Arachidonic Acid / Prostacyclin

[Soup Lady]

[moderator edit: separated from https://raypeatforum.com/community/threads/vitamin-b-6.19/#post-120490]

To Charlie,
I know this is an old post, but dermatitis is a classic sign of low arachidonic acid/prostacyclin. Theoretically, B6 would help increase AA and prostacyclin, but it doesn't help much. Chicken fat is the best source of arachidonic acid/prostacyclin, and would probably clear up your dermatitis. I know Ray Peat doesn't approve of eating chicken fat, but you might want to research this issue if you still have dermatitis. Dietary arachidonic acid, like in a rich chicken soup, is actually anti-inflammatory, as opposed to cellular arachidonic acid, which participates in the inflammatory response to free radicals, like those caused by unmetabolized vegetable oils. I think the key is to completely avoid vegetable oils. http://www.ncbi.nlm.nih.gov/pubmed/23528213

 

[haidut]

To Charlie,
I know this is an old post, but dermatitis is a classic sign of low arachidonic acid/prostacyclin. Theoretically, B6 would help increase AA and prostacyclin, but it doesn't help much. Chicken fat is the best source of arachidonic acid/prostacyclin, and would probably clear up your dermatitis. I know Ray Peat doesn't approve of eating chicken fat, but you might want to research this issue if you still have dermatitis. Dietary arachidonic acid, like in a rich chicken soup, is actually anti-inflammatory, as opposed to cellular arachidonic acid, which participates in the inflammatory response to free radicals, like those caused by unmetabolized vegetable oils. I think the key is to completely avoid vegetable oils. http://www.ncbi.nlm.nih.gov/pubmed/23528213

How is dietary arachidonic acid different from cellular arachidonic acid? How is it anti-inflammatory given that it is still a precursors to all inflammatory mediators. Am I missing something?

 

[jb116]

To Charlie,
I know this is an old post, but dermatitis is a classic sign of low arachidonic acid/prostacyclin. Theoretically, B6 would help increase AA and prostacyclin, but it doesn't help much. Chicken fat is the best source of arachidonic acid/prostacyclin, and would probably clear up your dermatitis. I know Ray Peat doesn't approve of eating chicken fat, but you might want to research this issue if you still have dermatitis. Dietary arachidonic acid, like in a rich chicken soup, is actually anti-inflammatory, as opposed to cellular arachidonic acid, which participates in the inflammatory response to free radicals, like those caused by unmetabolized vegetable oils. I think the key is to completely avoid vegetable oils. http://www.ncbi.nlm.nih.gov/pubmed/23528213

This is a bit odd since historically ray has mentioned quite a few times the rebuttal to the burr experiment that showed b6 is the usual culprit for these conditions and that the n-6 or arachidonic acid for that matter are not essential in any sense.

EDIT: haidut beat me to the punch lol

 

[Soup Lady]

This is a very complicated issue but, in a nutshell, dietary arachidonic acid is turned into an anti-inflammatory hormone called prostacyclin, which protects the stomach, fights cancer, is given to treat people who have heart attacks, produces cannibinoids (AKA pot), increases GABA, glutathione, and SOD, builds new synapses, repairs myelin, breaks down triglycerides, preventing fatty liver, prevents birth defects, and much more. Beef has very little AA, poultry is the best source. Cellular AA: All cells have some AA in them, and it is used to form pro-inflammatory hormones in the presence of free radicals, etc. So, AA is a very powerful fat, and is needed only in small amounts. But, it is absolutely needed. The problem is that the enzyme that is needed for the body to make arachidonic acid from plant linoleic acid is very often dysfunctional, esp. in Northern Europeans and in the case of illness, so chicken fat is very beneficial, I believe. I found all this when I was researching the benefits of chicken soup. Here's a good overall reference: http://www.brinkzone.com/articles/a...pplementation-safe-can-it-even-be-beneficial/

 

[haidut]

This is a very complicated issue but, in a nutshell, dietary arachidonic acid is turned into an anti-inflammatory hormone called prostacyclin, which protects the stomach, fights cancer, is given to treat people who have heart attacks, produces cannibinoids (AKA pot), increases GABA, glutathione, and SOD, builds new synapses, repairs myelin, breaks down triglycerides, preventing fatty liver, prevents birth defects, and much more. Beef has very little AA, poultry is the best source. Cellular AA: All cells have some AA in them, and it is used to form pro-inflammatory hormones in the presence of free radicals, etc. So, AA is a very powerful fat, and is needed only in small amounts. But, it is absolutely needed. The problem is that the enzyme that is needed for the body to make arachidonic acid from plant linoleic acid is very often dysfunctional, esp. in Northern Europeans and in the case of illness, so chicken fat is very beneficial, I believe. I found all this when I was researching the benefits of chicken soup. Here's a good overall reference: http://www.brinkzone.com/articles/a...pplementation-safe-can-it-even-be-beneficial/

