# Krebs cycle

Category: Metabolism

Also known as: citric acid cycle, TCA cycle, tricarboxylic acid cycle

The Krebs cycle, also known as the citric acid cycle or tricarboxylic acid (TCA) cycle, is the central oxidative pathway of metabolism, functioning as the primary engine for producing usable energy, carbon dioxide, and the electronically desaturated state of living matter. Peat…

11 passages · 3 authors · 2001–2024 · Most-cited: [Georgi Dinkov](https://bioenergeticoracle.com/md/voices/georgi-dinkov/index.md)

Canonical page: https://bioenergeticoracle.com/concepts/krebs-cycle

## Synthesis

**The Krebs cycle**, also known as the citric acid cycle or tricarboxylic acid (TCA) cycle, is the central oxidative pathway of metabolism, functioning as the primary engine for producing usable energy, carbon dioxide, and the *electronically desaturated state* of living matter. [Source 3, 5, 10] Peat framed the cycle not merely as a biochemical sequence but as the core of cellular respiration whose efficient operation is the defining characteristic of health, while its disruption is the common denominator of degenerative disease. [Source 2, 8] The cycle processes **acetyl-CoA**, derived from the decarboxylation of pyruvate, through a series of reactions that generate **NADH** and **carbon dioxide**, with the latter being essential for oxygen delivery via the Bohr effect. [Source 3, 5]

A critical regulatory point preceding the cycle is the enzyme **pyruvate dehydrogenase (PDH)**, which converts pyruvate into acetyl-CoA. [Source 2, 5] Dinkov has described PDH as a rate-limiting "bridge" that, when blocked by factors such as a low mitochondrial NAD+/NADH ratio or deficiency of cofactors like vitamin B1 and magnesium, causes a backlog of glycolytic products. [Source 5, 7] This obstruction forces pyruvate to be reduced to lactic acid instead of entering the Krebs cycle, a metabolic signature Peat associated with cancer, inflammation, and the generalized stress state. [Source 2, 9] The cycle itself can also experience a buildup of electrons if the downstream **electron transport chain** is malfunctioning, a condition that activates *fatty acid synthase* to convert excess citric acid into fat as an emergency electron sink. [Source 10]

Peat emphasized that the cycle's intermediates serve as crucial junction points for managing excitotoxicity and cellular energy. He noted that the amino acids glutamate and aspartate, which act as excitatory signals, are normally consumed in the Krebs cycle as **alpha-ketoglutarate** and **oxaloacetate**, respectively. [Source 6] A deficiency of carbon dioxide, resulting from impaired mitochondrial respiration, prevents the consumption of these excitatory amino acids and the synthesis of urea, creating a self-reinforcing loop of energy failure and cellular excitation that underlies conditions like epilepsy. [Source 6] Szent-Györgyi, whose work was foundational to discovering the cycle, viewed the donation of electrons to cellular systems as the trigger for the active, contracted state, while the high-energy oxidative function of the cycle was the answer to restoring the cell to its stable, resting state. [Source 8]

Dinkov has elaborated on the therapeutic implications of manipulating the cycle, noting that certain **alpha-keto acids** like pyruvate and alpha-ketoglutarate are intermediates that, when supplemented, can theoretically speed up oxidative reactions. [Source 4] He distinguishes these from **beta-keto acids** like acetoacetate, which can serve an oxidizing function, and beta-hydroxybutyrate, whose dangerous accumulation leads to diabetic ketoacidosis. [Source 4] Furthermore, substances like salicylic acid (from aspirin) are understood to reactivate the Krebs cycle and electron transport chain, the two steps that are characteristically suppressed in cancer while glycolysis rages unchecked. [Source 11] The cycle's proper function is thus the fulcrum of Peat's bioenergetic model, where the efficient oxidation of glucose to carbon dioxide is the fundamental process that sustains structure and prevents the *activated, electron-rich state* of pathology. [Source 1, 8]

## People also ask

### How does the Krebs cycle relate to lactic acid production?

Peat argued that when pyruvate dehydrogenase is blocked, pyruvate cannot enter the cycle and is instead reduced to lactic acid, a metabolic signature he associated with cancer and stress.

