# Cancer

Category: Conditions

Also known as: tumor, carcinoma

Cancer is fundamentally a metabolic disease characterized by a regression to a primitive, fermentative energy state, a process Otto Warburg identified as aerobic glycolysis—the conversion of glucose to lactic acid even in the presence of adequate oxygen. Peat argued that this…

11 passages · 2 authors · 2007–2025 · Most-cited: [Ray Peat](https://bioenergeticoracle.com/md/voices/ray-peat/index.md)

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

## Synthesis

**Cancer** is fundamentally a metabolic disease characterized by a regression to a primitive, fermentative energy state, a process Otto Warburg identified as *aerobic glycolysis*—the conversion of glucose to lactic acid even in the presence of adequate oxygen. [Source 3, 11] Peat argued that this shift is not caused by random genetic mutations, but by a **reduced redox state** within the cell, a condition where the flow of energy is blocked and the cell shifts toward a more reduced, electron-rich environment. [Source 1] This metabolic defect involves a failure of oxidative phosphorylation, where oxygen fails to act as the terminal electron acceptor, and instead, pyruvic acid accepts electrons, forming **lactic acid**. [Source 11] The resulting lactate production is not merely a byproduct but an active driver of the disease, modifying the extracellular matrix and activating pathways like mTOR that sustain the cancerous state. [Source 4]

The development of the cancer field is a cooperative phase transition driven by chronic stress and energy depletion, not a collection of "bad cells" to be killed. [Source 1, 6] When cells are stressed beyond their capacity to respire, oxygen and glucose are depleted, forcing a reliance on glycolysis. [Source 1] This state is self-reinforcing; lactate promotes the activation of mTOR, and mTOR in turn activates aerobic glycolysis, creating a vicious circle of *cancerization*. [Source 4] Peat emphasized that glucose deprivation, a common misinterpretation of Warburg's work, is countertherapeutic because it accelerates the tumor's consumption of the body's own protein and fat stores, leading to wasting and increased stress. [Source 1, 4] The tumor's high glucose uptake on a PET scan reflects a perceived lack of glucose due to inefficient oxidation, not a sugar addiction. [Source 7] Dinkov has elaborated that this metabolic state involves excessive fatty acid oxidation, which blocks complex II of the electron transport chain, causing a buildup of electrons and further oxidative stress. [Source 7]

Corrective therapy, in Peat's framework, reinforces the organism's health rather than attacking the tumor, aiming to restore oxidative metabolism and suppress lactate formation. [Source 4] Substances that favor the production of **carbon dioxide** over lactate include thyroid hormone, progesterone, and sodium bicarbonate. [Source 4] Progesterone, in particular, has been shown to be protective against cancer, and Peat extensively documented how studies claiming it is carcinogenic were methodologically flawed, often using known tumor-promoting vehicles like corn oil or toxic solvents like cyclodextrins without proper controls. [Source 2, 8, 10] The systemic nature of the disease is underscored by the fact that the ratio of lactate to pyruvate in the blood is abnormal in many chronic conditions, including mental health disorders, indicating a broader mitochondrial dysfunction. [Source 9] The protective effects of sodium are also relevant, as it improves immunity and reduces inflammation, while its absence activates the renin-angiotensin-aldosterone system, which is involved in degeneration. [Source 5]

The futile "War on Cancer," driven by the genetic theory of disease, has ignored this metabolic reality, leading to treatments that often cause harm without reducing mortality. [Source 6, 11] The mass screening and over-diagnosis of conditions like neuroblastoma and prostate cancer have not decreased death rates, and in the case of prostate cancer, the use of estrogen as a treatment likely increased them. [Source 6] The drug industry's focus on targets like angiogenesis inhibitors, proteins induced by lactate, has generated billions of dollars without a noticeable change in cancer mortality, as they neglected the basic needs of normal tissues. [Source 11] Peat maintained that the organism's state of health can be reinforced by a great number of synergistic substances that inhibit the inflammatory, degenerative processes at multiple levels, a supportive approach that has nothing in common with the ruling paradigm of attacking the disease. [Source 4]

## People also ask

### What metabolic shift defines cancer according to Peat?

Peat argued cancer is defined by a regression to aerobic glycolysis, where cells convert glucose to lactic acid even with oxygen present, due to a failure of oxidative phosphorylation and a reduced redox state.

