# Leptin

Category: Hormones

Leptin is a peptide hormone produced by fat cells that Ray Peat consistently identified as a central component of the inflammation-promoting system, rather than a simple appetite regulator. Peat argued that the pharmaceutical industry initially promoted leptin as a natural…

8 passages · 3 authors · 2007–2023 · Most-cited: [Ray Peat](https://bioenergeticoracle.com/md/voices/ray-peat/index.md)

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

## Synthesis

**Leptin** is a peptide hormone produced by fat cells that Ray Peat consistently identified as a central component of the **inflammation-promoting system**, rather than a simple appetite regulator. [Source 5] Peat argued that the pharmaceutical industry initially promoted leptin as a natural anti-obesity chemical after discovering it could limit appetite, but subsequent research revealed that it is produced in excess during overeating, especially on a high-fat diet, and is particularly abundant in obese individuals. [Source 3] He doubted the biological significance of the concept of *leptin resistance*, viewing it as an outgrowth of industry promotion rather than a meaningful physiological state, and suggested that being resistant to leptin might actually be beneficial given its harmful effects. [Source 1]

Mechanistically, Peat described leptin as a hormone that, when it reaches the brain, does shut off appetite but simultaneously **activates inflammatory processes**. [Source 3] He specifically identified leptin as the signal that turns on the cancer metabolism known as *aerobic glycolysis* in breast cancer, where cancer cells inefficiently burn sugar even in the presence of oxygen. [Source 3] Peat further elaborated that leptin, which is promoted by estrogen, activates the POMC-related endorphin stress system, and that these endorphins in turn activate histamine, another promoter of inflammation and cell division. [Source 4] He emphasized that progesterone opposes these effects in multiple ways, including by directly inhibiting leptin. [Source 4]

Peat noted that **fructose** uniquely suppresses leptin relative to other foods, a point he raised in the context of defending sugar against claims that high-fructose corn syrup blocks satiety signals. [Source 2, 3] This aligns with his broader view that sugary fruits, which come with high concentrations of potassium and other minerals, help metabolize sugar safely without turning it into fat. [Source 2] In contrast, Danny Roddy's early writing from 2010 presented a different framework, describing leptin as "possibly the most important hormone in the body" controlling metabolic rate and fuel regulation, and claiming that *leptin resistance*—caused by white sugar, grains, and vegetable oils—was the starting point of metabolic derangement and upstream of insulin resistance. [Source 7] Roddy later acknowledged this earlier enthusiasm for leptin as a period of confusion, noting he "didn't have any idea what he's talking about" at the time. [Source 6]

Georgi Dinkov has extended the discussion by noting that despite its bad reputation, leptin is actually known to **improve insulin sensitivity**, with several leptin-mimetic drugs in clinical trials for treating type 2 diabetes. [Source 8] This presents a more nuanced view of leptin's metabolic role, though it does not contradict Peat's core concern about its inflammatory and cancer-promoting actions when chronically elevated. [Source 3, 4] Peat's fundamental position remained that leptin is part of a regulatory system that, in obese individuals, becomes dysregulated and causes harmful effects rather than protective regulation, making it a mediator of the damage caused by obesity rather than a therapeutic target. [Source 3]

## People also ask

### How does leptin promote cancer according to Peat?

Peat argued that leptin activates aerobic glycolysis in breast cancer, a process where cancer cells inefficiently burn sugar even with oxygen present, and that it is promoted by estrogen while being opposed by progesterone.

### Why did Peat think fructose was relevant to leptin levels?

Peat noted that fructose uniquely suppresses leptin compared to other foods, which he used to defend sugar against claims that high-fructose corn syrup blocks satiety, and he believed sugary fruits with minerals help metabolize sugar safely.

### Does leptin have any beneficial metabolic effects?

Georgi Dinkov noted that leptin is known to improve insulin sensitivity, with leptin-mimetic drugs in trials for type 2 diabetes, though this does not contradict Peat's concern about its inflammatory and cancer-promoting actions when chronically elevated.