### What role do Krebs cycle intermediates play in brain excitability?

The corpus describes how glutamate and aspartate are normally consumed as cycle intermediates, and a carbon dioxide deficiency from impaired respiration prevents this, creating a loop of energy failure and excitation linked to epilepsy.

### How can aspirin affect the Krebs cycle?

Dinkov noted that salicylic acid from aspirin can reactivate the Krebs cycle and electron transport chain, which are characteristically suppressed in cancer while glycolysis remains elevated.

## Related concepts

- [Electron transport chain](https://bioenergeticoracle.com/md/concepts/electron-transport-chain/index.md)
- [Aspirin](https://bioenergeticoracle.com/md/concepts/aspirin/index.md)
- [Cancer metabolism](https://bioenergeticoracle.com/md/concepts/cancer-metabolism/index.md)
- [Cascara Sagrada](https://bioenergeticoracle.com/md/concepts/cascara-sagrada/index.md)
- [Epilepsy](https://bioenergeticoracle.com/md/concepts/epilepsy/index.md)
- [Estrogen dominance](https://bioenergeticoracle.com/md/concepts/estrogen-dominance/index.md)

## Cited passages

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

### Source 1 — Heart and hormones

Ray Peat · Article · 2015 · https://raypeat.com/articles/articles/heart-hormones.shtml

> Although Albert Szent-Gyorgyi is known mostly for his discovery of vitamin C and his contribution to understanding the tricarboxylic acid or Krebs cycle, his main interest was in understanding the nature of life itself, and he focused mainly on muscle contraction and cancer growth regulation. In one of his experiments, he compared the effects of estrogen and progesterone on rabbit hearts. A basic property of the heart muscle is that when it beats more frequently, it beats more strongly. This is called the staircase effect, from the way a tracing of its motion rises, beat by beat, as the rate of stimulation is increased. This is a logical way to behave, but sometimes it fails to occur: In shock, and in heart failure, the pulse rate increases, without increasing the volume of blood pumped in each contraction.
>
> Szent-Gyorgyi found that estrogen treatment decreased the staircase effect, while progesterone treatment increased the staircase. He described the staircase as a situation in which function (the rate of contraction) builds structure (the size of the contraction). Progesterone allowed "structure" to be built by the contraction, and estrogen prevented that.
>
> (It's interesting to compare these effects of the hormones to the more general idea of anabolic and catabolic hormones, in which more permanent structures in cells are affected.)
>
> The rapid and extensive alternation of contraction and relaxation made possible by progesterone is also produced by testosterone (Tsang, et al., 2009). Things that increase the force of contraction are called inotropic, and the things that promote relaxation are called lusitropic; progesterone and testosterone are both positively inotropic and lusitropic, improving contraction and relaxation. Estrogen is a negative lusitropic hormone (Filice, et al., 2011), and also a negative inotropic hormone (Sitzler, et al., 1996), that is, it impairs both relaxation and contraction.
>
> Another standard term describing heart function is chronotropy, referring to the frequency of contraction. Because of the staircase interaction of frequency and force, there has been some confusion in classifying drugs according to chronotropism. In a state of shock or estrogen dominance, an inotropic drug will slow the heart rate by increasing the amount of blood pumped.

