# Glycolysis

Category: Metabolism

The conversion of glucose to lactic acid, providing some usable energy, but many times less than oxidation provides. Lactic acid, produced by splitting glucose to pyruvic acid followed by its reduction, is associated with calcium uptake and nitric oxide production, depletes…

11 passages · 3 authors · 2010–2021 · Most-cited: [Ray Peat](https://bioenergeticoracle.com/md/voices/ray-peat/index.md)

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

## Synthesis

**Glycolysis** is the metabolic pathway that converts glucose to lactic acid, yielding a small amount of usable energy—many times less than mitochondrial oxidative phosphorylation provides. [Source 1, 5] Peat distinguished between *anaerobic glycolysis*, a normal response to insufficient oxygen during intense muscle action, and **aerobic glycolysis** (the Warburg effect), the pathological conversion of glucose to lactic acid even in the presence of adequate oxygen, as seen in cancer, shock, and extreme trauma. [Source 1, 3, 7] The presence of oxygen normally restrains glycolysis so that glucose is oxidized to carbon dioxide; when this restraint fails, the cell reverts to a more primitive form of energy production that supports only cell division and primitive function, not the complex differentiation supported by respiration. [Source 1]

Peat argued that the products of glycolysis, **lactic acid** and pyruvic acid, are not merely markers of respiratory failure but are themselves toxins that suppress mitochondrial respiration, creating a vicious cycle. [Source 4, 5] Lactic acid is associated with calcium uptake, nitric oxide production, and energy depletion, contributing to cell death and the systemic derangements of hyperventilation, including vascular leakiness, brain swelling, and multiple organ failure. [Source 1, 4, 5] He identified the **Crabtree effect**—the inhibition of cellular respiration by an excess of glucose—as a general stress phenomenon in which glycolysis is activated while oxidative metabolism is shut down, a maladaptive response given respiration's far greater efficiency. [Source 4, 5] This is distinct from the normal **Pasteur effect**, where respiration limits glycolysis to the rate at which its products can be oxidatively consumed. [Source 4, 5]

The regulation of glycolysis is tightly coupled to carbon dioxide and the systemic metabolic state. Peat explained that a high background of carbon dioxide promotes circulation and oxygenation, preventing the anaerobic glycolysis that produces toxic lactic acid. [Source 2] Conversely, when carbon dioxide is deficient, aerobic glycolysis is favored, and the resulting lactate suppresses glucose oxidation while increasing the oxidation of fats, further lowering metabolic efficiency through the **Randle effect**. [Source 5, 11] Peat noted that glycolysis, as the initial splitting of glucose to pyruvate, is a normal part of oxidative metabolism and is preferable to burning excessive fat, provided the pyruvate enters the Krebs cycle rather than being reduced to lactate. [Source 11] Dinkov has extended this framing, describing cancer as a reversal to a primitive state of metabolism where cells rely exclusively on glycolysis, producing very little ATP and large amounts of lactic acid, leading to structural degradation and uncontrolled growth. [Source 10]

Peat traced the conceptual history of glycolysis through the work of Warburg and Szent-Gyorgyi, who viewed it as a primitive energy system, and emphasized that the organized, enzyme-to-enzyme handoff of substrates within the cell challenges the dilute-solution assumptions of classical biochemistry. [Source 1, 6] He identified several factors that suppress glycolysis and promote oxidative metabolism, including thyroid hormone, palmitic acid, light, and vitamin B1, while estrogen, unsaturated oils, and phytoestrogens promote the glycolytic stress state by increasing free fatty acids and inhibiting thyroid function. [Source 2, 5] Roddy notes that Peat's focus on glycolysis often centers on the recycling of carbon units and the critical role of mitochondrial carbon dioxide output in determining whether the link reaction proceeds, rather than on the textbook depiction of glycolysis as merely the first step in glucose oxidation. [Source 8, 9]

## People also ask

### How does aerobic glycolysis differ from normal anaerobic glycolysis?

Peat distinguished anaerobic glycolysis, a normal response to low oxygen during intense muscle action, from aerobic glycolysis, a pathological conversion of glucose to lactic acid even with adequate oxygen present, as seen in cancer and shock.

