# Arachidonic Acid

Category: Foods & Substances

Also known as: AA

Arachidonic acid is a highly unsaturated fatty acid that Ray Peat identified as one of the most toxic stored fats in the body, acting as the primary precursor to the major inflammatory mediators known as prostaglandins, leukotrienes, and thromboxanes. Even if not consumed…

11 passages · 2 authors · 2007–2024 · Most-cited: [Ray Peat](https://bioenergeticoracle.com/md/voices/ray-peat/index.md)

Canonical page: https://bioenergeticoracle.com/concepts/arachidonic-acid

## Synthesis

**Arachidonic acid** is a highly unsaturated fatty acid that Ray Peat identified as **one of the most toxic stored fats** in the body, acting as the primary precursor to the major inflammatory mediators known as prostaglandins, leukotrienes, and thromboxanes. [Source 1, 7] Even if not consumed directly, the body synthesizes it from dietary linoleic acid, and its spontaneous release from phospholipids and triglyceride storage triggers a cascade of inflammatory and degenerative processes. [Source 1] Peat argued that this chronic, low-grade inflammation, driven by the continual liberation of small amounts of arachidonic acid, is a fundamental cause of conditions ranging from diabetes and osteoporosis to Alzheimer's disease and fibrosis. [Source 1, 3, 6]

The release of arachidonic acid is enzymatically controlled by *phospholipase A2*, an enzyme activated by virtually any inflammatory or stress signal, including estrogen, serotonin, and physical irritation. [Source 5, 10] Once liberated, arachidonic acid does not require enzymatic conversion to begin causing harm; its mere presence shifts a cell's affinity for water, causing cellular swelling that is sufficient to *turn off oxidative phosphorylation* and force a reliance on glycolysis. [Source 11] Georgi Dinkov has written that intact arachidonic acid reliably causes decreased mitochondrial function and reduced oxygen consumption, and can even structurally reduce the expression of electron transport chain complexes, making its anti-metabolic effects harder to reverse. [Source 2] This metabolic disruption is not tissue-specific, making arachidonic acid a pro-cancer agent both for the initiation and growth of tumors. [Source 2]

Peat detailed multiple self-reinforcing pathological loops involving arachidonic acid. It stimulates the secretion of **prolactin**, which in turn decreases thyroid activity and oxidative metabolism while increasing glycolysis and lactate production. [Source 3] Dinkov has described a positive feedback cycle between arachidonic acid and **serotonin**, where arachidonic acid inhibits the serotonin transporter (SERT), leading to increased serotonin availability, which then activates phospholipase A2 to liberate more arachidonic acid. [Source 8] This cycle implicates arachidonic acid as a known inducer of depression and suggests that SSRI drugs, by inhibiting SERT, are highly pro-inflammatory. [Source 8] Furthermore, arachidonic acid and DHA increase the excitatory effect of glutamate on its receptor and decrease its uptake, directly contributing to excitotoxicity and nerve damage seen in epilepsy, Parkinson's disease, and Alzheimer's disease. [Source 9]

The accumulation of arachidonic acid in tissues is a hallmark of aging and stress. As fat tissues become more burdened with it, they release it more easily in response to lipolytic stress signals, explaining the increased levels of free fatty acids and lipid peroxidation with age. [Source 10] Peat noted that the brain becomes increasingly enriched with polyunsaturated fats over time, leading to the spontaneous oxidation of these fats into neuroprostanes and isoprostanes, which are linked to the progression of Alzheimer's disease. [Source 6] This burden is diet-dependent; Peat observed that in animals "deficient" in polyunsaturated fatty acids, adrenaline does not have the lipolytic effect it does in animals on a standard diet, highlighting how dietary choices directly modulate the body's stress-induced release of stored toxins. [Source 10]

The therapeutic countermeasures to arachidonic acid's toxicity center on inhibiting its release and opposing its downstream effects. Progesterone inhibits the phospholipase that liberates arachidonic acid, while estrogen activates it. [Source 10] **Aspirin** exerts its broad protective effects partly by inhibiting the synthesis of prostaglandins from arachidonic acid, thereby reducing inflammation, stimulating bone formation, and protecting against excitotoxic nerve damage. [Source 3, 9] Peat maintained that the most fundamental intervention is dietary: consuming saturated fats instead of polyunsaturated fats prevents the initial storage of this toxin, as saturated fats are chemically unreactive and can even act as antioxidants to prevent the deterioration of unsaturated molecules. [Source 1, 10] He dismissed the concept of essential fatty acid deficiency as a misapplication of flawed experimental models, particularly when extrapolated to animals with higher metabolic rates. [Source 4]

## People also ask

### How does arachidonic acid disrupt cellular energy production?

Peat argued that its mere presence causes cellular swelling, which turns off oxidative phosphorylation and forces a reliance on glycolysis, while Georgi Dinkov noted it can also reduce the expression of electron transport chain complexes.

