving up its electrons to oxygen, creating water and carbon dioxide as oxygen is also added to the carbon skeleton of the glucose. Fats are metabolized in a a slightly different pathway also to oxygen but there is a competition between fats and glucose and the most efficient use of oxygen is when you're burning glucose and if you're forced to burn fats you lose efficiency and if they're unsaturated fats you not only lose efficiency but you damage the structure of the mitochondrion because the electrons are not taken up quickly enough by oxygen and they escape to oxidize the mitochondrion itself. So if you cut off the oxygen supply or use for any reason, you tend to create damage and destruction of the mitochondria by these escaping electrons the thyroid function is to activate the enzymes which take up electrons and so while thyroid intensifies oxidation it's the proper oxidation that's pulling electrons through the mitochondrion and turning them harmlessly into water And so if you interfere with thyroid, then you have the same effects that you get from cortisone or too much free fatty acids, especially pre-unsaturated fatty acids.

### Source 7 — Mitochondria and mortality

Ray Peat · Article · 2016 · https://raypeat.com/articles/articles/mitochondria-mortality.shtml

> (How did cells originate? How did mitochondria originate? "Germs.")
>
> Since I have a view of how cells came to exist, under conditions that exist on earth, I should consider whether that view doesn't also reasonably account for their various components. Sidney Fox's proteinoid microspheres provide a good model for the spontaneous formation of primitive cells; variations of that idea can account for the formation of organelles (such as mitochondria and nuclei within cells, and chromosomes within nuclei). The value of this idea, of a self-stimulating process in mitochondrial generation, is that it suggests many ways to test the idea experimentally, and it suggests explanations for developmental and pathological processes that otherwise would have no coherent explanation.
>
> Proteinoid microspheres and coacervates form by acquiring molecules from solution, condensing them into a separate phase, with its own physical properties. At every phase boundary, there are numerous physical forces, especially electronic properties, that make each kind of interface different from other kinds. Small changes of pH, temperature, of salts and other solutes can alter the interfacial forces, causing particles to dissolve, or grow, or fragment, or to move. In the way that carbon dioxide alters the shapes and electrical affinities of hemoglobin and other proteins, I propose that it increases the stability of the mitochondrial coacervate, causing it to "recruit" additional proteins from its external environment, as well as from its own synthetic machinery, to enlarge both its structure and its functions.
>
> In the relative absence of carbon dioxide, or excess of alternative solutes and adsorbents, such as lactic acid, the stability of the mitochondrial phase would be decreased, and the mitochondria would be degraded in both structure and function. As the back side of the idea that carbon dioxide stabilizes and activates mitochondria, the idea that lactic acid is involved in the degrading of mitochondria can also be tested experimentally, and it is already supported by a considerable amount of circumstantial evidence.
>
> This combination of sensitivity to the environment, with a kind of positive feedback or inertia either upward or downward, corresponds to what we actually see in mitochondrial physiology and pathology.
>
> The Crabtree effect, which is the suppression of respiration by glycolysis, is often described as the simple opposite of the Pasteur effect, in which respiration limits glycolysis to the rate that allows its product to be consumed oxidatively.

### Source 8 — Energy Production Diabetes Saturated Fats KMUD 2011

Ray Peat · Interview · 2011 · http://www.l-i-g-h-t.com/files/herb-doctors-energy-production,-diabetes-and-saturated-fats.mp4

> **Herb Doctor:** This is the system within every cell. The mitochondria are little factories that work in the cell.
>
> **Ray Peat:** Yah, it produces something like 35 times more energy per molecule of sugar than the diabetic pathway can produce.
>
> **Herb Doctor:** Cause the diabetics are forced, for want of a better word, into a fat-burning mode rather than glucose-burning.
>
> **Ray Peat:** Yah. And if it was purely saturated fat, that would be OK. When we’re at rest, our cells can burn saturated fat; they prefer that! The fat cells have been found to burn at rest. I mean, they are always at rest, where the heart or skeleton muscles only in a relatively quiet state will burn saturated fats. But the fat cells, being always at rest, slowly energize themselves by burning saturated fat. And that's why with age, our tissues become more and more concentrated with polyunsaturated fats; because the fat cells themselves are using the good stuff. So with age, it's seen all the way from birth to old age, there’s a progressive increase of polyunsaturated fats in all our tissues.
>
> **Herb Doctor:** Right. From our diets.