### Why did Peat consider lactic acid more than just a marker of low oxygen?

Peat argued that lactic acid and pyruvic acid are themselves toxins that suppress mitochondrial respiration, creating a vicious cycle of energy depletion, calcium uptake, and nitric oxide production that contributes to cell death and organ failure.

### What role does carbon dioxide play in restraining glycolysis?

The entry describes how a high background of carbon dioxide promotes circulation and oxygenation, preventing anaerobic glycolysis, while a carbon dioxide deficiency favors aerobic glycolysis and the production of lactate that suppresses glucose oxidation.

## Related concepts

- [Warburg effect](https://bioenergeticoracle.com/md/concepts/warburg-effect/index.md)
- [Aldosterone](https://bioenergeticoracle.com/md/concepts/aldosterone/index.md)
- [Cellular respiration](https://bioenergeticoracle.com/md/concepts/cellular-respiration/index.md)
- [Crabtree effect](https://bioenergeticoracle.com/md/concepts/crabtree-effect/index.md)
- [Lactic acid](https://bioenergeticoracle.com/md/concepts/lactic-acid/index.md)
- [Lipolysis](https://bioenergeticoracle.com/md/concepts/lipolysis/index.md)

## Cited passages

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

### Source 1 — Glossary

Ray Peat · Glossary

> Glycolysis
>
> The conversion of glucose to lactic acid, providing some usable energy, but many times less than oxidation provides. Lactic acid, produced by splitting glucose to pyruvic acid followed by its reduction, is associated with calcium uptake and nitric oxide production, depletes energy, contributing to cell death.
>
> ...The presence of oxygen normally restrains glycolysis so that glucose is converted to carbon dioxide instead of lactic acid.
>
> A point made by O. Warburg and A. Szent-Gyorgyi and others is that there is an important difference between the energy provided by glycolysis and that provided by mitochondrial respiration. They felt that glycolysis was a more primitive form of energy production, and supported only primitive function and cell division, while the more efficient respiration supported cell differentiation and complex functioning.
>
> Aerobic glycolysis is the conversion of glucose to lactic acid even in the presence of oxygen. The presence of oxygen normally restrains glycolysis so that glucose is converted to carbon dioxide instead of lactic acid.
>
> Anaerobic glycolysis is the increased conversion of glucose to lactic acid when the supply of oxygen isn't sufficient, which is a normal event during intense muscle action.

### Source 2 — Mitochondria and mortality

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

> Glycolysis produces both pyruvate and lactate, and excessive pyruvate produces almost the same inhibitory effect as lactate; since the Crabtree effect involves nitric oxide and fatty acids as well as calcium, I think it is reasonable to look for the simplest sort of explanation, instead of trying to experimentally trace all the possible interactions of these substances; a simple physical competition between the products of glycolysis and carbon dioxide, for the binding sites, such as lysine, that would amount to a phase change in the mitochondrion. Glucose, and apparently glycolysis, are required for the production of nitric oxide, as for the accumulation of calcium, at least in some types of cell, and these coordinated changes, which lower energy production, could be produced by a reduction in carbon dioxide, in a physical change even more basic than the energy level represented by ATP. The use of Krebs cycle substances in the synthesis of amino acids, and other products, would decrease the formation of CO2, creating a situation in which the system would have two possible states, one, the glycolytic stress state, and the other, the carbon dioxide producing energy-efficient state.
>
> Besides the frequently discussed interactions of excessively accumulated iron with the unsaturated fatty acids, producing lipid peroxides and other toxins, the accumulated calcium very probably forms some insoluble soaps with the free fatty acids which are released even from intracellular fats during stress. The growth of new mitochondria probably occasionally leaves behind such useless materials, combining soaps, iron, and porphyrins remaining from damaged respiratory enzymes.
>
> When the background of carbon dioxide is high, circulation and oxygenation tend to prevent the anaerobic glycolysis that produces toxic lactic acid, so that a given level of activity will be harmful or helpful, depending on the level of carbon dioxide being produced at rest.
>
> Preventively, avoiding foods containing lactic acid, such as yogurt and sauerkraut, would be helpful, since bacterial lactic acid is much more toxic than the type that we form under stress. 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.