### What dietary change did Peat recommend to reduce arachidonic acid's harm?

Peat maintained that consuming saturated fats instead of polyunsaturated fats prevents the initial storage of this toxin, as saturated fats are chemically unreactive and can even act as antioxidants.

### What is the relationship between arachidonic acid and serotonin?

Dinkov described a positive feedback cycle where arachidonic acid inhibits the serotonin transporter, increasing serotonin availability, which then activates the enzyme that liberates more arachidonic acid.

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- [Diabetes](https://bioenergeticoracle.com/md/concepts/diabetes/index.md)

## Cited passages

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

### Source 1 — Diabetes II and How to Restore and Protect Nerves KMUD 2014

Ray Peat · Interview · 2014 · https://www.youtube.com/watch?v=Lj4ewp2YH1k

> **Herb Doctor:** So that’s the thing behind what you’re describing now as the component free fatty acids (FFAs); if somebody’s eating a lot of saturated fat like butter, ghee, coconut oil then they’re not going to liberate the same free fatty acids that they would if they were consuming polyunsaturated ones in their diet?
>
> **Ray Peat:** Right
>
> **Herb Doctor:** Getting back to the classic description of diabetes as being a wasting disease, which actually we see very little of, as opposed to what now is generically diabetes, and it’s very largely linked to obesity in the general population, that obesity is probably directly linked to the polyunsaturated thyroid-suppressive diet some people consume?
>
> **Ray Peat:** It’s now increasingly seen as a fat inflammation condition, a mild chronic inflammation. And a major thing that causes that is the continual spontaneous release of small amounts of arachidonic acid, which is a highly unsaturated fatty acid. Even if you don’t eat it, linoleic acid for example will be turned into it by enzymes in the body. So, it becomes one of the most toxic stored fats, both in phospholipids and in the triglyceride storage. And when that’s released, that allows it to be turned into various things, but especially prostaglandins which are probably our biggest inflammatory problem.

### Source 2 — PUFA can cause male infertility by inhibiting oxidative metabolism (OXPHOS)

Georgi Dinkov · Article · Jun 3, 2024 · https://haidut.me/?p=2528

> The study looked at one of the members of the PUFA family that even mainstream medicine is not very fond of. Namely, arachidonic acid (AA). However, the reason medicine is not very fond of that PUFA is due to its role as a precursor to the major inflammatory mediators known as prostaglandins, leukotrienes, and thromboxanes. Medicine does not really have any criticism towards the intact AA or the other members of the PUFA family. Yet, the study below demonstrated that intact AA reliably caused decreased functioning, or even death, of the Sertoli cells (SC) and thus decreased (or even zero) spermatogenesis. The mechanism of action for the those negative effects of AA were purely metabolic – i.e. increased glycolysis and reduced oxygen consumption, paired with lower mitochondrial function. Worse, AA actually reduced the expression of several of the electron chain complexes (ETC), which means its effects were structural (and thus harder to reverse) in additional to functional (lower OXPHOS). Now, while the study was done with SC found in the male gonads, there is nothing SC-specific about the effects of AA. In other words, the same anti-metabolic effects are expected to occur in any type of cell regardless of its origin or maturation state. That automatically makes AA both pro-cancer both for de-novo cancerization and also for growth of already established tumors. It would be great to see a similar study done for other PUFA members, but the available evidence is already pointing in the same direction as the findings about AA below.
>
> [references]

### Source 3 — Osteoporosis, aging, tissue renewal, and product science

Ray Peat · Article · 2012 · https://raypeat.com/articles/articles/osteoporosis-aging.shtml