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## Cited passages

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

### Source 1 — Email Exchanges — Leptin

Ray Peat · Email · 2015

> # Leptin
>
> I doubt that there is any biological significance in the idea of leptin resistance. Leptin promotes inflammation and cancer, so it might be good to be resistant to it, but I think the concept is mainly an outgrowth of the pharmaceutical industry's promotion of leptin as a cure for obesity.

### Source 2 — Sugar Myths 1 – Sugar and the Link Between Cholesterol.

Ray Peat · Transcript · 2011

> **Andrew Murray:** So leptin is the bad guy?
>
> **Ray Peat:** And it so happens that fructose suppresses it relative to other foods. I know most people that listen to the show are way more conscious than to drink artificially sweetened juices or artificially sweetened sodas, but with the trend and fad to drink artificially sweeteners as a replacement to sugar. There are a few nasty replacers for sugar. Things like saccharine were shown to cause allergic reactions. Sucralose is a relative new one. I won’t go through the chemical process to make it, but let’s just say there is nothing in nature like it and it is not good for you and acelulfame-k is a known carcinogen, containing methylene chloride. Plenty of the alternative sweeteners are bad for you… Our engineer has a question: Someone with hypothyroidism and low cholesterol, what can their link be there?
>
> **Ray Peat:** Probably eating too much starch. That’s the commonest cause of that pattern. Fructose in particular acts very much like T3. Both glucose and fructose increase the conversion of the inactive thyroxine to the active T3. They do several things to increase the thyroid activity, lowering the stress hormone as well as increasing the active thyroid hormone and the energy provided by both the glucose and the T3 in the liver will give it the energy to produce the cholesterol that is needed if you are eating enough sugar and not producing toxins in the intestines, by eating hard to digest fibrous foods.

### Source 3 — Sugar Myths 1 – Sugar and the Link Between Cholesterol.

Ray Peat · Transcript · 2011

> **Ray Peat:** Well chocolate doesn’t have the protein. Maybe chocolate with a glass of milk.
>
> **Andrew Murray:** Okay next caller. Hi my name is Mike. I am calling from Eureka. Thank you for taking the call. My question is about and Lipoprotein A and collagen. Is there a loss of collagen when the LPA is high? If that’s true how do you lower the LPA and how do you raise the collagen? (Cut out caller) The gentlemen wanted to know the connection between lipoprotein A and collagen.
>
> **Ray Peat:** Lipoprotein A? I don’t know what he…
>
> **Andrew Murray:** Next caller? I heard that high fructose corn syrup blocks a chemical signal that goes to your brain when you have enough food to eat or enough to drink and it blocks that signal, causing people to want to eat or drink more.
>
> **Ray Peat:** That’s leptin that you are talking about.
>
> **Andrew Murray:** I think it came from one of those doctors that were anti sugar.
>
> **Ray Peat:** Yeah the pharmaceutical industry was hoping to promote leptin as a natural anti-obesity chemical, when they discovered it would limit appetite, but as it developed over the last twelve or so years, it turns out that it is produced when you over eat, especially on fat. It is produced by fat cells, especially by obese people a lot of it is produced. When you have a lot of it and the brain responds, it does shut off your appetite but it also happens to activate inflammatory processes, and for example in breast cancer, it is found to be the signal that turns on the cancer metabolism, called aerobic glycolysis where the cancer, even in the presence of oxygen needs sugar or will burn sugar at a higher inefficient rate. So leptin turns out to be one of the means by which obesity causes it damages, rather than being this mysteriously wonderful protective molecule. It’s part of our regulatory system that in fat people it gets out of whack and causes harmful effects, rather than regulatory effects.