### Why did Peat consider glucose deprivation harmful for cancer patients?

Peat argued that glucose deprivation accelerates the tumor's consumption of the body's protein and fat stores, leading to wasting and increased stress, because the tumor's high glucose uptake reflects inefficient oxidation, not a sugar addiction.

### How did Peat propose restoring metabolism to counteract cancer?

Peat proposed reinforcing the organism's health by restoring oxidative metabolism and suppressing lactate formation, using substances like thyroid hormone, progesterone, and sodium bicarbonate that favor carbon dioxide production over lactate.

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## Cited passages

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

### Source 1 — 100 Years of Cancer Metabolism

Ray Peat · Newsletter · 2016

> In physics, the idea of cooperative phase transition is familiarly used to explain water's change of state during freezing and melting, but the reductionist ideology that is so conspicuous in science makes biologists reluctant to see it in the changes of state that occur in cells. The idea that the bond energy of ATP is used to power muscle contraction, by causing little levers to move, is intimately associated with the belief in membranes, pumps, and random diffusion of enzymes and their substrates. To the mechanist, cells, organisms, and consciousness are just statistical abstracts of molecular events, and cancer is neatly explained as the product of random genetic mutations. The way energy flows through a system depends on the conductive and catalytic condition of the system, and the condition of the system depends on the flow of energy. When a cell is stressed, stimulated beyond its ability to respond with increased respiration to produce the energy needed to return to its resting state, the stress itself is a relatively reducing state, like the cytochrome color shift Keilin saw when muscles contracted or were poisoned.
>
> The reduced state leads to increased production of lactate, which produces enough energy to keep the cell alive, but the lactate contributes to the stressed redox shift in the cell that produces it, as well as in the surrounding cells. The new reductionist interpretation of Warburg's idea is that the shift to aerobic glycolysis and lactate production is the result of a genetic change that centers on increasing glucose use, but in reality glucose deprivation is one of the things that can lead to the shift to aerobic glycolysis, with the lactate then being derived from the breakdown of tissue protein instead of glucose. V.S. Shapot found that providing both glucose and oxygen to rats with Ehrlich ascites cancer could produce the Pasteur effect, inhibiting glycolysis and restoring cellular respiration (Tagi-zade and Shapot, 1971). The ability of glucose to reduce excitation in other situations probably involves the increased oxidative state; an important part of the cancer physiology is overexcitation of the brain, especially the hypothalamus, and just increasing the level of blood glucose can lower that excitation (Shapot, et al., 1983). When cells are dangerously overstimulated, oxygen and glucose are depleted.

### Source 2 — Estrogen, progesterone, and cancer: Conflicts of interest in regulation and product promotion.

Ray Peat · Article · 2007 · https://raypeat.com/articles/articles/estrogen-progesterone-cancer.shtml

> A different chemical carcinogen, 7,12-dimethylbenz(a)anthracene was used in another 1973 study (Jabara, et al.), in combination with progesterone. In this experiment, the carcinogen was administered to rats in one dose by stomach tube, dissolved in corn oil. The progesterone was injected subcutaneously in 3 mg doses in corn oil three times per week. Unfortunately, there was no control group in which the corn oil was injected alone. The progesterone was supposedly dissolved in the corn oil, one tenth ml per dose. That amount of progesterone (3% weight/volume) will dissolve in hot corn oil, but as the oil cools, the progesterone crystallizes and precipitates. That creates doubt regarding what the animals were actually receiving. Corn oil is one of the most effective vegetable oil tumor promoters/carcinogens, and it's now considered improper to use it as a solvent for testing even oral carcinogens, since some chemicals that are carcinogenic in the oil are relatively harmless when administered without the corn oil.
>
> The animals got 2 ml of corn oil in the stomach feeding with the carcinogen. One of the groups (group 5) received, in addition, more than 6 ml of corn oil in the injections. The experiment lasted only 135 days, and in the group that received only the carcinogen, the mortality was only 5%, and that death occurred shortly after the carcinogen was administered. All of the groups receiving the corn oil and progesterone injections had higher mortality, two with 25%, one with 37.5% mortality. Despite the unexplained general problem with prematurely dying rats, the authors found that "The relative incidence rates indicated that pretreatment with progesterone inhibited tumorigenesis, except in the group (5) in which progesterone treatment was continued for the duration of the experiment." Without progesterone, it is almost certain that the additional corn oil injected would have increased tumorigenesis in all experimental groups. Without that vehicle control group, the experiment can just as well be described as a test of corn oil, rather than of progesterone. If you claim to be testing the capacity of a substance to promote tumors, it shouldn't be administered in a standard tumor promoter.

