# Lipolysis

Category: Metabolism

The liberation of free fatty acids from triglycerides, the neutral form in which fats are stored, bound to glycerine.

11 passages · 3 authors · 1993–2022 · Most-cited: [Georgi Dinkov](https://bioenergeticoracle.com/md/voices/georgi-dinkov/index.md)

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

## Synthesis

**Lipolysis** is the breaking down of fats, specifically the liberation of fatty acids from storage triglycerides into the bloodstream. [Source 1, 4] In Ray Peat's framework, this process is not merely a metabolic convenience but a central axis of stress and disease. Peat noted that **Thyroid Stimulating Hormone (TSH)** itself can produce lipolysis, raising circulating free fatty acids and potentially contributing to *functional hypothyroidism* due to the antimetabolic effects of unsaturated fatty acids. [Source 2] Dinkov has extended this, arguing that the primary hormones determining the activity of lipolytic enzymes are **cortisol** and **adrenaline**, and that chronically elevated lipolysis is a hallmark of metabolic dysfunction. [Source 6]

The distinction between basal and excessive lipolysis is critical. Dinkov emphasizes that there is always *basal lipolysis* occurring because at rest, muscles—especially the heart—primarily burn fat. [Source 3, 7] Roddy has clarified that interventions like aspirin or niacinamide do not systemically block this process but inhibit it to a point where it will not overwhelm the liver or other vital organs. [Source 7] The danger arises from excessive lipolysis, which floods the bloodstream with free fatty acids, predominantly **polyunsaturated fatty acids (PUFA)**. This surge blocks the metabolism of sugar via the *Randle cycle*, directly poisoning the pancreas and preventing insulin from acting on glucose transporters, thereby locking glucose out of the cell. [Source 3, 11]

Excessive lipolysis is a primary driver of organ damage. Dinkov has detailed how fat cells undergoing stress shed not only fatty acids but also **mitochondrial fragments** into the bloodstream, which the organism interprets as a danger signal, activating the stress system (HPA axis) and suppressing gonadal and thyroid function. [Source 5] This process increases reactive oxygen species (ROS) production in organs like the heart, leading to long-term damage such as fibrosis and congestive heart failure. [Source 5] Furthermore, the liver has a fixed capacity to process fat; when lipolysis is elevated, the liver re-esterifies the excess into triglycerides and stores them internally, directly fattening the organ and causing insulin resistance. [Source 9] The kidneys and brain are also highly susceptible to this PUFA-driven damage. [Source 8]

The link between lipolysis and cancer is established through estrogenic signaling. Dinkov has cited evidence that elevated lipolysis and its product, free fatty acids, drive breast cancer growth by directly activating **estrogen receptors** and increasing inflammation, while simultaneously suppressing Krebs cycle activity. [Source 10] Conversely, lowering lipolysis reduces estrogenic signaling and abolishes cancer growth. [Source 10] This explains why anti-lipolytic interventions like aspirin and niacinamide, which inhibit the enzyme fatty acid synthase (FAS), demonstrate strikingly lower rates of chronic diseases. [Source 5, 10] Dinkov notes that the drug **Acipimox**, a niacinamide derivative, works primarily by lowering lipolysis, which allows insulin to function properly and decreases blood glucose, demonstrating that fat, not sugar, is the fundamental metabolic problem. [Source 11]

Maintaining a low baseline lipolysis is therefore a central therapeutic goal. Dinkov suggests that increasing lean muscle mass through *concentric exercise* is a key strategy, as muscle acts as a sink for fatty acids, burning them at rest and preventing them from overwhelming organs. [Source 3, 8] He warns that one can sense excessive lipolysis by the smell of **glycerol** on the breath, a byproduct of triglyceride breakdown, indicating a harmful state of overexertion. [Source 8] Populations with remarkably low baseline lipolysis, such as certain traditional tribes eating high-starch diets, exhibit high metabolic rates and low levels of stress hormones, supporting the hypothesis that keeping lipolysis low is essential for oxidizing glucose and maintaining metabolic health. [Source 6]

## People also ask

### How does excessive lipolysis interfere with sugar metabolism?

Peat’s framework describes how a surge of free fatty acids, especially polyunsaturated fats, blocks sugar metabolism via the Randle cycle, poisoning the pancreas and preventing insulin from acting on glucose transporters.

### Why is the smell of glycerol on the breath considered a warning sign?

Dinkov noted that glycerol is a byproduct of triglyceride breakdown, so its presence on the breath indicates a harmful state of excessive lipolysis and overexertion.

### What role does muscle mass play in controlling lipolysis?

Dinkov suggested that increasing lean muscle through concentric exercise helps because muscle acts as a sink for fatty acids, burning them at rest and preventing them from overwhelming organs.

