# Prostaglandins

Category: Hormones

Also known as: prostaglandin, PGE2, PGE1, PGD2

Prostaglandins are hormone-like inflammatory signaling substances synthesized from polyunsaturated fats (PUFAs), and Ray Peat argued that, contrary to the popular "yin and yang" theory of good and bad types, the accumulating evidence shows they all have seriously harmful…

11 passages · 3 authors · 2012–2023 · Most-cited: [Ray Peat](https://bioenergeticoracle.com/md/voices/ray-peat/index.md)

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

## Synthesis

**Prostaglandins** are hormone-like inflammatory signaling substances synthesized from **polyunsaturated fats** (PUFAs), and Ray Peat argued that, contrary to the popular "yin and yang" theory of good and bad types, the accumulating evidence shows they all have seriously harmful effects, making their absence beneficial. [Source 4, 5] They are formed from linoleic acid and arachidonic acid via the cyclooxygenase (COX) pathway, and Peat noted that the body's own endogenously produced **Mead acid** (an omega-9 PUFA) yields anti-inflammatory prostaglandins, but this natural defensive system is blocked by the accumulation of dietary vegetable and fish oils. [Source 1, 4, 8] Georgi Dinkov has reinforced that even mainstream medicine considers the ideal blood level of PGE2 to be zero, and that consuming PUFAs guarantees a certain amount of these metabolites will be produced, especially during stress-induced *lipolysis* when PUFAs are preferentially released from fat stores. [Source 11]

The pathological actions of prostaglandins form a central amplifying loop in degenerative disease. Peat detailed that **PGE2** directly activates *aromatase*, the enzyme that synthesizes estrogen from androgens, and also activates *heme oxygenase*, which produces carbon monoxide and releases toxic free iron. [Source 3, 6] Dinkov has written that PGE2 was found to be directly responsible for inhibiting oxidative glucose metabolism in the brain, diverting glucose to glycogen synthesis and producing an "aged brain" phenotype with significant cognitive deterioration. [Source 9] This metabolic suppression is compounded by prostaglandins' ability to synergize with estrogen, destroy the negative feedback mechanism of the adrenal axis to elevate cortisol, and activate *tryptophan hydroxylase* to increase serotonin synthesis. [Source 2, 10] Danny Roddy has highlighted that PGE2 is elevated in prostate and breast cancer, and that **PGD2** was found to be significantly increased in the scalps of men with androgenic alopecia, linking these metabolites directly to pattern hair loss. [Source 2, 5, 7]

The production and effects of prostaglandins are intimately tied to systemic energy failure and inflammation. Peat explained that the stressed or injured cell becomes incontinent, releasing ATP and producing lactic acid, while the peroxidation of PUFAs produces toxins that amplify cellular stress reactions. [Source 1, 3] Dinkov described a positive-feedback loop where increased prostaglandin levels result in increased COX enzyme expression and activity, creating a self-reinforcing spiral of inflammation. [Source 9] Roddy noted that many prostaglandins are *anti-respiratory*, directly inhibiting the production of useful energy, and that the liberation of free fatty acids into the blood promotes inefficient energy metabolism and inflammation. [Source 7] This cascade connects prostaglandins to a broader degenerative context where Peat observed that the accumulation of PUFA is one reason why baldness, heart attacks, and prostate cancer are strongly associated. [Source 8]

Therapeutic intervention focuses on blocking prostaglandin synthesis and avoiding their dietary precursors. Peat listed **aspirin**, caffeine, progesterone, and methylene blue as safe substances that lower carbon monoxide production or protect against its effects, with aspirin being the most direct method to inhibit the COX pathway. [Source 3, 9] Dinkov has emphasized that blocking the effects of PGE2, even peripherally, was sufficient to restore glucose metabolism and reverse the aged brain phenotype in animal studies. [Source 9] The foundational strategy, however, is the systemic avoidance of dietary PUFAs, as Peat argued that the relative absence of these fats improves fetal memory and development, and that non-metabolized PUFA itself suppresses glucose metabolism and increases inflammatory biomarkers independently of prostaglandin formation. [Source 1, 9]

## People also ask

### How do prostaglandins suppress brain energy metabolism?

Peat and Dinkov described that PGE2 directly inhibits oxidative glucose metabolism in the brain, diverting glucose into glycogen storage and creating an "aged brain" phenotype with cognitive deterioration.