### Source 3 — 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 4 — Carcinogenic Metabolism

Ray Peat · Newsletter · 2022

> A common misinterpretation of Warburg’s work has led to the idea of starving cancer by withholding sugar from the diet. That increases the tumor’s consumption of protein and fat, leading to the conversion of the body itself to fuel to support the cancer growth, creating immunodeficiency and intensified stress. Diabetes was originally known as a wasting disease, quickly leading to death because of the inability to oxidize sugar, with increased lactate production and generalized inflammation. Depriving the diabetic person of the sugar they crave accelerates the conversion of their tissues to fuel, with greatly increased free fatty acids in the serum, blocking the oxidation of glucose. Increased serum free fatty acids are associated with both diabetes and cancer (Zhang, et al., 2020; Li et al., 2021).
>
> Hysteresis is a general phenomenon in which an effect lags behind its cause—for example, it takes less energy to maintain a flow of electricity than to start it; it describes system inertia. Cancer demonstrates this property—a continuing stress gradually leads to an accumulation of functional and structural changes that sustain the stressed condition, such as changes in the extracellular environment as well as intracellular processes. For example, the presence of lactate modifies the extracellular matrix in ways that increase lactate formation (Sullivan, et al., 2018). An important factor in creating functional and metabolic inertia is a phosphate transfer enzyme that creates a general pattern of activation, the kinase called mTOR (mechanistic target of rapamycin).
>
> A bacterial fungicidal antibiotic, rapamycin, originally used to treat candidiasis, was found to be immunosuppressive, and is used to prevent rejection of kidney transplants. The mTOR enzyme inhibited by rapamycin has been found to promote growth, inflammation, fibrosis, and cancer growth, and to accelerate aging. Lactate promotes the activation of mTOR, and mTOR activates aerobic glycolysis, the defining feature of cancer. Interrupting the vicious circles of cancerization is essential for the survival of the organism.
>
> There are many substances that can inhibit the inflammatory, degenerative processes acting at multiple levels, and these substances tend to be synergistic, so that a great number of substances can be safely used at the same time. This kind of supportive therapy has nothing in common with the ruling paradigm of cancer treatment—it is reinforcing the organism’s state of health, rather than attacking the disease of cancer.

### Source 5 — Salt, energy, metabolic rate, and longevity

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

> Studies in which animals were fed popular Japanese foods--” salted cuttlefish guts, broiled, salted, dried sardines, pickled radish, and soy sauce “--besides a chemical carcinogen, showed that the Japanese foods increased the number of tumors.
>
> But another study, adding only soy sauce (with a salt content of about 18%) to the diet did not increase the incidence of cancer, in another it was protective against stomach cancer (Benjamin, et al., 1991).
>
> Several studies show that dried fish and pickled vegetables are carcinogenic, probably because of the oxidized fats, and other chemical changes, and fungal contamination, which are likely to be worse without the salt.
>
> Animals fed dried fish were found to have mutagenic urine, apparently as a result of toxic materials occurring in various preserved foods (Fong, et al., 1979).
>
> Although preserved foods develop many peculiar toxins, even fresh fish in the diet have been found to be associated with increased cancer risk (Phukan, et al., 2006).
>
> When small animals were given a milliliter of a saturated salt solution with the carcinogen, the number of tumors was increased with the salt.
>
> However, when the salt was given with mucin, it had no cancer promoting effect.
>
> Since the large amount of a saturated salt solution breaks down the stomach’s protective mucus coating, the stomach cells were not protected from the carcinogen.
>
> Rather than showing that salt causes stomach cancer, the experiments showed that a cup or more of saturated salt solution, or several ounces of pure salt, shouldn’t be ingested at the same time as a strong carcinogen.
>
> Some studies have found pork to be associated with cancer of the esophagous (Nagai, et al., 1982), thyroid ( Markaki, et al., 2003), and other organs, but an experiment with beef, chicken, or bacon diet in rats provides another perspective on the role of salt in carcinogenesis.
>
> After being given a carcinogen, rats were fed meat diets, containing either 30% or 60% of freeze-dried fried beef, chicken, or bacon. Neither beef nor chicken changed the incidence of precancerous lesions in the intestine, but the incidence was reduced by 12% in the animals on the 30% bacon diet, and by 20% in rats getting the diet with 60% bacon.
>
> Salt apparently made the difference.