## Related concepts

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## Cited passages

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

### Source 1 — Nutrition for Women

Ray Peat · Book · 1993

> We synthesize many fats, but some others must be included in the diet — essential fatty acids, or "vitamin F."
>
> Lipolysis: the breaking down of fats, it commonly refers to the breakdown of storage triglycerides into fatty acids and glycerol.
>
> Minerals: generally, these are all the elements that are needed by organisms, but which can be found in nature independently, though carbon, nitrogen, and water are not called minerals. They have structural, chemical, and catalytic functions.
>
> Mitochondria: small "compartments" in the cytoplasm (the viscous part of the cell, everything but the nucleus), they are responsible for much of the cell's energy production (as ATP) and oxygen consumption.
>
> Nutrition: a branch of biology or physiology, an area of scientific study which overlaps many other areas, including biochemistry, physiological chemistry, reproduction and growth, microbiology, general and comparative physiology. etc. Easily distinguished from dietetics, which tends to be concerned more narrowly with the regulation of food intake, but also with cooking and food prices, serving food, and professionalism.
>
> Proteins: with water, proteins are the main structural components of the animal body. They are also the catalysts (enzymes) which govern the rate of almost every chemical reaction in the organism. The third type of protein is used for immunity: antibodies. Proteins are synthesized in cells in a linear manner, connecting many (50 to a few hundred) amino acids in a row, but the most soluble (hydrophilic, water-loving) normally take on a compact, roughly spherical form. They are classed as "macromolecules," molecules which are so large that they have special properties; it is sometimes more useful to think of them as a "system" than as a unit. When proteins are digested, they are broken down (more or less completely) into amino acids. These smaller molecules (a little smaller than sugar molecules, they weigh roughly 100 times more than a hydrogen atom) are composed of carbon, hydrogen, oxygen, nitrogen, and sometimes sulfur. Along the "backbone" of a protein, the atoms nitrogen, carbon, and another carbon, from each amino acid, repeat regularly: N- C-C, -N-C-C, -N-C-C, etc.

### Source 2 — Glossary

Ray Peat · Glossary

> Thyroid Stimulating Hormone (TSH)
>
> TSH itself can produce lipolysis, raising the level of circulating free fatty acids. This suggests that a high level of TSH could sometimes contribute to functional hypothyroidism, because of the antimetabolic effects of the unsaturated fatty acids

### Source 3 — Episode 6: Georgi Dinkov (Haidut) on Diabetes and Insulin Resistance

Georgi Dinkov · Interview · May 1, 2020 · https://www.youtube.com/watch?v=e_OxeTCw6J8

> **Georgi Dinkov:** I understand you, I believe you, I see that the meaning is that when people have even measured this in their blood, they have measured the fatty acids and indeed, when the fatty acids rise, blood sugar also rises, because fatty acids block the metabolism of sugar. And they say, okay, but I am a fat person, so in order for me to be entirely cured, that is, to remove my type 2 diabetes, I have to lose weight. Which is known; medicine recognizes this too. And there are even special interventions with the idea of losing weight. Yes, this works, but 30% of these people can develop type 1 diabetes because while you are fasting, you are exposed to too many fatty acids and, as I said, if this level rises to a certain degree, you can fall into diabetic ketoacidosis or your pancreas can be completely destroyed. Usually these hunger treatments are under medical supervision, and if they have to fall into some state, immediately they are given an injection of insulin to lower the level of fatty acids. But the whole idea is the following. One must lose weight to defeat type 2 diabetes, to cure it completely. And the question or criticism I get from clients is the following: okay, but now when I take nicotinamide and when I take aspirin or acipimox or whatever, if I suppress lipolysis, then those fatty acids remain in me and I cannot burn them, that is, I will not have diabetes while I take these things, but practically the diabetes remains. That is, the moment I stop taking them, these fatty acids return to the blood and practically I again fall into a diabetic state. So if I want to be entirely healthy I have to lose weight. How can I lose weight if I am suppressing the burning of fatty acids, because I am keeping them in me in the adipose tissue by inhibiting... The drugs I mentioned—aspirin, nicotinamide, acipimox and so on—they do not suppress lipolysis 100%. They suppress so-called excessive lipolysis, which leads to diabetes.

### Source 4 — #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

> **Danny Roddy:** Again, there's different ways to approach it, but a person doing anything to improve their health from the standard American stuff is probably beneficial. And I think we've said that like two or three times. So...
>
> **Kyle Mamounis:** There's a super chat question. Oh, yeah.
>
> **Danny Roddy:** I was going to do them at the very, very, very end, but we should probably do them now. Okay. Ellie says, how's it going with a GIF? Thank you, Ellie. Steph, for $31.41. Thank you so much, Steph. You're amazing. You're the best moderator ever. And Soma says, Kyle, can you clarify the difference between lipolysis and fat oxidation, also re-esterification? Keto and Ray Peat followers use these terms incorrectly.