### Source 2 — Episode 2: Georgi Dinkov (Haidut) - Personal History, the Metabolic Process in the Body, Heroic Medicine

Georgi Dinkov · Interview · Dec 22, 2019 · https://www.youtube.com/watch?v=BFku5gD73-k

> **Georgi Dinkov:** Glycolysis, the Krebs cycle, or the citric acid cycle, and the last step is the electron chain. So the first step, glycolysis, in it there are eight substeps, the glucose that you have eaten is converted into a molecule called pyruvate. And in this process, the first phase, the result of metabolizing one molecule of glucose is two molecules of ATP. After that this pyruvate has to enter the Krebs cycle, or the so-called citric acid cycle. There is a very important enzyme, which has to take pyruvate as raw material and convert it into something else that the Krebs cycle can use as raw material for itself, to continue producing and, so to speak, transferring electrons down the pathway, and to produce ATP and carbon dioxide. This enzyme is called pyruvate dehydrogenase. And it has been shown that this enzyme works almost not at all in cancer cells. There are some drugs that are not approved for cancer, but there are very successful experiments with them. One of them is dichloroacetate, which if you type DCA into Google, cancer, it will immediately bring up all these studies that have come out with it. They are mainly done in Canada, because there medicine is more or less not as commercialized, but it activates this enzyme. It shows that activation of the main enzyme that is responsible almost for glucose metabolism in the body leads to very rapid disappearance of very advanced stages of deadly cancers. Brain cancer, pancreatic cancer, melanoma, and so on. It does not work for all cancers, but the very fact that there are cases and a significant option with humans, the very fact that it leads to such rapid disappearance of such advanced cancer, I think for me it shows unambiguously that cancer is not a genetic disease, because if it were a genetic disease, then the metabolic approach should not work. Because genetic theory says, once the cell mutates and turns into a cancerous one, the patient's only chance is burn, poison, cut.

### Source 3 — Carbon Dioxide: The "Cure" for Male Pattern Baldness?

Danny Roddy · Video Transcript · Sep 6, 2016 · https://www.youtube.com/watch?v=6PBKLRtp30E

> Pyruvate is being decarboxylated into acetyl-CoA, releasing carbon dioxide. The acetyl-CoA is going into the Krebs or citric acid cycle, producing water, ATP, and carbon dioxide. Really simplistic. I know it's much more complicated. But that is the basic view of mitochondrial respiration and the production of carbon dioxide. So you have to metabolize glucose efficiently in order to produce carbon dioxide. And the reason why that is important is hemoglobin carries oxygen in the blood and you need a sufficient amount of carbon dioxide via the Bohr effect to release the oxygen from the hemoglobin. So the cells, tissues and organs, the hair follicle is a mini organ, can absorb the oxygen and produce their energy and maintain their structure and all their fulfill all their duties they need. So I think in 1958 Montagna said that a hair follicle needs two basic things. It needs energy substrate like glucose or pyruvate or fructose and it needs oxygen. So if you just think of an extremely basic way and lots of things are happening in baldness to inhibit that energy metabolism. And so just to kind of prove this point, in 2007 they say, carbon dioxide facilitates oxygen delivery to the tissues by changing the affinity of oxygen to hemoglobin and increases cerebral blood flow by effects of arterial blood pressure and on cerebral vessels. Recent clinical studies show improved brain oxygenation when hypoxia is combined with hypercapnia, which is lots of carbon dioxide. anti-inflammatory and protective against organ injury. Properties of CO2 may have therapeutic importance. So just to tag onto that, azetazolamide, a drug that inhibits the breakdown of carbon dioxide through inhibiting the enzyme carbonic anhydrase. That has been used to treat male pattern baldness. I haven't heard much talk of it. I'm still looking for additional information on it. But just knowing that, it's kind of a proof of concept that this isn't just complete, total theory, and it has been applied that something like azetazolamide would be used for baldness.