> Calcium activates mitochondrial respiration, and lowers adrenaline (Luft, et al., 1988), parathyroid hormone (Ohgitani, et al., 1997), and prolactin (Kruse and Kracht, 1981). Copper, which is the co-factor for the cytochrome C oxidase enzyme, activated by thyroid, is essential for bone formation and maintenance, and is consistently deficient in osteoporosis. Thyroid hormone increases the body's ability to assimilate copper.
>
> Aspirin, which stimulates bone formation, has other thyroid-like actions, including activation of mitochondrial respiration and energy production, with an increase of cytochrome C oxidase (Cai, et al., 1996), and it lowers serotonin (Shen, et al., 2011). It also apparently protects against calcification of the soft tissues, (Vasudev, et al., 2000), though there has been surprisingly little investigation of that. "Aspirin can promote trabecular bone remodeling, improve three-dimensional structure of trabecular bone and increase bone density of cancellous in osteoporotic rats by stimulating bone formation. It may become a new drug for the treatment of osteoporosis" (Chen, et al., 2011).
>
> A wide range of inflammatory mediators that accelerate inflammation and bone loss also inhibit thyroid function. People who ate more polyunsaturated fat, which inhibits thyroid and oxidative metabolism, were several times more likely to have osteoporotic fractures (that is, essentially spontaneous fractures) than people who ate the least (Martinez-Ramirez, et al., 2007).
>
> Arachidonic acid stimulates prolactin secretion, and prolactin acts on the thyroid gland to decrease its activity, and on other tissues to increase their glycolysis (with lactate production), while decreasing oxidative metabolism (Spatling, et al., 1982; Strizhkov, 1991).
>
> Living at high altitude, which strengthens bones, increases thyroid activity and decreases prolactin (Richalet, et al., 2010) and parathyroid hormone (Khan, et al., 1996). It lowers free fatty acids, which lower bone mass by reducing bone formation and increasing bone resorption (Chen, et al., 2010).

### Source 4 — Ray Peat Email Advice Depository — Post 245

Ray Peat · Email · May 17, 2016

> **Question:** if EFAs are absolutely unessential then what is the explanation for symptoms carnivore animals such as cats get when their diet are devoid of Arachidonic acid ?
>
> **Ray Peat:** I think people have extrapolated ideas from EFAD rats to cats, without recognizing that carnivores have higher metabolic rates and nutritional needs, so that the mistakes of the Burrs are even easier to make. [references]

### Source 5 — One Radio Network: Ray Peat with Patrick Timpone — April 18, 2022

Ray Peat · Interview · Apr 18, 2022

> **Ray Peat:** Oh, no, but like anything toxic, if you mess up your... nucleic acids, that causes a series of problems and among other reactions that can activate phospholipase.
>
> **Patrick Timpone:** So again, phospholipase, how does this fit into this whole picture? I'm just quite sorry, I'm not the sharpest tool in the shed here on the phospholipase thing.
>
> **Ray Peat:** When you eat something bad or get a cold, Anything that starts an inflammatory process, be it in your intestine or your nose or even in your skin, that irritation activates the phospholipases. There are several different kinds, but the one that most people think about is the phospholipase A2 type. that liberates arachidonic acid from the phospholipids that are part of our structural system of lipids and proteins and water that make up the cell. So there's always a lot of phospholipid around to be acted on by the phospholipids, and anything that disrupts your cells will activate that And that liberating arachidonic acid immediately brings up your prostaglandins, which then activate many other cytokines and inflammatory processes.

### Source 6 — Thyroid, Hypothyroidism & Diet, Lifestyle, Exercise to Fix it!

Ray Peat · Interview · Jul 20, 2019 · https://www.youtube.com/watch?v=HNTgD6djJtE

> **Ray Peat:** of having the arachidonic acid prostaglandin rise as you accumulate fat with aging the brain gets more and more polyunsaturated fats and they're starting to look at the role of prostaglandin in brain has lots of spontaneous oxidation of fats into substances called isoprostanes and neuroprostanes, which are spontaneous equivalents of the enzyme produced prostaglandins, but they are made from both enzymes. in the stressed brain and go with our increase in Alzheimer's disease. Following the idea of essential fatty acids in the 60s, people were told to eat more linoleic acid because it's an essential fatty acid. When it was found that that was increasing both cancer and heart disease, the marketers turned to the fish oil type of N-3. But still, those are accumulating in the tissues, in the blood vessels, leading to plaque formation in the brain, leading to various kinds of under functioning of the brain tissue.
>
> **Jodelle Fitzwater:** So you've heard it here, folks. You don't need to take a fish oil pill. You can eat sugar and you want to make sure that you get rid of the ones they are calling the essential fatty acids like linoleic acid. Instead, you can eat a really awesome pro thyroid diet of things like cheese and milk and, um, good seafood and, um, you know, well cooked vegetables occasionally and getting some good starches from your fruits. Yes, Dr. Peat.