### Source 5 — How lipolysis may damage organs such as the heart

Georgi Dinkov · Article · Aug 27, 2021 · https://haidut.me/?p=1606

> It is well-known in endocrinology, and especially among doctors specializing in diabetes, that excessive lipolysis is highly detrimental not only for the overall progression of metabolic diseases like diabetes, but also for most of the organs of the patient. Lipolysis is known to be elevated in most obese people, and especially in people with diabetes. One of the most common morbidities observed in diabetes patients is cardiovascular disease. In fact, most type II diabetic patients eventually succumb to either kidney failure or heart attacks. However, despite the well-established connection between diabetes and heart disease medicine still does not have an explanation as to how diabetes causes heart disease. The study below demonstrates that lipolysis may play a key role in damaging the heart, not only by supplying the highly inflammatory PUFA, but also by increasing production of ROS. While the study only looked at ROS production in the heart, the mechanism is generic enough to apply to all other organs and as such explain their damage in diabetic patients as well. Namely, during lipolysis (which is elevated during stress) fat cells shed their contents into the bloodstream. The contents includes not only fatty acids (predominantly PUFA) but also mitochondrial fragments from the fat cells. Fat cells are, after all, structurally similar to other cells (except red blood cells, which do not have mitochondria) and as such contain mitochondria. Multiple studies have demonstrated that the presence of mitochondrial debris in the bloodstream is interpreted as a stress signal by the organism, with the subsequent activation of the stress system (HPA axis), suppression of gonadal/thyroid axis, and activation of various defense systems such as the heat-shock proteins, serotonin, estrogen, etc at the expense of overall systemic health of the organism. The study below confirms that the presence of fat cell mitochondria in the blood stream triggers the activation of such stress systems in the heart, with the resulting increase in ROS production. This ROS burst “primes” the heart to be prepared in the case of a future ischemic event. However, that “preparedness” for stress comes at the cost of long-term damage, usually in the form of fibrosis. So, while the study suggests chronically elevated lipolysis may help the heart survive a single ischemic event, it essentially guarantees long-term (usually terminal) pathology such as congestive heart failure.

### Source 6 — Georgi Dinkov, Brad Marshall on Obesity Causes and Solutions

Georgi Dinkov · Interview · Jul 11, 2022

> **Georgi Dinkov:** And it turns out that these people have a remarkably low rate of baseline lipolysis, which is the breakdown of fat from the fatty tissue to go into the bloodstream. Why? Well, I guess they, I mean... at this point it's probably accumulated enough to be either either genetic or at very least epigenetic throughout the generations but it looks like they have a very very low baseline levels of cortisol and adrenaline which are the two hormones that determine essentially how active your your lipolytic enzymes will be they're

### Source 7 — 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

> **Danny Roddy:** just to touch on this it's so often stated that ray or or the idea is that you're completely inhibiting lipolysis and this is just impossible you're always burning fat to some extent i know we've mentioned that before but it's probably worth mentioning again like taking aspirin or taking niacinamide does not systemically inhibit lipolysis

### Source 8 — The ThermoDiet Podcast Episode 114 - Georgi Dinkov

Georgi Dinkov · Interview · Nov 27, 2022 · https://www.youtube.com/watch?v=Twpszx115qQ

> **Tyler Woodward:** and that's like one of the main benefits of having more muscle mass right it's just that you burn more fat at rest so that's going to take away some of the fat in the bloodstream which is going to decrease the randall cycle so that the organs and everything else can increase more
>
> **Georgi Dinkov:** So try to do whatever's possible to increase lean muscle mass, right? And you keep your organs as healthy as possible. Elevated lipolysis will not do the latter, right? So basically concentric exercises such as actually lifting weights is a mix, is a concentric and eccentric, but things like climbing stairs. um or like rowing um sprinting like even biking or swimming yes exactly jumps things like that those are almost purely concentric exercises and it's been shown that your muscles can actually act almost identical to your gonads and produce much more testosterone the new gonads produce when you stimulate the muscles with concentric exercise so it's going to produce testosterone locally which is going to have to lead to that basically anti-cortisol hypertrophic effect on muscles you're going to have more muscles you're going to burn more fat at rest right or at least with mild exercise you don't you don't want to get to a point where you basically you can actually tell about a smell you start smelling like glycerol uh and i think actually they sell uh they sell you can get like the ketone strips right but they're only good for for full-blown ketosis for people that are against diabetic or practicing the low-carb diet for a long time but they also have these devices they're these breathalyzer devices when they can tell you when you're basically like exhaling too much glycerol And that is a byproduct of fatty acid oxidation, right? Because the fatty acids exist in the form, storage form are triglycerides. So when they start getting broken down for oxidation or any other purpose, the glycerol basically like start floating around. It also gets metabolized. But accumulation of glycerol, rising of glycerol in the blood is an indication of excessive lipolysis. And you can feel it on your breath if you get trained enough.