### What is the connection between prostaglandins and hair loss?

Danny Roddy highlighted that PGD2 was found to be significantly elevated in the scalps of men with androgenic alopecia, directly linking this prostaglandin metabolite to pattern hair loss.

### Why is avoiding dietary PUFAs central to reducing prostaglandin damage?

Peat argued that prostaglandins are synthesized from polyunsaturated fats, and Dinkov noted that consuming PUFAs guarantees their production, especially during stress when PUFAs are released from fat stores.

## Related concepts

- [ATP (Adenosine Triphosphate)](https://bioenergeticoracle.com/md/concepts/atp-adenosine-triphosphate/index.md)
- [Autophagy](https://bioenergeticoracle.com/md/concepts/autophagy/index.md)
- [Cellular respiration](https://bioenergeticoracle.com/md/concepts/cellular-respiration/index.md)
- [Estrogen-serotonin axis](https://bioenergeticoracle.com/md/concepts/estrogen-serotonin-axis/index.md)
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## Cited passages

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

### Source 1 — Regeneration and degeneration - Types of inflammation change with aging

Ray Peat · Article · 2012 · https://raypeat.com/articles/articles/regeneration-degeneration.shtml

> Two prostaglandins, PGE2 and PGF2a, potently produce inflammation in fetal rabbits, but not in adult rabbits. (Morykwas, et al., 1994). Tissue injury that would produce inflammation in adults causes other signals in the fetus that activate repair processes.
>
> When a cell is injured or stressed, for example when deprived of oxygen, it becomes incontinent, and releases ATP into its surroundings. The extracellular ATP, and its breakdown products, ADP, AMP, adenosine, and inorganic phosphate or pyrophosphate, stimulate cells in various ways. ATP causes vasodilation, increasing circulation, and usually signals cells to divide, and can activate stem cells (Yu, et al., 2010). The lactic acid produced by distressed cells also has signalling effects, including vasodilation and stimulated division. Stressed cells digest their own proteins and other structural materials (autophagy), and the breakdown products act as signals to guide the differentiation of their replacement cells. Mobile phagocytes, ingesting the material of decomposing cells, are essential for guiding tissue restoration.
>
> In adults, prostaglandins are known to be involved in many of the harmful effects of inflammation. They are formed from the polyunsaturated fats, linoleic acid and arachidonic acid, which we are unable to synthesize ourselves, so the adult’s exposure to the prostaglandins is influenced by diet. Since the fetus is able to synthesize fat from glucose, the newborn animal usually contains a high proportion of saturated fats and their derivatives, such as stearic acid, oleic acid, and Mead acid, which can be synthesized from glucose or amino acids. Newborn calves have very little polyunsaturated fat in their tissues, but even the small percentage of PUFA in milk causes its tissues to gradually accumulate a higher percentage of PUFA as it matures. The fatty acids of newborn humans, and other non-ruminants, reflect their mothers’ diets more closely, but Mead acid is still present in human newborns (Al, et al., 1990).
>
> In a study of prenatal learning (habituation rate), the experimenters found that the relative absence of the supposedly essential fatty acids improved the short term and long term memory of the fetus (Dirix, et al., 2009).

