# Beta oxidation

Category: Metabolism

Also known as: fatty acid oxidation

Beta oxidation is the mitochondrial process that breaks down fatty acids into acetyl-CoA, and in the bioenergetic framework it is treated not as a neutral alternative fuel pathway but as a fundamental stress signal and a metabolic brake on optimal glucose oxidation. The…

12 passages · 2 authors · 2015–2023 · Most-cited: [Georgi Dinkov](https://bioenergeticoracle.com/md/voices/georgi-dinkov/index.md)

Canonical page: https://bioenergeticoracle.com/concepts/beta-oxidation

## Synthesis

**Beta oxidation** is the mitochondrial process that breaks down fatty acids into acetyl-CoA, and in the bioenergetic framework it is treated not as a neutral alternative fuel pathway but as a *fundamental stress signal* and a metabolic brake on optimal glucose oxidation. [Source 6, 7] The evolutionary purpose of fatty acid oxidation is to tap into reserves when high-quality food is unavailable, signaling the organism to compensate by turning off energetically expensive functions such as reproduction, cognition, and tissue maintenance. [Source 6] This shift is described as a **slow-down system** associated with torpor and hibernation, in contrast to the pro-thyroid, structure-renewing oxidation of glucose. [Source 1]

Mechanistically, beta oxidation and glucose oxidation are linked through the **Randle Cycle**, where the products of fat breakdown directly suppress the use of glucose. [Source 2, 4] One product of beta oxidation, malonyl-CoA, specifically inhibits the **pyruvate dehydrogenase complex**, the enzyme that commits pyruvate from glycolysis into the mitochondria. [Source 2] More broadly, when beta oxidation is highly active, it generates an excess of NADH, lowering the *NAD to NADH ratio* and placing the cell in a reductive state. [Source 4, 10] Because pyruvate dehydrogenase requires NAD, this reductive state downregulates the enzyme, causing a buildup of pyruvate. The cell then uses pyruvate as an emergency oxidant to regenerate NAD, producing **lactic acid** as a byproduct. [Source 4, 10] This explains why states of predominant fat oxidation, such as diabetes and cancer, are characterized by elevated lactate and an inability to fully oxidize glucose, which is partially metabolized in the cytosol but stops before entering the Krebs cycle. [Source 2, 4, 10]

Excessive beta oxidation is positioned as the *prima causa* linking stress, diet, and a spectrum of pathologies. [Source 12] Georgi Dinkov has argued that the pathological effects exist on a gradient: the more beta oxidation is increased, the more reductive the cell becomes, driving a progression from mild insulin resistance to diabetes, cardiovascular disease, liver disease, and ultimately cancer. [Source 12] This is because cancer cells produce most of their ATP via beta oxidation, wasting glucose into lactate, and shifting metabolism away from fat oxidation by inhibiting CPT1 with agents like **niacinamide** or **aspirin** can force cancer cells to either normalize or undergo apoptosis. [Source 5, 9] Dinkov notes that while aspirin and niacinamide inhibit lipolysis, they only inhibit the beta oxidation process itself in very high, potentially toxic doses; at physiological doses they do not completely block the pathway. [Source 3] The stress hormone **cortisol** reinforces this pathological shift by increasing fatty acid oxidation and suppressing glucose oxidation, making chronic stress a direct promoter of the beta-oxidation-dominant state. [Source 6]

The consequences of a beta-oxidation-dominant metabolism extend to tissue structure and specific disease states. Hair follicles, described as mini-organs, require glucose as their primary fuel and cannot sustain growth on fatty acids or ketones; their function depends on efficient oxidative metabolism producing carbon dioxide, a process that beta oxidation provides less of, thereby slowing the metabolic rate that maintains structural cohesion. [Source 7] Dinkov has highlighted that conditions like **pulmonary arterial hypertension** and **heart failure** are driven by dramatically elevated fatty acid oxidation and ketogenesis with concomitantly decreased glucose oxidation, framing them as organ-specific manifestations of stress metabolism or "diabetes of the lungs." [Source 8] Even interventions aimed at weight loss through increased fatty acid oxidation have been shown to decrease insulin sensitivity, leading researchers to conclude that promoting this pathway does not have the desired effect. [Source 11]

## People also ask

### How does beta oxidation suppress glucose metabolism?

Peat’s framework describes the Randle Cycle, where products of fat breakdown inhibit glucose use. Specifically, malonyl-CoA blocks the pyruvate dehydrogenase complex, and excess NADH from beta oxidation lowers the NAD to NADH ratio, further downregulating that enzyme and causing pyruvate to be converted into lactic acid instead of entering the Krebs cycle.