### Source 4 — [EP.18] Georgi Dinkov - on Keto Acids, PUFA, and Kompirin

Georgi Dinkov · Interview · Feb 14, 2022 · https://www.youtube.com/watch?v=gk7dvEWTSlA

> **Veselin Velichkov:** Start recording. We are recording. Hi! Hello! Well, good. Greetings to everyone from those two who have gotten together for a little chat. In the podcast Feel, Think, Act, we are supposed to follow some rules, a bit more marketing-like, so to speak. But we simply like to chat and talk about interesting things without following all the marketing rules. I wondered for a long time what topic we should talk about, because there are always topics that repeat for you and we say somewhere, even in English or like that, the same thing repeated, there has to be some uniqueness and... surely there are things that still have not been said, but the thing that was interesting to me, and I think will be interesting to our viewers too, is keto acids. They have been mentioned lightly, but not much is said about them, even in the Ray Peat environment, let's say. We are not talking about people in general; there it is not at all. In reality, when a person looks, there are few articles, little like that. Over time it has not been something very deeply explored, maybe. Maybe if you have gone deeper into it, you will tell us a little more about keto acids, what they are. In general, let's start from the most general things, because many people will already say, what is this, man? Yes.
>
> **Georgi Dinkov:** Keto acids, in principle, are such organic substances, complex molecules, which have a carboxyl group and a ketone. And in practice there are three types of keto acids: alpha, beta, and gamma. And depending on their type, that is, which group they fall into, they have different functions in the human body. Alpha-keto acids, for example, are very important for the Krebs cycle. Pyruvic acid, or pyruvate, I suppose that is how it is translated in Bulgarian, is very important, because this is the first step of the Krebs cycle. The first step of oxidative metabolism. Another alpha-keto acid is alpha-ketoglutarate. You may have seen it; it is sold as a supplement. And quite a few bodybuilders stuff themselves with it, because the explanation is, to some extent it is true, that if you take some of the intermediate products of the Krebs cycle, such as succinate, succinic acid, fumarate, alpha-ketoglutarate, pyruvate, this will speed up the reactions in the Krebs cycle and in practice metabolism will increase, you will have more energy, and eventually, so to speak, you may lose weight. And that is one of the reasons alpha-ketoglutarate is sold as a supplement. And it is quite expensive, by the way, if you start looking at it as such. But, so... It turns out that these are the alpha-keto acids; the beta-keto acids are of the type acetoacetate, which is present in our product Pyrucet. In fact, it is a combination of an alpha-keto acid and a beta-keto acid. You have pyruvate and acetoacetate. Beta-keto acids are usually created when there is an accumulation of fats in the blood. Whether it is from increased lipolysis, whether it is because the person is diabetic, but again, whether this is due to increased lipolysis. In practice, if there is no source of glucose in the body, the level of beta-keto acids, such as acetoacetate and beta-hydroxybutyrate, rises.

### Source 5 — #15: NAD+/NADH Redox Balance, Vitamin D, Sugar, Genetic Determinism & Vitamin E with Georgi Dinkov

Georgi Dinkov · Interview · Jan 4, 2020 · https://open.spotify.com/episode/1gP8sg3BC6RsOGu46ePtCS

> **Georgi Dinkov:** So, okay, so the liver converted this extra lactic acid back to glucose, right? But you're back at step one. So this glucose has to go through glycolysis, right? Generate NADH again and pyruvate, and you're back at the step, the rate-limiting step of metabolism of glucose is pyruvate dehydrogenase. So the things that determine the function, the primary factors that determine the function of this enzyme is the availability of vitamin B1, the availability of magnesium, and actually, ironically, the ratio of NAD to the NADH. But it's the mitochondrial ratio of NAD to the NADH. And in order for this ratio to be high inside of the mitochondria, this means that the Krebs cycle and the electron transport chain have to be working well in order for this intermitohondrial NADH to be reoxidized back into NAD. Because inside the mitochondria, the cell doesn't have the emergency option of using pyruvate or another emergency oxidant unless, again, I'm giving the disclaimer, unless you're supplementing with something. like quinols, things like emergency oxidizing agents. So if the pyruvate dehydrogenase enzyme is working well, then basically it takes that pyruvate and it converts it into acetyl-CoA. And then you have the Krebs cycle, which I think has like six or 10 different sub-steps. There are several sub-steps, and then they create additional... So the acetyl-CoA can basically get converted into alpha-ketoglutarate, succinic acid, fumaric acid. And ultimately, there's no end because it's a cycle, right? But there's a step in the Krebs cycle from which the succinic acid can actually jump into the electron transport chain. And the first step is known as succinic dehydrogenase. That is the enzyme that is the first one of the electron transport chain. And along all of these steps, you're basically oxidizing NADH, accepting that electron, reoxidizing the NADH back into NAD, and also generating carbon dioxide.