### Source 6 — Comments on cancer therapy

Ray Peat · Newsletter · 2016

> Limiting the number of doctors was very effective for increasing their income, but increasing the number of diagnosed diseases per patient is also very effective. By expanding the definition of diabetes, the sale of drugs increased tremendously, with only moderate harm to the patients. Starting in the 1940s, "pre-cancerous" conditions became "carcinoma in situ," and mass media campaigns warned the public to watch for changes in moles or in bowel functions, because having surgery in time would save your life. Despite the escalation of diagnosis, cancer deaths increased. While watching for changes in moles, deaths from melanoma increased five-fold.
>
> In the 1980s, a protein, the so-called prostate specific antigen, PSA, was identified as a possible indicator of the presence of prostate cancer, and it became popular as a way to diagnose prostate cancer, with the result that many symptom-free men were given prostate biopsies and treatment for prostate cancer and the mortality rate increased sharply from 21/100,000 population in 1981, before PSA was known, to 30/100,000 in 1992. At that time (and for the preceding 30 or 40 years) estrogen was the most popular treatment for prostate cancer, so it was probably an important factor in the suddenly increased death rate.
>
> There have been several studies of the effects of x-ray mammography screening on women's health and mortality. When some of the authors have concluded that there is either no decrease in mortality from that screening, or a very small decrease, but a very significantly harmful effect on the women's health, they have been furiously denounced by the cancer specialists, who say that people who aren't specialists in treating cancer have no right to say such things. The specialists apparently still believe that over-diagnosis isn't a big problem, and that very large numbers of deaths (e.g., 28%, Weedon-Fekjrer, et al., 2014; 15%, but with 30% over-diagnosis, Gotzsche and Jorgensen, 2013) are prevented by mammography. The women who have been screened seem to be even more enthusiastic than the oncologists about the number of lives the mammograms save, guessing 80 times as many as estimated in three studies (Gotzsche and Jorgensen, Independent UK Panel on Breast Cancer Screening, and Miller, et al.).

### Source 7 — #367 Cancer pt2. Inflammation, Metabolism, & Ozempic. With Georgi Dinkov & Alannah Connealy.

Georgi Dinkov · Interview · Mar 29, 2025

> **Georgi Dinkov:** keeping that machinery takes energy, the cells will simply become more effective and say, why am I keeping this energetically expensive machinery in the form of all these proteins involved in oxidative phosphorylation? I'm going to get rid of it and start producing energy the dirty, cheap way, which is glycolysis. So really, glycology is like the coal plant, while the oxidative phosphoration is like the, I don't want to say nuclear plant because there's a bad connotation, but in terms of efficiency, that's really the comparison. So let's say we'll go back to coal burning, which creates a lot of bad byproducts. It really doesn't produce that much energy compared to per unit of raw material used compared to, let's say, the nuclear power plant, putting radiation aside completely in terms of efficiency. And that's really cancer. The cancer metabolism is that excessive glycolysis, overproduction of lactic acid, and then really lack of complete oxidation of glucose to carbon dioxide in water, which is what happens when you're using oxygen properly. Combined with that, we also see in cancer patients, insulin resistance, which should immediately kind of like, you know, if there's an endocrine doctor there, he or she should immediately think, okay, there's an oversupply of fatty acids because we now know that is the fatty acids that are causing the insulin resistance. It's not the sugar. Yes, the sugar is being wasted. And because the sugar is wasted in the cancer cell, the cancer cells increase their uptake of sugar to compensate for the perceived lack of it because they don't oxidize it properly. So a common test for cancer is to inject radioactive glucose solution into a patient and then put them in a PT scan and then see which part of the body starts to light up because that means that part is really uptaking a lot more glucose than the rest. And because the glucose is radioactive, they can pinpoint it. That usually means there's a tumor there.