### Why is beta oxidation linked to hair loss?

The corpus notes that hair follicles are mini-organs requiring glucose as their primary fuel and cannot sustain growth on fatty acids or ketones. Beta oxidation provides less carbon dioxide, slowing the oxidative metabolic rate needed to maintain the structural cohesion of the follicle.

### What role does cortisol play in promoting fat oxidation?

Peat argued that the stress hormone cortisol reinforces a pathological metabolic shift by increasing fatty acid oxidation and suppressing glucose oxidation, making chronic stress a direct promoter of a beta-oxidation-dominant state.

## Related concepts

- [Fatty Liver Disease](https://bioenergeticoracle.com/md/concepts/fatty-liver-disease/index.md)
- [Lipolysis](https://bioenergeticoracle.com/md/concepts/lipolysis/index.md)
- [Acidosis](https://bioenergeticoracle.com/md/concepts/acidosis/index.md)
- [Estrone](https://bioenergeticoracle.com/md/concepts/estrone/index.md)
- [GABA](https://bioenergeticoracle.com/md/concepts/gaba/index.md)
- [Glycogen](https://bioenergeticoracle.com/md/concepts/glycogen/index.md)

## Cited passages

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

### Source 1 — How to Burn Fat on a Keto Diet (And Why You Shouldn’t) [Generative Energy #29]

Danny Roddy · Interview · Oct 13, 2016 · https://www.youtube.com/watch?v=BN3wx5IW9RI

> **Kyle Mamounis:** I don't have every step in beta-oxidation memorized. But essentially, the acyl chain will get pulled off two carbons at a time, and they'll eventually make their way to acetyl-CoA. the same as the carbons that get pulled off two at a time from glucose. Unless you have a very short fatty acid, there's more carbon lengths there. So you can make more acetyl-CoA. Of course, there's other problems. You know, if you skip the pyruvate dehydrogenase step, then you run out of oxaloacetate. But that's a good thing to them because then you get to make ketones. That's not a bug. That's a feature of fat metabolism.
>
> **Danny Roddy:** And then the pyruvate dehydrogenase, that's a step where carbon dioxide is produced as well.
>
> **Kyle Mamounis:** yes that's the difference in the respiratory quotient between glucose metabolism oxidation and fat oxidation
>
> **Danny Roddy:** you had some amazing points i felt like in the talk just talking about like a broad stroke view of fatty acids being like a break on the metabolism basically and associated with torpor torpor and hibernation and things like that and being a slow down system versus glucose or sugars being useful for maintaining the system and promoting renewal and thyroid and things like that.

### Source 2 — #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 3 — Q&A: Weight Loss, Dating, Red Light, Authorities, Starch Diets [Generative Energy #23]

Danny Roddy · Interview · Mar 3, 2016 · https://www.youtube.com/watch?v=kcU2Mt98nxQ

> **Georgi Dinkov:** It inhibits it, but it doesn't block it, right? There's a difference here. Basically, it inhibits to the point where it will not overwhelm your liver or your brain or some of the other vital organs. Just like I said, there's always some lipolysis going on. That's just how the organism is designed and because the muscles prefer that fat for burning. And basically, in order for you to suppress actual fatty acid oxidation, which is what I think people mean, so let's say like if your liver was really really well functioning if you had let's say you had four livers then then yeah then it would be okay to actually flood the bloodstream with PUFA because all of it will go to these livers they'll glucuronidize it and excrete it but since that is not happening basically you know um you should not be releasing that much PUFA and it's really the i think what people are confusing here is the pulses versus the beta oxidation And aspirin and niacinamide only inhibit beta oxidation in very high doses. And that's actually the mechanism through which the potential toxicity of niacinamide and aspirin has been observed. If you take like six grams of aspirin or more or six grams of niacinamide or more. that starts to inhibit the beta-oxidation process of the actual fats. So basically that may trigger some toxicity. But it has to be done systemically and for very long term and with all these high doses in order for you to observe it. In the doses that Ray recommends and the doses that really most people can tolerate without having other side effects, I don't think you can inhibit lipolysis to the point of reaching that cycle where you're basically inhibiting the oxidation as well. I mean, again, not many people, only the old studies with schizophrenia use 6 grams of niacinamide and more.