### Source 6 — Epilepsy and Progesterone

Ray Peat · Article · 2006 · https://raypeat.com/articles/articles/epilepsy-progesterone.shtml

> Once an excitotoxic state exists, the consequences of cell exhaustion can increase the likelihood that the condition will spread to other cells, since any excitation can trigger a complex of other excitatory processes. As calcium enters cells, potassium leaves, and enzymes are activated, producing free fatty acids (linoleic and arachidonic, for example) and prostaglandins, which activate other processes, including lipid peroxidation and free radical production.
>
> Protein kinase C (promoted by unsaturated fats and estrogen) facilitates the release of excitatory amino acids. (See J. W. Phillis and M. H. O'Regan, "Mechanisms of glutamate and aspartate release in the ischemic rat cerebral cortex," Br. Res. 730(1-2), 150-164, 1996.) Estrogen supports acetylcholine release, which leads to increased extracellular potassium and excitatory amino acids. (See R. B. Gibbs, et al., "Effects of estrogen on potassium-stimulated acetylcholine release in the hippocampus and overlying cortex of adult rats," Br. Res. 749(1), 143-146, 1997.) Estrogen also stimulates the production of free radicals. Calcium, free radicals, and unsaturated free fatty acids impair energy production, decreasing the ability to regulate potassium and calcium.
>
> The increased estrogen associated with seizures is associated with reduced serum calcium (Jacono and Robertson, 1987). Feedback self-stimulation of free radicals, free fatty acids, and prostaglandins create a bias toward increased excitation. Ammonia is produced by stimulated nerves, and normally its elimination helps to eliminate and control the excitotoxic amino acids, glutamate and aspartate. The production of urea consumes aspartic acid, converting it to fumaric acid, but this requires carbon dioxide, produced by normal mitochondrial function.
>
> A deficiency of carbon dioxide would reduce the delivery of oxygen to the brain by constricting blood vessels and changing hemoglobin's affinity for oxygen (limiting carbon dioxide production), and the failure to consume aspartate (in urea synthesis) and glutamate (as alpha-ketoglutarate) and aspartate (as oxaloacetate) in the Krebs cycle, means that as energy becomes deficient, excitation tends to be promoted.

### Source 7 — How To Unblock Your Metabolism - Georgi Dinkov

Georgi Dinkov · Interview · May 8, 2024 · https://www.youtube.com/watch?v=skeXyC1_MVA

> **Georgi Dinkov:** He's saying cancer cells, when I look at them structurally, they have nothing wrong with them but for some reason once they decide to become cancer state cancer cells and we give them oxygen they don't revert back to normal but he said it still is metabolic i don't see any structurally any structural damage to them so he didn't know at the time there is this enzyme peruvian hydrogenase and they can be blocked so if it gets blocked or completely destroyed the bridge collapses then peruvian the cars will accumulate right and at some point they'll probably start falling into the river because there's too much of an accumulation you're always eating there's always food coming in right so biotin will take some of these cars and you know route them through an alternative bridge and then the you know that that later area after the bridges is known as the Krebs cycle which is now part of the mitochondria once you enter the mitochondria then usually all things are fine uh very rare diseases genetic ones have damages to one of the enzymes of the Krebs cycle right but they're but they're so this is a soul severe most people don't survive beyond the first year after birth so it's like chances are you don't have that okay if there's any issue it's the deficiency of a cofactor or whatnot otherwise you wouldn't make it past one series of age and then there is there is potentially another blockage that can happen at the electron transport chain right but it can also be reversed uh usually the the the big block is a complex one which is dependent on the nad plus to the nadh ratio so by giving niacinamide you're also unplugging that block as well And finally, there can be, you know, commonly blocked complex IV, which is known as cytochrome C oxidase. In people in an extremely stressed state, they produce a lot of nitric oxide. Nitric oxide, a lot of bodybuilders and sports people take it because it's a viral dilatory molecule.