### Source 2 — #95: The Anti-Stress Youth Steroids | Finasteride, Inflammation, and The Gut | PUFA | Prostaglandins with Georgi Dinkov

Georgi Dinkov · Interview · Jan 14, 2023 · https://open.spotify.com/episode/1f0ImDpFnuMdwToUcuqufC

> **Danny Roddy:** This is where like the – so that anti-seed oil thing has become pretty popular on the internet. And I think it just kind of stops short of talking about the prostaglandins. And then also like it's so not controversial that PGE2 is high in prostate cancer, high in breast cancer, and then activates aromatase. And so like it – Ray's stuff is so coherent because you can't fully understand how bad PUFA is until you understand the prostaglandins. And then it activates estrogen, which is also harmful. And so it just all fits together in a nice little box. And so the anti-seed oil stuff on the internet just kind of doesn't get there. And it just— I

### Source 3 — From 'heroic medicine' to 'hormesis': First deny that harm is done

Ray Peat · Newsletter · 2017

> Reacting with oxygen, the peroxidation of PUFA produces many toxins, including carbon monoxide (Wolff, 1976), and one of the basic enzymes induced by stress is cyclooxygenase, producing prostaglandins. One of those, PGE2, activates heme oxygenase (Park, et al., 2009), the enzyme that produces carbon monoxide from the breakdown of heme, and it also activates aromatase, the enzyme that produces estrogen from androgens. The result is that the accumulating PUFA function as amplifiers of the cellular stress reactions. In experimental situations, the epigenetic changes produced by stress are reversible, but when the organism stays in the same sort of environment that started the process, reversals become less likely with increasing age.
>
> Emotional stress is organized by the nervous system, changing hormones and cell functions that improve immediate survival. Glucose deprivation seems to be a feature of stress that activates the cell survival enzymes, including heme oxygenase and aromatase. In the state of learned helplessness or chronic despair, the relative dominance of the cholinergic system keeps the body in the inflamed, hypometabolic condition, in which rheumatoid arthritis, fibromyalgia, and sleep apnea are likely to occur.
>
> When carbon monoxide is produced in stress, the breakdown of the heme molecule also releases iron, and biliverdin, which is quickly turned into bilirubin. Increases of bilirubin and carbon monoxide in the body fluids or breath can be seen in many chronic conditions, along with changes in tissue iron content.
>
> Most publications have been concentrating on the increase of heme oxygenase and carbon monoxide during injury, sickness, and stress, with suggestions that treatments (chemicals or radiation) to increase its production could be beneficial. (Existing drugs that have been proposed for increasing heme oxygenase include resveratrol, metformin, and the statins.) However, many researchers have recognized that the short-term, local benefits are associated with very serious long-term harmful effects, including cancer, dementia, Parkinson’s disease (Song, et al., 2017) and other neurodegenerative diseases (Schipper, 2000; Song, et al., 2006; Schipper and Song, 2015), arthritis (Devesa, et al., 2005), liver disease, and heart failure.

### Source 4 — Dr. Ray Peat, Day Two: Full Interview from On the Back of a Tiger

Ray Peat · Interview · Feb 18, 2021 · https://www.youtube.com/watch?v=Z3yVUELD2ZA

> **Ray Peat:** And I think it was the F type of prostaglandin imitated the sunburn. electrically it created a a reducing area on my skin and the around that time a few people started saying well they're natural hormones but some of them have really bad effects such as knocking out progesterone production in the ovaries. And so there was the yin and yang theory of prostaglandins, the good ones and the bad ones. But when you look at the good ones, as the evidence accumulates, they all have some really bad effects causing pain or... atrophy or inflammation or such, so not having any of these ordinary prostaglandins would be good. And when you're really deficient, absolutely lacking the vegetable N-6 or N-3 fatty acids, the body produces its own polyunsaturated fats but they're stable because they have this tail of a hydrocarbon chain of nine carbons they're the n minus nine and these are anti-inflammatory rather than pro-inflammatory and so our body tends to make those when it isn't being blocked by the vegetable or fish oils. And so our natural defensive anti-inflammatory system seems to be a casualty of the accumulation of these environmental fats.