### Source 4 — Estrogen, Progesterone and Resveratrol with Georgi Dinkov

Georgi Dinkov · Interview · Sep 16, 2021

> **Matt Blackburn:** That was an awesome, awesome explanation. Yeah, it's palmitic and stearic acid, right? I eat a lot of classified local beef and I feel so good after I eat it. Could you give an explanation of the Randall cycle? Because I came out of the keto community, like a lot of us did, trying lots of crazy stuff. And I heard somewhere where someone was saying it's the closest thing to an on-off switch. But then I've also heard that... our cells are always oxidizing glucose and fatty acids to some degree. Is that kind of, because there's like a keto leader that talks about metabolic flexibility and how we want to be able to oxidize both. That's like a big selling point for his stuff. So I'm just curious about that.
>
> **Georgi Dinkov:** I don't think it's a completely on and off switch, but there's no doubt that the more towards fat oxidation you are, the more the beta oxidation mechanism of the cell is activated. This deactivates the enzyme pyruvate dehydrogenase, which is the first mitochondrial enzyme that takes the output of glycolysis, which is pyruvate, and then basically helps import it inside the mitochondria and continue metabolizing it through the Krebs cycle. and through the electron transport chain. So it's almost like if beta-oxidation is active, then pyruvate dehydrogenase will not work well, or, I mean, it will be down-regulated, so to speak, its activity, right? And then what happens is that this means you'll have a buildup of pyruvate. But because, like, the oxidation of fats produces an excess of NADH, which is – that's really – our fuel is hydrogen, right? We extract hydrogen from the food. and then we passed hydrogen through different portions of the cell through this molecule called NADH, right? And NADH is just the NAD plus a hydrogen ion. So NADH carries this hydrogen, you know, throughout the cell across different steps, and eventually this hydrogen is given to oxygen, and then it becomes water, right? And then in the Krebs cycle, it also generates water, and carbon dioxide is a byproduct. So what happens is that when you have a buildup of NADH, the cell, in order for the cell to continue to exist, the cell still needs to perform a little bit of glycolysis. But glycolysis needs NAD. The cell needs the oxidized version of NAD in order to survive. So it's going to get that NAD any way it can. So what happens is that if you have a buildup of NADH, basically the pyruvate dehydrogenase is not working and then you have a buildup of pyruvate so what do you do to oxidize nadh back to nad if if basically if the if the the pyruvate dehydrogenase is not working you use pyruvate as the emergency oxidant.

### Source 5 — How to Best Optimize Your Muscular Health - Discussion Between Georgi Dinkov, Tyler Lebaron, & Dr. Mercola

Georgi Dinkov · Interview · Jul 23, 2023

> **Georgi Dinkov:** And the latest offshoot of that approach is basically they're saying, let's not worry about the absolute levels of ATP. Let's look at how the ATP is produced. And if you look at the cancer cells, every single type of tumor seen so far produces most of its ATP as a result of beta oxidation. And that's why it's wasting the glucose into lactate. Because when you oxidize predominantly fat, that lowers the NAD to the NADH ratio, which puts the cell in a more reductive state. And also NAD to the NADH ratio is one of the controlling levers on pyruvate dehydrogenase. So some studies lately, over the last maybe not two or three years, one of them used meldonium, which is a drug that inhibits the transport and, of course, the oxidation of the longer chain fatty acids, a Russian drug invented back in the 70s. It's also a doping drug. Because it increased endurance. So they demonstrated complete removal of human neuroglioblastoma in a mouse model by doing nothing else, but lowering basically the excessive oxidation of fats, which allows more glucose to be oxidized and shifts the cancer cell. First, it doesn't change the ATP production. It remains the same. But the mitochondrial NADH to the NADH ratio rises and the cell acidifies, which basically allows it to either return to normal metabolic state or commit apoptosis if it's too damaged to continue.