### Source 7 — #01: Thyroid, CO2, Redox Balance, and Hans Selye's Stress with Georgi Dinkov

Georgi Dinkov · Interview · May 3, 2019 · https://open.spotify.com/episode/2lolRyxtgPXLaCvEAmSZyQ

> **Georgi Dinkov:** So I'll start by basically discussing the topic of inflammation because I think many people will be familiar with that. I just saw a blog on Harvard Medical School website today, and it basically said, we've got it all wrong. Inflammation is the true cause of all chronic disease and even infectious disease. And they do a very good job of explaining in very simple language that there hasn't been a single disease that they've picked up and looked – try to analyze it, and they did not find that inflammation was a major cause, if not the main cause of that disease. Of course, they give the examples of diabetes, metabolic syndrome, cancer, Alzheimer's. But then they also talk about viral and bacterial infections. Apparently, inflammation plays a role there as well. It's just if you're under chronic low-grade inflammatory stress, you're much more susceptible to both bacterial and viral infections. So again, so the doctors at this point, mainstream medicine as I like to call them, they're saying, wow, scratching their heads. Well, I guess inflammation is indeed a major cause. There is no such thing as healthy inflammation. That's one of the most poisonous ideas that's been promoted over the last 100 years, that we need inflammation because it's part of the repair mechanism. Yes, but remember, repair mechanisms can get out of hand unless they're accompanied by sufficient energy production, which can restrain them. If you don't restrain them, then they're adaptive, but in a bad way. They become maladaptive. Well, guess what? I guess about 80% of the inflammatory reaction in the body is controlled by the precursor arachidonic acid. And arachidonic acid is derived from the dietary omega-6, basically fatty acids. known as PUFA. PUFA also includes omega-3, right? They're considered less inflammatory.

### Source 8 — PUFA and serotonin promote each other, and likely cause mental illness

Georgi Dinkov · Article · Oct 17, 2019 · https://haidut.me/?p=655

> I neat new study that draws a direct parallel between PUFA-driven inflammation, serotonin and depression. As the study demonstrated, high levels of the PUFA arachidonic acid (AA) are highly correlated with lower density (expression) of the serotonin transported (SERT, 5-HTT), and the relationship is actually causative in both directions (AA<->serotonin). This results in increased serotonin availability/buildup since the primary role of SERT/5-HTT is to deactivate serotonin, using sodium as a co-factor.
>
> [references]
>
> What’s even worse, the study demonstrates that serotonin and AA form a positive feedback cycle with the increased serotonin due to AA inhibiting SERT/5-HTT resulting in activation of the enzyme Phospholipase A2 (PLA2) that synthesizes AA from linoleic acid, which then results in stronger SERT/5-HTT inhbition and even higher serotonin availability. While the study tries to dance carefully around the role of serotonin in depression and states that “conflicting” results have been seen in other studies, it readily admits that AA is a known inducer of depression in animal models. Well, if AA is a highly inflammatory depressant and forms a positive feedback cycle with serotonin then I don’t see how serotonin could possibly be an anti-depressant…Another immediate takeaway from the study is that SSRI drugs are highly pro-inflammatory since they activate the AA<->serotonin cycle by inhibiting SERT/5-HTT (which is their primary mechanism of action). All in all, another great reason to avoid PUFA and eat plenty of salt (to taste).
>
> [references]

### Source 9 — The Gaba System Defenses and Tissue Renewal

Ray Peat · Article · 2007

> Excitation increases the production of free radicals by the mitochondria themselves (Duan, et al., 2007). Just eliminating most PUFA from the diet decreases the risks of excitotoxicity.
>
> DHA and arachidonic acid increase the excitatory effect of glutamate on its receptor (Yeh, et al., 1995), and decrease the uptake of glutamate by the protein that binds it to stop the excitatory process (Yu, et al., 1986). These fats cause swelling of mitochondria and cells, and increase vascular permeability. Saturated fats don't have those excitatory effects.
>
> Fish oils and other omega-3 oils are being promoted as treatment for many diseases, especially heart disease, arthritis and other inflammatory diseases, and depression. They do have an anti-inflammatory effect, at least in the short term, partly associated with their inhibition of prostaglandin synthesis, but their anti-inflammatory effects have been found to result from their oxidized products (Chaudhary, et al., 2004), which have many toxic effects. Although claims are made regarding their beneficial effect on the circulatory system, there are good reasons to think that they contribute to atherosclerosis (for example, Wang and Oram, 2002, 2005). And they suppress the immune system and thyroid function.
>
> The PUFA (especially the omega-3 fatty acids) spontaneously decompose into a variety of toxins, and arachidonate is also enzymically converted into prostaglandins, some of which exacerbate the excitatory damage (Pepicelli, et al., 2005); aspirin's neuroprotective effect (Riepe, et al., 1997) is probably partly caused by inhibiting prostaglandin synthesis. Besides the prostaglandins, other mediators of inflammation including nitric oxide and interleukins are produced by excessive excitation, as cells lose their ability to retain magnesium, and to control excitatory intracellular calcium.
>
> Nitric oxide, associated with unbalanced excitation, is involved in the nerve damage of epilepsy, amyotrophic lateral sclerosis, Parkinson's disease, Alzheimer's disease, and Huntington's disease. An energy deficit increases excitation and cellular calcium uptake, increasing nitric oxide synthesis (Schulz, et al., 1997).