### Source 8 — Estrogen, progesterone, and cancer: Conflicts of interest in regulation and product promotion.

Ray Peat · Article · 2007 · https://raypeat.com/articles/articles/estrogen-progesterone-cancer.shtml

> Twenty years later, Horsky and Pitha at NIH reported that the cyclodextrins can synergize with carcinogens, and in 1982 a group in Japan reported that cyclodextrins can increase the production of kidney cancers by another carcinogen (Hiasa, et al.). The intrinsic carcinogenicity of a more water soluble cyclodextrin, that was considered "more toxicologically benign," was found to cause pathological changes in lungs, liver, and kidney, and to increase the formation of tumors in the pancreas and intestines of rats (Gould and Scott, 2005).
>
> In 1974, D. W. Frank and others at Upjohn had begun testing the effects of progesterone and medroxyprogesterone acetate in beagle dogs, using an "aqueous suspension." Their 1979 publication describing that four year study didn't mention the way in which the "aqueous solution" had been made, and didn't mention cyclodextrins at all. Frank's published observation during the beagle study that cyclodextrins are toxic to the kidneys suggests that someone at Upjohn had noticed a problem with the "wetting agent" that was already in use in the beagle study.
>
> Another remarkable feature of the four year beagle study was that, of 140 dogs that began the intended 7 year study, 28 had died by the time they published the report, and none died of cancer, but the causes of death were not reported. The only experimental group in which there were no deaths by the end of four years was the low dose progesterone group. The dogs in the high dose progesterone group received weekly intramuscular injections of 1140 mg of progesterone suspended in 11.4 ml of "aqueous vehicle." 2345 ml of the vehicle was received by each dog during the four years. Only four dogs in that group were still alive at the time of publication, but the cause of death of the other 16 wasn't mentioned. Quarts of a toxic material that had never before been used in this way, injected into their muscles, and the unexplained deaths of so many animals, make this a unique experiment that is unlikely ever to be repeated. Their failure to mention injection-site muscle damage is just another indication of the study's low quality.

### Source 9 — The Metabolic Cancer Revolution with Dr. Thomas Seyfried, Georgi Dinkov

Georgi Dinkov · Interview · Apr 3, 2025

> **David Gornoski:** Georgi, have you found that to be the case, that there's a fermentation basis for cancer? What have you found in your research and your rodent experiment?
>
> **Georgi Dinkov:** So, yes, absolutely. Even as Otto Warburg found out about 100 years ago, cancer cells do something called aerobic glycolysis. So they basically ferment even if you give them a sufficient amount of oxygen. And he thought that, you know, he never thought the genes were the issue, even though genomics wasn't as developed back then. He thought there was a dysfunction in the mitochondria, which could be repaired if the cell is put into more optimal environment. I don't think he got the chance to expand on what this more optimal environment means. But even to this day, the Warburg effect is a... one of the hallmarks of cancer, and it's used to basically diagnose cancer by giving patients radioactive glucose, and then it's uptaken by all the tissues. But since the tumor has a much higher uptake of glucose than regularly respiring tissue, on a PET scan, you can see the tumor uptaking the glucose and converting it into radioactive lactate. So, yeah, the fermentation is definitely a hallmark of cancer, but also, as Dr. Seyfried said, almost every other chronic disease that we know of, Parkinson's disease, Alzheimer's disease, you know, a lot of the so-called mental health conditions, you can actually see abnormal ratio of the pyruvate to lactate into the blood. In other words, in favor of lactate, which means that even people with mental health conditions are experiencing some kind of a mitochondrial dysfunction, most likely, mostly into the brain, but probably in the rest of the body as well. So my research really has been focused on trying to reduce the fermentation, shift the redox ratio of the cell, especially the mitochondrial ratio, towards oxidation, especially things like the NAD plus to the NADH or the... ubiquinol to ubiquinol or acetoacetate to hydroxybutyrate and this can be done via a number of very simple methods utilizing cofactors that all cells require in order to properly convert the fuel into carbon dioxide and ATP and water.