### Source 6 — Food Metabolism & Diets | Georgi Dinkov

Georgi Dinkov · Interview · Jul 24, 2023

> **Georgi Dinkov:** which a lot of people think is a good thing, but it's actually the natural, the evolutionary purpose of fatty acid oxidation is basically a stress signal. It means that you don't have sufficient access to good, high-quality food. So the body taps into its reserves. And that is a signal for the body that it needs to actually compensate and balance the trade-off by turning off a lot of other functions that are highly energetically expensive. And since the body doesn't have the proper amount of glucose, which is what it prefers to oxidize for really for optimal metabolism, then the body will turn off a lot of other functions such as reproductive function, cognitive function, mood, skin quality, hair quality. You already mentioned it. You've seen a lot of these women going on a low-carb diet for a long time. Eventually, these problems manifest. That's completely normal. And it's been seen in nature too. Basically, there's a study that I posted a couple of years ago on my blog, which showed that the hibernating animals, they gorge themselves up on food during the warm months of the year. And during that time, their health is perfect. And then once they start hibernating, they actually, because they're not eating anymore, they tap into their fat resources. Once they start getting predominantly fat, they meet all of the diagnostic criteria for diabetes. And they stay diabetic while they're hibernating because they're not eating. which is kind of like a surrogate for a low carb diet or chronic fasting or even intermittent fasting. Also surrogate for stress because when you're under stress, when cortisol rises, it increases the level of fatty acid oxidation and suppresses the oxidation of glucose. So basically it shows that, you know, when you're... When you oxidize in fat, it is a sign for the organism that things are not optimal. So the organism is going to compensate and turn off a lot of things that are considered non-essential for survival.

### Source 7 — [2/4] The Male Pattern Baldness Myth - A Bioenergetic View of Pattern Baldness

Danny Roddy · Interview · Aug 3, 2015 · https://www.youtube.com/watch?v=N-KSdzki0-Y

> What about using fat as fuel? Everyone is using fat as fuel to some extent. However, using fat as fuel or beta oxidation skips glycolysis and the link reaction and provides acetyl-CoA for the Krebs cycle. This provides less carbon dioxide in addition to other mechanisms which can slow the rate of metabolism. Why does this matter again? Cells form tissues, tissues form organs, and organs form you. Again, the key idea was that energy and structure are interdependent at every level. Life supports life, function builds structure, and structure produces function. Once the function ceases, the structure collapses. It maintains itself by working. The structure and function of the tissue depend on the energy that the tissue is producing. The mini organ. The hair follicle is often referred to as a mini-organ. The hair follicle maintains its structure by the cohesion of cells. The hair follicle requires oxygen and an energy source to grow. Pathways to yield ATP or energy should be accelerated to meet energy requirements for the growth of hair. Growing hair requires two times the amount of glucose that resting follicles do. However, hair follicles are extremely inefficient at producing energy, converting proportionally more glucose to lactic acid rather than carbon dioxide. Glucose and not fat is the primary fuel of hair follicles. In fact, fatty acids or ketone bodies cannot sustain hair growth in vitro. Tying this all together was a landmark paper describing the association between mitochondrial dysfunction and hair aging. The group concluded that thyroid hormone could be repositioned as mitochondrial hair medicine. This is no surprise as thyroid hormone is often called the hormone of respiration and is needed for the efficient production of energy. Carbon dioxide cannot be produced efficiently without thyroid hormone. Moreover, thyroid hormone is needed to energize cells, which maintains their structure. When thyroid hormone is absent, the cell loses its organization and damage to the mitochondria occurs. While it may seem far-fetched to influence how our cells produce energy, there are many known factors which influence energy metabolism. Free fatty acids. Although all fats and oils, whether of vegetable or plant origin, contain a mixture of saturated, monounsaturated, and polyunsaturated fats, they differ in the proportions of each of these fats. That is to say, the main difference is a matter of degree, not kind.