### Source 3 — Biochemical Health, Reduction and Oxidation — Politics & Science 2015

Ray Peat · Interview · 2015

> **Jon Barkhausen:** That's called glycolysis?
>
> **Ray Peat:** It's aerobic glycolysis when you make lactic acid in the presence of oxygen, and ordinary anaerobic glycolysis is what happens when you exercise too hard. You can build up lactic acid in getting out of breath. The blood lactate increases if you exercise faster than you're breathing, and that's normal. You can a little later consume and oxidize the lactic acid and that's OK. But when you start producing lactic acid even in the presence of oxygen, as in the case of cancer, or extreme trauma or shock, the same thing happens; something turns the trigger, so that even though oxygen is present in shock, you will waste your sugar and make lactic acid.
>
> **Jon Barkhausen:** I see; oxygen is there, but you are unable to use it.
>
> **Ray Peat:** Yah, and in the case of shock at least, the nervous system is involved in making that aerobic glycolysis. So there are quite a few people who have suggested that the nervous system is involved in the cancer transition, doing the same thing that shock and trauma can do acutely.
>
> **Jon Barkhausen:** I want to ask you more about not being able to use oxygen, even though it’s there. It’s called anaerobic glycolysis ?

### Source 4 — Mitochondria and mortality

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

> 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. But the Pasteur effect is a normal sort of control system; when the Pasteur effect fails, as in cancer, there is glycolysis which is relatively independent of respiration, causing sugar to be consumed inefficiently. Embryonic tissues sometimes behave in this manner, leading to the suggestion that glycolysis is closely related to growth. Unlike the logical Pasteur effect, the Crabtree effect tends to lower cellular energy and adaptability. Looking at many situations in which increasing the glucose supply increases lactic acid production and suppresses respiration, leading to maladaptive decrease in cellular energy, I have begun thinking of lactic acid as a toxin. The use of Ringer's lactate solution in medicine has led many people to assume that lactate must be beneficial, or they wouldn't put it in the salt solution that is often used in emergencies; however, I think its use here, as a buffer, is simply a convenience, because of the instability of some bicarbonate solutions.
>
> On the organismic level, it is clear that lactic acid is "the essence of hyperventilation," and that it produces edema and malfunction on a grand scale: The panic reaction, shock lung, vascular leakiness, brain swelling, and finally multiple organ failure, all can be traced to an excess of lactic acid, and the related features of hyperventilated physiology.
>
> Otto Warburg apparently thought of lactate as simply a sign of the respiratory defect that characterizes cancer. V. S. Shapot at least hinted at its possible role in turning on the catabolic reactions leading to cancer cachexia (wasting). I think a good case can be made for lactate as the *cause* of the respiratory defect in cancer, just as it is usually the immediate cause of the respiratory derangement of hyperventilation on the organismic level.
>
> The Crabtree effect is usually thought of as just something that happens in tumors, and some tissues that are very active glycolytically, and some bacteria, when they are given large amounts of glucose.

### Source 5 — Mitochondria and mortality

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

> # Mitochondria and Mortality: Diet, Exercise, and Medicine, Damaging or Repairing Respiratory Metabolism
>
> ## MAIN IDEAS AND CONTEXTS
>
> Lactic acid and carbon dioxide have opposing effects.
>
> Intense exercise damages cells in ways that cumulatively impair metabolism. There is clear evidence that glycolysis, producing lactic acid from glucose, has toxic effects, suppressing respiration and killing cells. Within five minutes, exercise lowers the activity of enzymes that oxidize glucose. Diabetes, Alzheimer's disease, and general aging involve increased lactic acid production and accumulated metabolic (mitochondrial) damage.
>
> The products of glycolysis, lactic acid and pyruvic acid, suppress oxidation of glucose.
>
> Adaptation to hypoxia or increased carbon dioxide limits the formation of lactic acid. Muscles are 50% more efficient in the adapted state; glucose, which forms more carbon dioxide than fat does when oxidized, is metabolized more efficiently than fats, requiring less oxygen.
>
> Lactic acidosis, by suppressing oxidation of glucose, increases oxidation of fats, further suppressing glucose oxidation.
>
> Estrogen is harmful to mitochondria, progesterone is beneficial.
>
> Progesterone's brain-protective and restorative effects involve mitochondrial actions.
>
> Thyroid hormone, palmitic acid, and light activate a crucial respiratory enzyme, suppressing the formation of lactic acid. Palmitic acid occurs in coconut oil, and is formed naturally in animal tissues. Unsaturated oils have the opposite effect.
>
> Heart failure, shock, and other problems involving excess lactic acid can be treated "successfully" by poisoning glycolysis with dichloroacetic acid, reducing the production of lactic acid, increasing the oxidation of glucose, and increasing cellular ATP concentration. Thyroid, vitamin B1, biotin, etc., do the same.
>
> ## SOME DEFINITIONS
>
> **Glycolysis**: The conversion of glucose to lactic acid, providing some usable energy, but many times less than oxidation provides.
>
> **Lactic acid**, produced by splitting glucose to pyruvic acid followed by its reduction, is associated with calcium uptake and nitric oxide production, depletes energy, contributing to cell death.
>
> **Crabtree effect**: Inhibition of cellular respiration by an excess of glucose; excess of glucose promotes calcium uptake by cells.
>
> **Pasteur effect**: Inhibition of glycolysis (fermentation) by oxygen.