### Source 10 — Fats and degeneration

Ray Peat · Article · 2013 · https://raypeat.com/articles/articles/fats-degeneration3.shtml

> But, in the face of the immense amount of propagandistic "health" claims that have been made against the saturated fats, it's instructive to look at some of their actual effects, especially on the clotting system, and the related fibrotic reactions.
>
> The saturated fatty acids are very unreactive chemically. Coconut oil, despite containing about 1% of the unstable PUFA, can be left in a bucket at room temperature for a year or more without showing any evidence of deterioration, suggesting that the predominance of saturated fat acts as an antioxidant for the unsaturated molecules.
>
> In the body, the saturated fats seem to act the same way, preventing or even reversing many of the conditions caused by oxidation of fats.
>
> The stress-induced liberation of arachidonic acid causes blood vessels to leak, and this allows fibrin to escape from the blood stream, into the basement membrane and beyond into the extracellular matrix, where it produces fibrosis. (Cancer, autoimmune diseases, and heart disease involve the same inflammatory, thrombotic, fibrotic processes as the nominal fibroses.) Scleroderma, liver cirrhosis, fibrosis of the lungs, heart, and other organs, and all the diseases in which fibrous tissue becomes dense and progressively contracts, involve similar processes, and the treatments which are successful are those that stop the inflammation produced by the oxidation of the polyunsaturated fatty acids.
>
> Retroperitoneal fibrosis is now known to be produced by estrogen, and is treated by antiestrogenic and antiserotonergic drugs, but as early as 1940 Alejandro Lipschutz demonstrated that chronic exposure to very low doses of estrogen produced fibromas in essentially every part of the body.
>
> Earlier, Loeb had studied the action of large doses of estrogen, which produced fibrosis of the uterus, as if it had accelerated aging.
>
> Following Lipschutz' work, in which he demonstrated the "antifibromatogenic" actions of pregnenolone and progesterone, several Argentine researchers showed that progesterone prevented and cured abdominal adhesions and other fibrotic conditions, including retroperitoneal fibrosis.
>
> Since estrogen produces both leakiness of the capillaries and excessive formation of fibrin, its effects will be seen first in the organs where it concentrates, but eventually anywhere capillaries leak fibrin.

### Source 11 — Generative Energy #102: Ray Peat's Popularity | Synchronicity | PUFA and Bowel Disease | DHT and Testosterone | Estrogen with Georgi Dinkov

Georgi Dinkov (with Danny Roddy) · Interview · Jul 17, 2023 · https://open.spotify.com/episode/22fZxBBeQaEPARh9qZclcz

> **Danny Roddy:** What do you think? I was making fun of Paul Saladier.
>
> **Georgi Dinkov:** I can tell by the start of here, Sweet Green, which was a few other classmates, well, not classmates, other alumni from Georgetown, they started it, and it was booming for a while, and I think it's basically, at this point, it's all but dead. It's a dietary fad. People eat it for a while, and then they find out, the good thing is they find out they're not getting the benefits, so eventually they just stop eating them, except the most hardcore people. At this point, I think veganism, the only reason veganism is still a thing is because it's being pushed by the WEF and the UN Agenda 2030. 100%.
>
> **Danny Roddy:** What, didn't we, did we talk about it or did Ray reference an article that just like the presence of arachidonic acid caused stress to cells? It didn't even have to be converted into prostaglandins or anything. It was just, and so I think I had Chris Masterjohn on the podcast a few times ago, and I wish I had brought this up because I thought it like shifted a cell towards glycolysis just by being around, like nothing, didn't even have to do anything.

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