### Source 8 — Pulmonary hypertension (usually fatal) likely driven by increased fat oxidation (FAO)

Georgi Dinkov · Article · Feb 28, 2020 · https://haidut.me/?p=907

> Most of my medically inclined readers are familiar with the “mysterious” condition pulmonary arterial hypertension (PAH). I put “mysterious” in quotes, because mainstream medicine claims that its cause is unknown, its onset is unpredictable, there is no cure, and females are affected 4-5 times more often than males. Sounds familiar? Yet, while we are being lied to publicly, behind the scenes and without ANY of the usual publicity that Big Pharma loves so much, Pfizer bought the commercial rights for the serotonin antagonist terguride known to not only prevent but also cure the condition. Terguride’s chemical name is dihydro–lisuride, so it is just the slightly-modified, patented version of lisuride.
>
> The fact that serotonin causes PAH is highly indicative of a metabolic cause in this condition, but mainstream medicine keeps vehemently denying any possibility that the condition might be of metabolic origin. Well, such denials will become much more difficult as a result of the study below. It discovered that fatty acid oxidation (FAO) and ketogenesis are dramatically elevated in PAH patients, while glucose oxidation is concomitantly decreased. In other words, PAH may be nothing but just another organ-specific manifestation of the “stress metabolism” – a sort of “diabetes of the lungs” analogous to the recently proposed label for Alzheimer as “diabetes of the brain”. Now, this study did not look at what happens if you inhibit FAO and promote glucose oxidation, but I think the answer is already pretty much known. Why do I think that? Well, just a few days ago, I posted about another study that found switching from fat to glucose oxidation can treat another chronic, lethal, mysterious condition – heart failure.
>
> [references]
>
> Some people may accuse me of jumping the gun and trying to draw parallels between two conditions that have nothing in common. I wonder what those critics would say if I showed them that Pfizer is already testing the drug terguride for heart failure as well. So, apparently the two “mysterious” conditions are quite closely related, and what works for one in terms of metabolic treatments works for the other. So, the next time you meet a doctor who tells you that PAH is incurable and mysterious, just laugh maniacally and show him/her a bottle of aspirin or niacinamide 🙂
>
> [references]

### Source 9 — Fatty acid oxidation (FAO) inhibition abrogates triple-negative breast cancer

Georgi Dinkov · Article · Apr 9, 2020 · https://haidut.me/?p=965

> The evidence for the role of excessive FAO in cancer keeps piling on. As many of my readers know, triple-negative breast cancer is one of the most difficult to treat and its proportion of total breast cancer cases has been steadily rising over the last 20 years. When a patient is diagnosed with such a cancer, oncologists waste no time and put the patient on an aggressive regimen of radiation and cytotoxic chemotherapy as they think this is the patient’s only chance of surviving it. Unlike the more common hormone-sensitive cancers, oncologists do not believe this type of cancer can be slowed down or controlled to the point where the patient lives with it as a form of chronic disease without it becoming life-threatening. Needless to say, metabolic therapies are not even mentioned to the patient simply because oncology does not believe such therapies stand any chance at treating the cancer. Well, the study below begs to disagree. It not only highlights yet again the crucial role of FAO in cancer initiation/progression but it also demonstrates that simply inhibiting FAO can fully stop the cancer growth and ensure 100% survival (see Fig. 4e/4f below). The FAO drug used in the study was etomoxir and it is a so-called CPT1 inhibitor. The HED of etomoxir that abrogated the cancer was about 5mg/kg daily. Unfortunately, etomoxir is severely hepatotoxic and as such its clinical use has been halted, so it would be next to impossible to obtains it for human use or convince a doctor to prescribe it. Fortunately, niacinamide is also a CPT1 inhibitor and can achieve the same effects as etomoxir with a human dose of about 7mg/kg. Needless to say, other FAO inhibitors like aspirin, Mildronate/Meldonium, ethyl pyruvate + ethyl acetoacetate, progesterone, etc can also be used as interventions and will likely be highly synergistic with niacinamide.
>
> [references]