### Source 6 — Politics & Science: A Self-Ordering World — How Do You Know? — Patients, Students, and Discovery

Ray Peat · Video Transcript · Nov 10, 2010 · http://l-i-g-h-t.com/files/politics-science-a-self-ordering-world.mp4

> **Ray Peat:** So it isn't a random diffusion of material through water randomly finding an enzyme, but it's a totally organized enzyme-to-enzyme handoff of the material that they're working on. And he did that simply by counting molecules, which anyone could have done, but they were so committed to the idea of randomness in a watery solution that they totally missed the point of what's happening in the cell.

### Source 7 — Biochemical Health, Reduction and Oxidation — Politics & Science 2015

Ray Peat · Interview · 2015

> **Ray Peat:** No. Aerobic glycolysis ( or “Warburg effect”: it’s the observed phenomenon that cancer cells ferment the glucose even in presence of adequate oxygen) (“Anaerobic glycolysis” means “fermentation”, the conversion of glucose to lactic acid in the total, or partial absence of oxygen).
>
> **Jon Barkhausen:** How does the mitochondria burn fat ? How is that even possible ? What are the problems with that ?
>
> **Ray Peat:** It produces less carbon dioxide, for example. I think that’s the main problem. If you develop fat stores, you get particles of fat accumulating in the cytoplasm, and maybe even in the nucleus. That, probably, have a disruptive effect, from your...heavily shifted over to a fat economy. The tumor makes saturated fat, as it’s first product in converting sugar to saturated fat. But when it’s shifting in the presence of stress, when it shifts to burning fat, usually that will go through your fat stores, burning up your subcutaneous fat quickly. So, when a person is very sick with cancer, for example, they get a gaunt, emaciated look as their superficial fat stores are used up. And at the same time, they convert amino acids to energy, converting some of it to sugar, and some of it to fat. And so, it starts a wasting process. But, our stores, the older a person gets, generally the higher the amount of polyunsaturated fat in their stores. And when you’re oxidizing polyunsaturated fats, that produces more oxidative damage to the mitochondria. So, it tends to lower the oxidative part of the metabolism, and slow things down in general.

### Source 8 — #08: Mitochondria, Low-Carb Advocates, Metabolic Stress, and Gilbert Ling with Kyle Mamounis

Danny Roddy · Interview · Aug 16, 2019 · https://open.spotify.com/episode/6mXcU4jilQVGWrvJr1eJI6

> **Kyle Mamounis:** Okay. So yeah. I guess the relevant, really the only relevant points with the whole glycolysis thing is that, I mean, it's the Randall cycle thing, right? As far as like glucose versus fatty acids.
>
> **Danny Roddy:** Yeah, so I guess, so, well, yeah, the idea that the fatty acids are blocking the use of glucose and that's like an acute thing that happens, correct?
>
> **Kyle Mamounis:** Yeah, it's the, you know, while these, um, pathways are happening. Like if you look at the cartoon and it'll show, um, say in the TCA cycle or something like that, it'll show all of these products and it's in a big circle. Uh, and they go from, you know, thing to thing to thing. And then it goes back to Acetyl-CoA. Uh, a lot of those products in the, in the middle, in the cycle will spit off at different areas. Or if you have like extra, um, They can come in from outside and get thrown into that cycle. So in that in that way Glycolysis and beta oxidation which are the two first steps to get glucose and fatty acids respectively ready for the TCA cycle the products of those can go off into other things and the products of the TCA cycle can go into other things so one of the products of beta-oxidation of fatty acids as malonyl-CoA, and that specifically inhibits the pyruvate dehydrogenase complex enzyme.