### Source 4 — Preventing and treating cancer with progesterone.

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

> Both endorphins and ACTH can be found in tumors such as breast cancer. The ACTH stimulates the production of cortisol, that protects against some of the immediate causes of inflammation and growth, but that contributes to the loss of resistance, and increases estrogen synthesis.
>
> A protein called the sigma receptor, known for its role in cocaine's action, binds progesterone, and can inhibit the growth of cancer.
>
> Some anesthetics have similar effects on tumors, acting through this protein.
>
> The sigma receptor, in association with progesterone or pregnenolone, is protective against the excitatory amino acids.
>
> The extracellular medium changes during the development of a tumor. Irritated hypoxic cells, and estrogen-stimulated cells, increase their production of collagen, and the increase of collagen interferes with normal cell functions.
>
> Progesterone reduces the formation of collagen, and probably contributes to its removal.
>
> Naloxone or naltrexone, which blocks the actions of the endorphins and morphine, is being used to inhibit the growth of various kinds of cancer, including breast cancer and prostate cancer.
>
> Leptin (which is promoted by estrogen) is a hormone produced by fat cells, and it, like estrogen, activates the POMC-related endorphin stress system. The endorphins activate histamine, another promoter of inflammation and cell division. Progesterone opposes those various biochemical effects of estrogen in multiple ways, for example by inhibiting the ACTH stress response, by restraining cortisol's harmful actions, and by inhibiting leptin.
>
> Mediators of the radiation bystander effect include NO, TNF, COX, and prostaglandins. These are produced by other things that cause inflammation and injury, including estrogen.
>
> Cell division, when it is part of the body's continuous renewal and adaptation, isn't a source of mutations or degeneration, but when it is induced by the mediators of inflammation produced in response to injury, it leads to inherited changes, loss of differentiated function, and eventually to genetic instability.
>
> When cell division is so disturbed that the number of chromosomes becomes abnormal, the instability of these cells decreases their ability to survive, but when the causes of the inflammation persist, they will continue to be replaced by other abnormal cells.
>
> The toxic products of dying cells can reach a point at which the debris can't be removed, adding to the injury and inflammation.
>
> The damaged bystander cells spread their influence through a cancer field, injuring more cells.

### Source 5 — Source Nutritional Show: Brain And Tissue ll

Ray Peat · Interview · May 12, 2012 · http://l-i-g-h-t.com/files/source-nutritional-show-brain-and-tissue-2.mp4

> **Karen:** That’s so fascinating.
>
> **Damian Paul:** Well, we have a caller on the line, Hello, welcome to the Source Nutritional radio show. You had a question for our guest today, Dr. Raymond Peat.
>
> **Caller:** Yes, I had two and I listen on the radio. What then do you think is the best ratio between omega-6 and omega-3, and also have you ever heard of leptins?
>
> **Ray Peat:** Leptins. Yeah, leptin is part of the inflammation promoting system.
>
> **Caller:** They said it is sticky protein.
>
> **Ray Peat:** A what?
>
> **Caller:** A sticky protein that interrupts a lot of things in your body.
>
> **Karen:** This is a sticky protein.
>
> **Ray Peat:** Leptin as L-E-P-T-I-N?
>
> **Caller:** Yes.
>
> **Ray Peat:** It’s a little peptide produced by the fat cells which – it was promoted by the drug industry 10 or 15 years ago as a cure for obesity, but then it turned out that it also promotes inflammation and cancer.

### Source 6 — #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:** Well, that it stuck out to me because it's like, that's the first time I've heard of a health person getting their YouTube deleted like that. I don't know. I think I don't necessarily trust him. I don't know if he said something like kind of maybe like that YouTube would really not like, you know, like he had the channel Jimmy rants. Did you ever watch any of this?
>
> **Kyle Mamounis:** No, man.
>
> **Danny Roddy:** Maybe I have too much time on my hands.
>
> **Kyle Mamounis:** Yeah. You know, one of the only times I listened to that guy was when you were on his like thing. Was it like 2011 maybe?
>
> **Danny Roddy:** Yeah. 11 or 10 for sure. Yeah.
>
> **Kyle Mamounis:** Yeah. Um, That was funny. That's when you were into leptin. Everybody was into leptin.
>
> **Danny Roddy:** Yeah. I haven't listened to it for years, but I remember re-listening to it at one point and just cringing. I couldn't even... I remember being pass-out nervous for it, though, at the time. So I, and I, and I think I remember working in that leptin idea, like really close to the interview and like, I just have no idea.