### Source 9 — #06: Glutathione, Consciousness, Electronic Universe, and Statins with Georgi Dinkov

Georgi Dinkov · Interview · Jul 12, 2019 · https://open.spotify.com/episode/6Wo4K7UD9mpMzEcyu88MEc

> **Georgi Dinkov:** So anything extra, the liver has to re-esterify and convert it to triglycerides. And actually, before the liver releases it back into the bloodstream, the liver actually stores the majority of it inside of itself. So anytime you have elevated lipolysis, even if it looks like you're losing body fat and you may be losing body fat, keep in mind that simultaneously you're also fattening up your liver because the liver has a fixed capacity of how much fat it can process. So when you elevate lipolysis artificially by running or cycling or doing anything that's basically depleting glycogen and you're going into ketosis, into fatty acid oxidation mode, that directly damages your liver. And it makes the damages that much more worse if the fat is PUFA. So, you know, keeping lipolysis at bay and then, you know, or at the very least increasing the ratio of saturated fat to polyunsaturated fat, all of these are good ways to protect the liver.

### Source 10 — Lipolysis / FFA drive breast cancer by promoting estrogen signalling

Georgi Dinkov · Article · Sep 10, 2020 · https://haidut.me/?p=1200

> The evidence for the fat-loving nature of cancer just keeps on accumulating. During the last podcast with Danny and Ray, I mentioned that in cancer cells the enzyme fatty acid synthase (FAS) is actually part of the estrogen receptor (ER) complex. As such, anything that increases the expression/activity of one promotes the other as well. FAS is by now a well known target for cancer therapy and multiple FAS inhibiting drugs are being developed/tested by Big Pharma. The fact that aspirin is a dirt cheap and widely available FAS inhibitor is never mentioned, but that is a topic for another post.
>
> [references]
>
> To make matters worse, there has been evidence dating back to early 20th century that fatty acids (whether produced by FAS or obtained through the diet) also promote estrogen signalling. However, the power of the pro-estrogen industry has managed to suppress any discussions of the possible relevance of this fact for breast cancer development. Moreover, recently the estrogen industry has even started to criticize the findings of the WHI study and has pushed for return of HRT (with estrogen) for all post-menopausal women. If you ask an oncologist if fats promote breast cancer or if they are estrogenic, you are likely to get a blank stare at best or be chased out of his/her office at worst. I am hoping that the study below will change that attitude. It demonstrated directly that elevated lipolysis and its “product” free fatty acid (FFA) levels not only drive cancer growth, but do so by directly activating estrogen receptors and by increasing inflammation. In addition, it found that elevated lipolysis/FFA increased aerobic and fatty acid oxidation while suppressing Krebs cycle activity (classic example of the Randle effect). Conversely, lowering lipolysis/FFA reduced estrogenic signalling and abolished cancer growth.
>
> [references]

### Source 11 — Georgi Dinkov, Brad Marshall on Obesity Causes and Solutions

Georgi Dinkov · Interview · Jul 11, 2022

> **Georgi Dinkov:** How do I build muscle if I'm already obese? But if I, you know, if you already build the muscle, then it will be more difficult to become obese. Anyways, long story short is that you want to, you don't want to have excessive lipolysis because it poisons your pancreas. It blocks also the effects of insulin at the receptor level. The fatty acids have a receptor. And basically when they activate it, it largely prevents insulin from acting on the glucose transporters, GLUT1 through GLUT4. And this prevents the glucose from actually being absorbed into the cell. You may be producing a ton of insulin, but if there is a sufficient amount of fatty acids in the blood, you will not be able to absorb the glucose from the bloodstream. So keeping lipolysis low, there is a drug on the market, which is a derivative of niacinamide. The drug is called ACP-MOX. A-C-I-P-I-M-O-X. Actually, its main effect is lowering lipolysis. And that drug, just by taking it, results in decreased blood glucose, even though it actually decreases the fatty acids. It tells you that ultimately it's the fat that's the problem, the reductive stress, right? It decreases the excessive lipolysis, which allows insulin to do its job, which means blood glucose declines, also drops because it's being uptaken by the cell, right? And also it decreases cortisol, which tells you that the reason cortisol is there partially is basically because of the high insulin and... and the high free fatty acids and the high glucose. So cortisol and insulin always go hand in hand. Cortisol is there to keep your blood glucose from going too low. That's the primary role of cortisol. It's not inflammation. Your brain, you can go into hypoglycemic coma and actually die. Diabetic people know that very well. If your blood glucose levels drop below a critical level. Cortisol's job is to make sure that never happens.

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