### Source 8 — Suppression of Cancer Treatments — Politics & Science, 2001

Ray Peat · Interview · 2001

> **Jon Barkhausen:** Is this why he received the Nobel Prize for?
>
> **Ray Peat:** Yes, for his discoveries that led to the Krebs cycle, and ascorbic acid, and so on (respiration). And muscle studies, too. The muscle action was another one of Krebs things – you know, the methyl-guanidine causing muscle contraction by donating electrons to a system that should have the electrons withdrawn by the oxidative catalyst. And this became clearer and clearer in Szent-Györgyi's work (why he was working both on muscle contraction and oxidative metabolism). At the time, it seemed like he was working on two separate lines. But Koch is the explanation of Szent-Györgyi's whole career, basically. He later became explicit in showing why the donation of electrons to muscles causes them to contract. And another theory that just becomes an obstacle to understanding (besides the *Bronsted-Lowry* proton theory of acids), is the membrane theory of cell function, which explains cell electricity in terms of ions and protons. And Szent-Györgyi was working on the direct involvement of electrons and respiration as the primary thing that regulates those electrons. And in consciousness for example, consciousness disappears instantly when oxygen is no longer available to accept electrons, before there is any detectable change in cellular energy level. Szent-Györgyi was focusing on these things that really work, really explain cell physiology, and basically ignoring the silliness about protons, and cell membranes, and so on. And one of Szent- Gyorgyi's experiments involved adding electron donor chemicals and electron acceptor chemicals to a living muscle; and if the donor and acceptor were related to each other in terms of their oxidation potential, the muscle would contract in their presence. But if these two groups were not tuned to each other, the muscle wouldn't react.

### Source 9 — Cancer: Disorder and Energy

Ray Peat · Article · 2014 · https://raypeat.com/articles/articles/cancer-disorder-energy.shtml

> When glutamine enters the Krebs cycle to be used as fuel, this interferes with the ability to oxidize glucose, causing more lactic acid to be formed, contributing to the excitation and increased energy requirement.
>
> Lactic acid activates the other major mediators of inflammation, including prostaglandins (made from PUFA), free fatty acids (including arachidonate, that forms prostaglandins; Schoonderwoerd, et al., 1989), nitric oxide, carbon monoxide, proteolytic enzymes that degrade the extracellular matrix, TNF (Jensen, et al., 1990), hypoxia inducible factor (Lu, et al., 2002; McFate, et al., 2008), interferon, and interleukins. Arachidonic acid itself can increase lactate production (Meroni, et al., 2003). TNFalpha and interferon gamma activate lactic acid production by increasing prostaglandins (Taylor, et al., 1992).
>
> Most of the present information about cancer cells' behavior, such as reactions to radiation and chemical toxins, has been based on the study of cells in culture dishes. For more than 70 years, it was generally believed that radiation caused mutations and cancer by directly modifying the cells' genetic material. Then, it was discovered that fresh cells that were added to a dish of irradiated cells also developed mutations. The radiation causes cells to emit excitatory, inflammatory, substances such as serotonin and nitric oxide, which injure the cells that are later put near them.
>
> Applying this information to the existing knowledge that radiation induces cancer in animals, the doctrine of genetic determinism inferred that the radiation "bystander effect" is just another mechanism by which radiation produces the "mutant cancer cell" or clone of cancer cells. But the difference between events in vitro and in vivo is that cells which are injured in the organism immediately initiate a process of healing, and in that situation each of the substances emitted by injured cells is acting both locally and systemically to activate repair or regeneration of the damaged tissue. Cells isolated in a culture dish can't call on the organism for the necessary materials, so the responses of the "bystander" cells, leading to mutations and death, seem meaningless. The injured cells are merely toxic, rather than potentially being a stimulus to healing.