### Source 10 — Estrogen, Progesterone and Resveratrol with Georgi Dinkov

Georgi Dinkov · Interview · Sep 16, 2021

> **Georgi Dinkov:** So in other words, pyruvate oxidizes NADH back to NAD, and the output of this process is lactate. So that's why when you're oxidizing fat, you tend to have elevated levels of lactic acid because your cell cannot properly metabolize the glucose, right? If you eat the glucose, and there's always glucose circulating in your bloodstream because the brain relies mostly on glucose. So this glucose is going to go inside the cells, but if the beta-oxidation process is highly active, you will be in a fairly reductive state, and this glucose cannot be oxidized. In other words, the main determinant of whether glucose is oxidized is the NAD to the NADH ratio, because that's what controls the function of the enzyme pyruvate dehydrogenase. And it just so happens that when beta-oxidation is active, it suppresses that enzyme and also creates this excess of NADH. So you're going to end up wasting what I call the glucose into lactate. Now, I don't think you can completely turn off the glucose oxidation because at least glycolysis is still active, right? That's why we're having this overproduction of lactate that we see in diabetes and cancer cells, right? Because otherwise this lactate wouldn't be there, which means that somehow glucose is being partially metabolized but not fully. It doesn't go through a Krebs cycle. It doesn't go through electron transport chain.

### Source 11 — #04: Endotoxin, Otto Warburg, Cancer, Ketosis, and PUFA with Georgi Dinkov

Georgi Dinkov · Interview · Jun 14, 2019 · https://open.spotify.com/episode/1JcrW0U6ajwgFaDVe04f0m

> **Georgi Dinkov:** So what this study really shows in my opinion is that, at least the way I'm reading, is that they're saying, look, we have to come up with something else because increased fatty acid oxidation will not actually lead to weight loss. And what's more... Towards the end, they say that fatty acid oxidation is actually really controversial. Some studies have shown that insulin sensitivity is decreased when fatty acid oxidation is being promoted. So long story short, they're kind of saying we have to pull the plug on telling people to increase fatty acid oxidation somehow, whether it's through diet. exercise, or getting these drugs that the athletes do because it doesn't have the desired effect. And we're not even talking about the health effects. They're just saying strictly about weight loss. This is not going to work.

### Source 12 — Fatty acid oxidation – linking all illness (especially cancer) with stress and diet (fasting / low-carb)

Georgi Dinkov · Article · Oct 14, 2022 · https://haidut.me/?p=1994

> The study below is one perhaps the most comprehensive review published to date, challenging the medical dogma that cancer is a genetic/mutation disease. As the study aptly explains, the evidence, spanning as far back as Otto Warburg’s original work on this disease, is overwhelmingly in support of cancer being entirely metabolic in origin. Warburg stated that the metabolic defects seen in cancer are “irreversible”, but that does not mean they are of genetic origin! To the contrary – the accumulated evidence strongly suggests that any genetic mutations observed in “cancer” cells are secondary and downstream effects of those cells’ deranged metabolism. When Warburg said the metabolic changes are “irreversible”, apparently he meant that in a strictly “functional” context – i.e. irreversible for as long as the factor driving them is still present. Remove that factor and the “cancer” cells likely revert to normal behavior/metabolism. So, what is that mysterious prima causa of cancer, causing initially its functional derangement (e.g. Warburg Effect) and subsequently its structural changes (genetic mutations)? Well, as the article convincingly demonstrates, (excessive) fatty acid oxidation (FAO), also known as β-oxidation, through the reductive state (lowered mitochondrial NAD/NADH ratio) it leads to is both a necessary and sufficient factor for the initiation, growth and metastasizing of cancer. Thus, FAO is likely that prima causa medicine has been searching for more than century. Conversely, inhibiting FAO is likely the most promising avenue for truly curing that disease, and likely other metabolic (all?) diseases. Speaking of other diseases, as the study demonstrates, there does not seem to be some critical, specific threshold beyond which FAO becomes detrimental. The pathological effects of FAO are basically on a spectrum – the more it is increased the more reductive the redox state of the cell becomes, and the more deranged its metabolism becomes in desperate attempt to allow the cell to survive in this pseudo-hypoxic environment. As such, the “seeds” of cancer development can be seen even in states that medicine considers perfectly normal, and even desirable. Namely, glucose deprivation (through fasting and/or low-carb diets), acute/chronic stress (e.g. exhaustive exercise), or even administration of “beneficial” drugs such as metformin.

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