### Source 7 — The Four Horsemen of The Hairpocalypse

Danny Roddy · Article · Jul 15, 2010

> # The Four Horsemen of The Hairpocalypse
>
> Thursday, July 15, 2010 at 11:46PM
>
> Hair loss is pedestrian if you ask the pharmaceutical industry. You see they have it all figured out. Inhibit the manhood-promoting hormone, dihydrotestosterone (DHT), and you stop hair loss.
>
> The pharmaceutical drug Propecia is based on this very concept. Also called finsasteride, Propecia cripples the 5-alpha reductase enzyme that produces DHT from testosterone.
>
> So, how effective is this approach? Let's trek over to propeciasideeffects.com and ask the gentlemen suffering lifelong erectile dysfunction about it. They have some interesting things to say.
>
> Like all diseases of civilization, hair loss pathology is rooted in the dysregulation of the hormones within our bodies. High DHT, which is public enemy number one to the pharmaceutical industry, is a symptom of the body going metabolically awry and not the sole problem. So what do we do? Do we take a drug to fix the problem? Do we rub goop in our hair every morning? Do we take fifty designer supplements with each meal?
>
> All of these questions can be answered with a resounding no.
>
> Hair loss, if not too far advanced, can be halted with a little knowledge and determination. Let's go over the key players in what some have dubbed "the hairpocalypse"... Okay, only I have dubbed it the hairpocalypse.
>
> Out of Whack Hormones
>
> - Research and bloggers smarter than I, are reporting that the dysregulation of leptin is the starting point where the body starts to derail itself. Leptin is possibly the most important hormone in the body, as it controls both metabolic rate and fuel regulation. Leptin is secreted from your fat mass, and to function properly must travel through your circulatory system to your hypothalamus (brain).
>
> White sugar, grains, and vegetable oils disrupt leptin's message on it's way to the hypothalamus, so that your brain "cannot hear" this message. Interestingly enough, insulin resistance is downstream from leptin resistance. This point is integral, considering that insulin resistance is an early marker for premature hair loss.
>
> Inflammation
>
> - Inflammatory messengers interleukin-6 (IL-6) and C-reactive protein (CRP) come to the rescue when hormonal chaos ensues.

### Source 8 — Does SUGAR CAUSE RESISTANCE?  Does it MAKE YOU FAT? Interview with GEORGI DINKOV

Georgi Dinkov · Interview · Mar 9, 2023 · https://www.youtube.com/watch?v=WBluwv-WrVA

> **Georgi Dinkov:** but if this continues chronically which is what the chronic fasters are going to experience i don't think it's a good idea and in fact multiple studies demonstrated that chronically fasted organisms are at a much higher risk of cancers of the gastrointestinal tract specifically pancreatic liver and stomach um and um as a you know sort of like an anecdotal story steve jobs who was known to chronically fast uh acquired a cancer uh which was known to be not genetic his father and mother are still alive nobody in their head in the family had the cancer that he did um and basically the doctors thought that it may be due to a chronically elevated levels of ghrelin which he got to because he fasted for days at a time and then when he didn't fast he was eating mostly a fruitarian diet uh ashton kutcher who played steve jobs into the the movie the biopic i think it's called it's called jobs actually ended in the hospital ended up in the hospital with acute pancreatitis when he tried to implement the exact same uh feeding regimen as as steve jobs just check it out it was freaky he basically said you know what I think Jobs did it to himself because he did it for two or three days just to get into the mood for the role, and he ended up in the hospital with acute pancreatitis. So yeah, I don't think ghrelin is something that you want to play with. And leptin, which gets released when there's satiety, is actually something that's known to improve insulin resistance, despite the fact that most doctors view it as a bad biomarker.

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