### Source 9 — Protective CO2 and aging

Ray Peat · Article · 2011 · https://raypeat.com/articles/articles/co2.shtml

> When mitochondria are “uncoupled,” they produce more carbon dioxide than normal, and the mitochondria produce fewer free radicals. Animals with uncoupled mitochondria live longer than animals with the ordinary, more efficient mitochondria, that produce more reactive oxidative fragments. One effect of the high rate of oxidation of the uncoupled mitochondria is that they can eliminate polyunsaturated fatty acids that might otherwise be integrated into tissue structures, or function as inappropriate regulatory signals.
>
> Birds have a higher metabolic rate than mammals of the same size, and live longer. Their tissues contain fewer of the highly unsaturated fatty acids. Queen bees, which live many times longer than worker bees, have mainly monounsaturated fats in their tissues, while the tissues of the short-lived worker bees, receiving a different diet, within a couple of weeks of hatching will contain highly unsaturated fats.
>
> Bats have a very high metabolic rate, and an extremely long lifespan for an animal of their size. While most animals of their small size live only a few years, many bats live a few decades. Bat caves usually have slightly more carbon dioxide than the outside atmosphere, but they usually contain a large amount of ammonia, and bats maintain a high serum level of carbon dioxide, which protects them from the otherwise toxic effects of the ammonia.
>
> The naked mole rat, another small animal with an extremely long lifespan (in captivity they have lived up to 30 years, 9 or 10 times longer than mice of the same size) has a low basal metabolic rate, but I think measurements made in laboratories might not represent their metabolic rate in their natural habitat. They live in burrows that are kept closed, so the percentage of oxygen is lower than in the outside air, and the percentage of carbon dioxide ranges from 0.2% to 5% (atmospheric CO2 is about 0.038). The temperature and humidity in their burrows can be extremely high, and to be very meaningful their metabolic rate would have to be measured when their body temperature is raised by the heat in the burrow.
>
> When they have been studied in Europe and the US, there has been no investigation of the effect of altitude on their metabolism, and these animals are native to the high plains of Kenya and Ethiopia, where the low atmospheric pressure would be likely to increase the level of carbon dioxide in their tissues.
>
> Consequently, I doubt that the longevity seen in laboratory situations accurately reflects the longevity of the animals in their normal habitat.

### Source 10 — The Gaba System Defenses and Tissue Renewal

Ray Peat · Article · 2007

> When mitochondria are functioning fully, either glucose or saturated fats can safely provide energy. Some glucose or saturated fat can be converted to polyunsaturated fats, that can be used as regulators or signals, for example to activate the formation of stem cells. But those PUFA don't create disruptive cascades of increasing excitation or inflammation or excessive growth, and, from the evidence of animals that are fed fat free diets, or diets lacking omega-3 and omega-6 fatty acids, they aren't toxic to mitochondria.
>
> When a healthy cell is excited, the mitochondria become more active, and their energy needs may exceed the amount of glucose available, leading to the formation of ketone bodies. Glucose deprivation seems to be a fundamental signal of stress, and the formation of ketone bodies is possibly the most primitive defensive reaction to stress. They protect nerves from excitatory oxidative damage (Noh, et al., 2006), inhibit mitochondrial production of reactive oxygen species during excitation (Maalouf, et al., 2007) and inhibit tumor growth and lactate production (Magee, et al. 1979). Increased thyroid hormone can increase ketone formation (Riou, et al., 1980; Bartels and Sestoft, 1980).
>
> The idea of synaptic membrane receptors often leads people to think of cellular inhibition in terms of raising a cell's threshold for producing an all-or-none membrane response to stimulation. But the inhibitory and excitatory systems interact at all levels of function and structure, reciprocally modifying each other. In response to signals for excitation or inhibition, for example, the quantity of GABA and GABAergic steroids such as progesterone will change, in response to increases or decreases in the enzymes that produce or eliminate them, and changes in concentrations of precursor molecules. The quantity and sensitivity of the various types of "receptor" will change. Proteins that bind and inactivate GABA and other regulators will change in quantity and effectiveness. The rate at which energy is produced will change, along with the rates of cellular reconstruction and decomposition. The cells' metabolic changes will produce signals that affect adjoining cells and the organism's physiological processes, including circulation, respiration, and readiness for stress.
>
> In the "normal" course of aging, good tissues atrophy, and may be partly replaced by fibrotic tissues, and in that environment, tumors and disorganized structures of various kinds develop.

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