### Source 5 — Do "Essential Fatty Acids" Cause Pattern Hair Loss?

Danny Roddy · Article · Apr 23, 2013

> Prostaglandins, like PGD2, are hormone-like proinflammatory signaling substances.
>
> Arachidonic Acid: The Essential Fat That Makes You Bald?
>
> Forum members began theorizing methods of inhibiting PGD2 almost immediately. However, members who were overzealous about limiting arachidonic acid (i.e., through diet or supplementation) were reminded that arachidonic acid is part of the membrane lipid bilayer of our cells.
>
> Back in October I wrote about Dr. Ling's Associated-Induction (AI) hypothesis, which is an alternative view of cellular physiology. Immediately after I wrote that article, I promised myself I would never write about the subject again, but a few months later regained interest due to various articles by Phil from Pranarupa, Andrew Kim, and reading The Living State and Bioenergetics by Albert Szent-Györgyi.
>
> Viewing baldness in the context of energy metabolism lends itself to Dr. Ling's AI hypothesis, which details a unique role for ATP as a "cardinal adsorbent" and rejects the idea of the membranous-water-sack, in favor of a gel-like assortment of cell water that is structured through electronic interactions with the cytoskeletal proteins. I won't rehash all the details of the original article, but the essentiality of arachidonic acid can seriously be questioned if the membrane lipid bilayer doesn't exist.
>
> Arachidonic Acid & The "Ivory Dome" Theory of Baldness
>
> Over the last few weeks I've been writing about Frederick Hoelzel's "Ivory Dome" theory of baldness:
> The Myth of Male Pattern Baldness
> The "Ivory Dome" Theory of Pattern Hair Loss
> The "Ivory Dome" Theory of Pattern Hair Loss Part II: Putting It All Together
>
> I have since expanded on Hoelzel's theory linking various hormones and signaling substances that influence the abnormal deposition of calcium in the context of promoting energy metabolism. In addition to providing the raw material for the production of PGD2, arachidonic acid and the other prostaglandins can contribute to pattern baldness a myriad of ways:
>
> Arachidonic acid is metabolized into prostaglandin E2, which increases estrogen (Bulunn et al., 2000).

### Source 6 — A Bioenergetic View of Osteoporosis [Generative Energy #25]

Danny Roddy · Interview · Mar 24, 2016 · https://www.youtube.com/watch?v=8wAlMUFN1g0

> **Danny Roddy:** we talk about lipolysis and the randall cycle and the polyunsaturated fats really often did you want to touch on less often i think we probably talk about the prostaglandins and to my surprise that's news to a lot of people of like what prostaglandins are and if you dig a little bit of the the so-called alternative view they think that some prostaglandins are good and some are bad whereas repeat usually says hey they're mostly linked to these degenerative conditions and one of those degenerative conditions is the prostaglandin PGE2, which not only, it seems to be part of this vicious cycle of lactic acid, estrogen, et cetera. And this, the increase in prostaglandins can only happen when there's an increase in lipolysis and the unsaturated fats, the so-called essential unsaturated fats are substrate for the production of these prostaglandins.

### Source 7 — Evil Sugar Radio # 33: Danny Roddy, Hair Loss, Ray Peat, Thyroid, Stress

Danny Roddy · Interview · Mar 7, 2014 · https://www.youtube.com/watch?v=vXw0VGYRpRQ

> **Scott:** Well, so you mentioned prostaglandins. Can you kind of talk about that? Even that was beyond me. So can you tell us what prostaglandins are?
>
> **Danny Roddy:** Yeah, so, okay, so prostaglandins are like hormone-like inflammatory substances. In stress, they are metabolized from, I'm sure you guys have heard it, arachidonic acid. So Chris Masterjohn writes a lot about this.
>
> **Scott:** Yep.
>
> **Danny Roddy:** And so this is where, again, Ray kind of diverges from other people, but a lot of the prostaglandins are anti-respiratory, so that means they'll inhibit the production of useful energy. But also the particular prostaglandin, I think it's called prostaglandin E2 or PGE2, activates aromatase. So this is an enzyme that converts testosterone into estrogen. And we definitely don't want that. And then I think even what made me even more interested in it was I think two years ago, prostaglandin D2, so this is just another derivative prostaglandin, was found to be increased in the scalps of those who were diagnosed with male pattern baldness. So at least from the balding point of view, it doesn't look like any of these prostaglandins, when they're metabolized from free fatty acids, are doing any helpful things. And then kind of when you map the idea that estrogen isn't the female hormone, and also prostaglandins tend to, or free fatty acids, tend to increase the activity of the enzyme that converts tryptophan into serotonin. I think it's called tryptophan hydroxylase. But when you kind of consider all these things, it just seems like a very bad idea to liberate a bunch of fat into the blood because it can promote inefficient energy and inflammation and things like that.