### Source 10 — #15: NAD+/NADH Redox Balance, Vitamin D, Sugar, Genetic Determinism & Vitamin E with Georgi Dinkov

Georgi Dinkov · Interview · Jan 4, 2020 · https://open.spotify.com/episode/1gP8sg3BC6RsOGu46ePtCS

> **Georgi Dinkov:** So I forgot to mention another emergency mechanism the body has to deal with, and I posted, I think I sent you that link, is that synthesizing fat. So actually there was a study published that showed that actually, like basically the accumulation of fat, aside from other reasons such as high cortisol, I mean, they're all correlated, but the primary driver behind this process is that these actual electrons have to go somewhere. And once they enter the Krebs cycle, if something else is malfunctioning, such as the electrode transport chain, so the Krebs cycle can also have a buildup of electrons, right? So if there is a buildup of electrons in the Krebs cycle, the only other thing that can get them out of there is fatty acid synthase. That enzyme gets activated when there is a buildup of citric acid, which is one of the intermediaries inside the Krebs cycle. So if there's extra electrons, they cannot go to the electron transport chain and meet with oxygen. Then the only other thing they can do inside the Krebs cycle is get converted to fat by the enzyme fatty acid synthase, which happens to be. non-coincidentally, upregulated tremendously in every single cancer type known to medicine so far. To the point that, even though your doctor is not going to tell you this, but you can Google and verify this yourselves, there are multiple clinical trials right now with fatty acid synthase inhibitors as treatments, as hopefully cures for some of the worst cancers that we know, like pancreatic cancer, melanoma. neuroglioblastoma, a number of these cancers that have no known treatments. Well, maybe melanoma is kind of changing lately because they're starting to be immune therapy. But... Cancers that were considered that essentially untouchable, something as simple as inhibiting the ability of the body to synthesize fat, turns out to be tremendously therapeutic.

### Source 11 — Episode 9: Georgi Dinkov on Methylene Blue, Progesterone, Pregnenolone, DHEA, Quinones, Aspirin, and Vitamin C

Georgi Dinkov · Interview · Aug 9, 2020 · https://www.youtube.com/watch?v=tFEFk4s3R98

> **Georgi Dinkov:** So salicylic acid by itself is not absorbed very well by the stomach, and when it is acetylsalicylic acid, that is, with this additional acetyl group attached to it, it is absorbed much better and enters the cell much more easily, where after about 15, when you drink an aspirin, after about 15 minutes, if they check you, if they take blood, they will not find aspirin in the blood. They will find only salicylic acid and acetic acid. That is, it has already broken down into the main components. Also, the acetyl group has its own unique effect, and it is connected a little with anticoagulation. So acetylsalicylic acid, in other words aspirin, has a slightly stronger anticoagulant effect than salicylic acid, and this is due to the acetyl group aspirin has. Another thing is that because of this acetyl group, aspirin also has a slightly stronger antipyretic effect than salicylic acid. In other words, it is a little more effective at reducing temperature if you have a high temperature. But in general the metabolic effects of aspirin are almost identical to those of salicylic acid, because after about 15 minutes, whatever dose of aspirin you take, after about 15 minutes it has already broken down into salicylic acid and acetic acid. And from then on, salicylic acid stimulates metabolism, specifically these last two steps. You have glycolysis, the Krebs cycle or citric acid cycle, and the electron transport complex. And we already know that in all diseases, whether we call them metabolic or others, especially in cancer, the first step is very well expressed, glycolysis, an enormous amount of lactic acid is produced because of it, but the other two steps do not work. Acetylsalicylic acid and salicylic acid and the phenols in nature reactivate these two last steps, which do not work in cancer. Also, salicylic acid and most phenols in nature function as aromatase inhibitors.

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