### Source 10 — Estrogen, progesterone, and cancer: Conflicts of interest in regulation and product promotion.

Ray Peat · Article · 2007 · https://raypeat.com/articles/articles/estrogen-progesterone-cancer.shtml

> But California's OEHHA identifies those eight publications as "the relevant evidence that clearly shows through scientifically valid testing according to generally accepted principles that progesterone causes cancer." In 2004, the agency was petitioned to remove progesterone from the list. In the document rejecting that petition, they mentioned that IARC in 1999 had reviewed newer evidence confirming the carcinogenicity of progesterone. After months of asking the man in charge of rejecting the petition to identify that very important new data, I hadn't received an answer, so I wrote to IARC, and the man in charge there responded: "The IARC (1999) review is actually an IARC Monographs volume (Vol.72) . . . . This volume focuses on contraception and post-menopausal therapy. Progesterone is not used for these indications and, hence, after a quick search in the book I found only one reference that clearly reports an experiment with progesterone." [Wednesday, October 04, 2006 12:44 AM]
>
> That article (Grubbs CJ, Peckham JC & McDonough KD (1983) Effect of ovarian hormones on the induction of 1-methyl-1-nitrosourea-induced mammary cancer. Carcinogenesis 4(4):495-497) reported that progesterone reduced the incidence of mammary cancers caused by a carcinogen administered in vegetable oil. I don't think it's possible that anyone could read articles like this, that don't even claim to show that progesterone causes cancer, and conclude that they provide evidence of progesterone's carcinogenicity. The choice of "evidence" seems to have been a selection of titles of unread articles. And even the title of the 1999 IARC volume would have suggested to most people that it wasn't a review of progesterone.
>
> The lack of vehicle controls in some of the studies, the use of an unnamed vehicle in one beagle study, and the use of tumor-promoting vehicles in most if not all of the studies, means that no scientifically competent or valid studies have been cited by IARC, NTP, or the California state bureaucracy, OEHHA, to support California's claim that they know progesterone is a carcinogen.
>
> In their 2004 document, OEHHA mentioned 17 articles that had been submitted regarding progesterone's protective effects.

### Source 11 — Lactate, metabolic regression, & political-medical implications

Ray Peat · Newsletter · 2020

> The futile “War on Cancer” looked for the cause of cancer in viruses and mutant genes, and denied that metabolism could be relevant. The Human Genome Project and the application of genetic engineering to virology, immunology, and other branches of medicine involved a similar belief in the irrelevance of metabolism.
>
> Otto Warburg and Albert Szent-Györgyi shared a general view of life, in which simple life forms could be sustained by glycolysis (forming lactic acid), while oxidative metabolism, with its capacity to extract many times more energy from a given amount of fuel, is necessary to produce and maintain more complex forms of life. Both of them understood cancer to involve a regression to a primitive form of energy metabolism, glycolysis, which produces lactic acid rather than carbon dioxide. (When glycolysis occurs despite the presence of oxygen, it’s called aerobic glycolysis.)
>
> Warburg showed that in cancer, cellular respiration fails to suppress the production of lactic acid, as it does in normal cells, and that cancer can develop as a result of prolonged oxygen deprivation (with the associated lactic acid production). He observed that anything (including carcinogenic chemicals and radiation) that interferes with oxidative metabolism can lead to a series of changes: inflammation, followed by fibrosis, followed by atrophy and death, or sometimes instead of cell death, some of the cells become cancerous, losing their fixed identity as a differentiated element of a specific kind of tissue, and regress, dedifferentiate, to a primitive lactate-producing metabolism with a tendency to migrate to new locations.
>
> Szent-Györgyi, ten years younger than Warburg, recognized the importance of his work, and began a long project of attempting to understand what it is about oxidative metabolism that not only suppresses the formation of lactic acid, but that accounts for the properties of differentiated life. He believed that it was the movement of electrons in the cell substance that animated cells, and that in the living state there are characteristic differences in the force with which the cell substance manages its electronic system. In the primitive, dedifferentiated state, pyruvic acid is the electron acceptor, turning into lactic acid, and in the fully differentiated state, oxygen is the more powerful electron acceptor, making possible a more intense energy flow (through several intermediate steps), at higher voltage.

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