### Source 8 — Lost Conversations with Ray Peat #1: The Purpose of Hair, Luciferianism, and Obama as a CIA Creation

Ray Peat (with Ray Peat) · Interview · May 12, 2017 · https://dannyroddy.substack.com/p/lost-conversations-with-ray-peat

> **Danny Roddy:** To tag on to what you just said, the Larson et al. finding that the prostaglandin D-synthase, this is interfering with that normal hypoxia leading to renewal and with the accumulation of the PUFA in the prostaglandins. It basically just creates that typical baldness shape, basically?
>
> **Ray Peat:** Yeah, and I think the accumulating PUFA is one of the reasons why people get bald and heart attacks and prostate cancer. You know, prostate cancer is well associated with baldness?
>
> **Danny Roddy:** Mm-hmm (affirmative).
>
> **Ray Peat:** It's the same with heart attacks, many times more heart attacks in extremely bald men.
>
> **Danny Roddy:** Something that's funny is if you go to their hair loss forums, they're all under the impression that there are good and bad prostaglandins. They say prostaglandin D2 is bad and PGE2 is good, but then if you go to the prostate cancer research ... You've obviously pointed me in this direction, but almost all of the PGE2 is intimately associated with the development of prostate cancer.
>
> **Ray Peat:** Yeah, because they believe in the essentiality of PUFA, they have to think there must be some good prostaglandin. It turns out, I think, that when you metabolize sugar, you make it into fat. Then you make the fat into the mead acid, down that chain, you get the Omega-9 PUFA. Those are made into things like prostaglandins but we seldom get the chance to make them because we're drowned in the omega minus-6.

### Source 9 — Blocking prostaglandins restores (glucose) metabolism, reverses brain aging

Georgi Dinkov · Article · Oct 30, 2023 · https://haidut.me/?p=2378

> It is rare to find a study like the one below that combines so many crucial topics into a unified message. Namely, the role of energy in aging and disease, the role of oxidative glucose metabolism in aging and health, the pathological role of PUFA as a negative (glucose) metabolic regulator and thus a major pathological factor, the reversibility of this PUFA-driven state and even aging, and finally the positive feedback loop that so many of the pathological mediators form in the organism (i.e. sickness reinforces itself, as does health). In this specific case, the (in)famous PUFA metabolite (through the cyclo-oxygenase (COX) pathway) prostaglandin E2 (PGE2) was found to be directly responsible for inhibiting oxidative glucose metabolism in the brain and thus instead of glucose being used to synthesize ATP and support brain function (cognition) and structure, the glucose was instead diverted to glycogen synthesis. That condition alone was sufficient to produce an “aged brain” phenotype with significant deterioration in cognition. While the study did not investigate it, if glucose oxidation is suppressed, then lactate levels will rise as well as fatty acid oxidation (as a result of Randle cycle dynamics). So, another way to state the findings of the study is that lower glucose oxidation and elevated fatty acid oxidation drives brain aging by lowering brain energetic reserves (ATP) and this entire process is driven by the PUFA metabolites known as prostaglandins. Conversely, blocking the effects of PGE2 even only peripherally (i.e. not in the brain) was sufficient to restore glucose metabolism, and reverse the “aged brain” phenotype as demonstrated by the completely restored cognition in the aged animals. Speaking of PUFA, while the study only examined its PGE2 metabolites and speaks of other prostaglandins as “beneficial”, I don’t think this is the case as other studies have demonstrated pathological roles of PGD2 and PGF2 as well. Just as importantly, even non-metabolized PUFA is perfectly capable of suppressing glucose metabolism and increasing inflammatory biomarkers such as IL-1, IL-6, TNF-a, NF-kB, histamine, serotonin, etc.