### Source 9 — #08: Mitochondria, Low-Carb Advocates, Metabolic Stress, and Gilbert Ling with Kyle Mamounis

Danny Roddy · Interview · Aug 16, 2019 · https://open.spotify.com/episode/6mXcU4jilQVGWrvJr1eJI6

> **Kyle Mamounis:** Yeah. Yeah. Ray uses it as like to just talk about splitting glucose into two units where you get a little bit of energy. I think like three ATP or something and or four, something like that. And and then that. that peruvia that gets made can turn into lactate and sent out like if it's made in a muscle cell or something it can get sent out and picked up by the liver and turned back into glucose so that's that's what he's mostly talking about it's like a recycling of the same carbon units whereas most people would learn it as the first step in oxidation of glucose
>
> **Danny Roddy:** yeah Yeah, so Ray talks about it being half that step. But again, I think his general point is that, and I'm getting ahead of ourselves here, but you don't know how much of that link reaction is happening if the mitochondria aren't putting out the carbon dioxide.
>
> **Kyle Mamounis:** Right. Yeah.
>
> **Danny Roddy:** Okay. So I have on screen, Chris Masterjohn has a great masterclass with Masterjohn, though I stole this graphic from, but this is our little cheat sheet for glycolysis and mitochondrial metabolism and the TCA cycle and the decarboxylation of pyruvate. So I don't know where you want to start with that, but.

### Source 10 — Episode 31: Debunking The Biggest Health Myths With Georgi Dinkov

Georgi Dinkov · Interview · May 17, 2021 · https://www.youtube.com/watch?v=vgqbaubsQd4

> **Georgi Dinkov:** Even amoebas and bacterias and very primitive slimes like kind of organisms, multicellular organisms have it. It's called glycolysis. And basically, the glycolysis is a very inefficient way of producing energy from food. And the resulting, so it produces very little ATP, but it consumes a lot of oxygen. And then one output of the excessive glycolysis is lactic acid. So if you add the three steps, which are glycolysis, curbs cycle, and electron transfer chain, those are the three steps of the metabolism. If you have only the first one working, glycolysis, you're producing very low amount of energy. and producing a lot of lactic acid, which lactic acid itself is a toxic molecule. The body doesn't like it, tries to get rid of it as soon as it's produced. But more importantly, if you're not producing sufficient amount of energy, just as I mentioned earlier, it leads to structural degradation over time, leads to inflammatory processes, because one way the body tries to repair damage is basically triggering a localized inflammatory reaction. which awakens the immune system and basically the immune system starts sending all of these cells in that direction where the inflammation is coming from, trying to repair. But in order to repair the damage, a lot of these primitive growth processes are being triggered and to synthesize new tissues, new cells, new machinery for the cells, DNA, RNA, enzymes, everything that the cell needs. And unfortunately, if that growth process is not inhibited, which also requires energy, eventually you get uncontrolled growth, which is the hallmark of cancer. And it just so happens that cancer cells can only produce energy through glycolysis. So a recent study came out about four years ago. which one of the leading cancer biologists in the United States, actually the world really, was a team of three of them, who wrote an editorial article in the journal Nature and said, we've been looking at cancer the wrong way.

### Source 11 — Ray Peat Email Advice Depository — Post 6

Ray Peat · Email · Jan 16, 2013

> ## Thread 10
>
> **Question:** When you say several effects of co2 shuts off glycolysis, do you mean anaerobic glycolysis or all glycolysis, if all glycolysis how does glucose enter mitochondria without breaking down to pyruvate?
>
> **Ray Peat:** Meaning the entry of lactate into the blood stream inappropriately, which would usually be called aerobic glycolysis, though you can't be sure how much oxygen is getting to the cells when CO2 is deficient, since its absence causes many problems in oxygen delivery and use.
>
> **Question:** So when CO2 isn't deficient glycolysis, meaning glucose to pyruvate, is fine?
>
> **Ray Peat:** Yes, as part of oxidative metabolism, it's better than burning too much fat.

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