### Source 10 — #95: The Anti-Stress Youth Steroids | Finasteride, Inflammation, and The Gut | PUFA | Prostaglandins with Georgi Dinkov

Georgi Dinkov · Interview · Jan 14, 2023 · https://open.spotify.com/episode/1f0ImDpFnuMdwToUcuqufC

> **Danny Roddy:** Oh, sorry. Prostaglandins are like hormones made from PUFA, right? They're not hormones because...
>
> **Georgi Dinkov:** Okay, so it depends on the definition. Basically, it has a hormone-like effect, right? So it's basically, it can trigger multiple endocrine systems and usually not in a good way. It synergizes with estrogen. So if you're producing a small amount of estrogen, but you have a sufficient amount of prostaglandins floating around, it will be the equivalent of basically being poisoned by massive amounts of estrogen. It also destroys the negative feedback mechanism between cortisol and the adrenal axis, like the ACTH and the CRH. So there was, I don't know if you remember that old study that showed that eating PUFA basically increases cortisol even in the absence of ACTH. So you're gonna have basically, you're gonna trigger the stress system, right? And simultaneously they're pro-inflammatory. So anytime you have the prostaglandins that are derived from arachidonic acid, Basically, you're going to trigger a lot of other inflammatory mediators downstream. Again, the interleukins, the tumor necrosis factor alpha, nuclear factor kappa B, I think is another one that's called. And of course, the prostaglandins are known to activate tryptophan hydroxylase. So you're going to be synthesizing more serotonin. Serotonin also gets involved in these multiple feedback cycles. It promotes the synthesis of cortisol through the serotonin receptor 5-HT2C. It promotes, actually increases the activity, not only the activity of aromatase, but also the expression of aromatase. We'll be able to produce more estrogen. Really nasty stuff. And basically, the prostaglandins are probably one of the most dietarily ubiquitous, even though you don't digest them in such big amounts directly, even though they are.

### Source 11 — #95: The Anti-Stress Youth Steroids | Finasteride, Inflammation, and The Gut | PUFA | Prostaglandins with Georgi Dinkov

Georgi Dinkov · Interview · Jan 14, 2023 · https://open.spotify.com/episode/1f0ImDpFnuMdwToUcuqufC

> **Georgi Dinkov:** think the CETO industry threw a lot of money and power towards propaganda to stop short of making the connection. Because if that connection was made in the public consciousness, then basically the industry is finished. Because there's no doubt, nobody's denying that the prostaglandin E2 or F2 are really bad, or D2. They're very bad for many different conditions, right? And then things like aspirin or like the different NSAIDs are actually beneficial because they inhibit the sense of those things. But in most people's minds, it's like eating PUFO does not directly correlate to having higher levels of prostaglandins. And I've seen multiple articles and doctors argue that basically, well, just because you eat more of the precursor and they're kind of using our argument too. Just because you're eating more of the precursor doesn't mean you're going to get more of the really bad downstream metabolite. But in this case, it seems to be the case because every time you have lipolysis, which happens under stress, or you're eating this high PUFA diet or low carb or whatnot, every time you're under stress or you have elevated lipolysis, PUFA gets preferentially released from the fatty stores. So if the PUFA gets preferentially released, it's got to go through the prostaglandin pathway. Some of it will get oxidized, but if a sufficient amount gets into the bloodstream, you're guaranteed to have a certain amount of prostaglandins. And even mainstream medicine admits that as far as PGE2 is concerned, the ideal amount of it in the blood is zero, which if the connection has been made in the public conscience that eating PUFA means no zero amount of PGE in the blood, then the public will say, you know what? Not anymore seed oils. And then, I don't know, then I think then the seed industry will say, okay, it's time to go to war in China because the situation is becoming desperate.

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