I don't really agree with the idea that prostacyclin is a "good" substance. It is a prostaglandin after all and as such it activates aromatase, increases angiogenesis, and stimulates cancer spread. Also, if the cells have arachidonic acid in them they would be able to synthesize prostacyclins if they needed it without the need for dietary arachidonic acid due to it being somehow special. Some things below to consider:
http://raypeat.com/articles/articles/fats-degeneration3.shtml
"...PGI2, or prostacyclin, is considered to be a good prostaglandin, because it causes vasodilatation, and so drug companies have made their own synthetic equivalents:Epoprostenol, iloprost, taprostene, ciprostene, UT-15, beraprost, and cicaprost. Some of these are being investigated for possible use in killing cancer. But many very useful drugs that already existed, including cortisol and aspirin, were found to achieve some of their most important effects by inhibiting the formation of the prostaglandins. It was the body's load of polyunsaturated fats which made it very susceptible to inflammation, stress, trauma, infection, radiation, hormone imbalance, and other fundamental problems, and drugs like aspirin and cortisone, which limit the activation of the stored “essential fatty acids,” gain their remarkable range of beneficial effects partly by the restraint they impose on those stored toxins."

http://www.ncbi.nlm.nih.gov/pubmed/12576509
"...During the pregnancy-lactation period, mother mice were fed either a high-fat diet rich in linoleic acid, a precursor of arachidonic acid (LO diet), or the same isocaloric diet enriched in linoleic acid and alpha-linolenic acid (LO/LL diet). Body weight from weaning onwards, fat mass, epididymal fat pad weight, and adipocyte size at 8 weeks of age were higher with LO diet than with LO/LL diet. In contrast, prostacyclin receptor-deficient mice fed either diet were similar in this respect, indicating that the prostacyclin signaling contributes to adipose tissue development. These results raise the issue of the high content of linoleic acid of i) ingested lipids during pregnancy and lactation, and ii) formula milk and infant foods in relation to the epidemic of childhood obesity."

http://onlinelibrary.wiley.com/doi/10.1002/path.4453/abstract
"...Although we do not provide direct evidence of a relationship between tumour vascularization and radiotherapy efficiency, our results suggest that the effect of PGI2 is related to its ability to promote vascularization. These results also support the concept that co-adjuvant therapy with PGIS enhancers, such as retinoids, could have therapeutic value for HNSCC treatment."

http://www.biochemistry.org/Portals/0/Conferences/abstracts/SA151/SA151P018.pdf
"...
Consistent with the apparent role for prostacyclin and PGE2, the IP receptor antagonist (CAY10441, 10μM, AA 20μM) and EP4 receptor antagonist (L-161,982, 0.05μM, AA 20μM), also decreased cell migration (45±10 versus 123±10, P<0.05 and 86± 6 versus 123±10, P<0.05 respectively). In contrast antagonists of alternate prostanoid receptors did not influence tumour cell migration out of matrigel droplets. These findings implicate prostacyclin as well as PGE2 in the metastatic activity of MDA-MB-468 breast cancer cells that over-express COX-2. Current investigations are focusing on potential mediators of increased cell migration caused by activation of IP and EP4 receptors."

http://www.cell.com/abstract/0092-8674(81)90117-3
"...Histamine stimulates the production of prostacyclin (PGI2) in cultured human endothelial cells. We have examined the cell specificity of histamine-mediated PGI2 synthesis in primary and subcultured human cells. Venous and arterial smooth muscle cells and skin fibroblasts synthesized PGI2 from exogenous arachidonic acid, but they did not synthesize a significant amount of PGI2 when treated with histamine. Endothelial cells, however, produced similar amounts of PGI2 in response to histamine and arachidonic acid. Thrombin also stimulates PGI2 production in endothelial cells. Histamine and thrombin yielded an additive production of PGI2 when added simultaneously to endothelial cells. When histamine and thrombin were added sequentially, the amount of PGI2 produced was not additive but equaled the amount characteristic of the first agonist alone."

Just b/c something is a vasodilator and and anti-inflammatory does not automatically make it a good substance. Nitric Oxide (NO) does both and it is involved in virtually all pathological conditions. So far, the same seems to be true about prostaglandins.
NO is given to newborn babies with pulmonary hypertension and destroys their lungs. Lactate is given to people with heart attacks and shock to "revive" them. These are all criminally bad therapies.
So, I need to see an explanation of the mechanism of beneficial action of prostacyclin. Right now, the biochemistry behind it points to it being far from beneficial.

 

[haidut]

A few other things. The link you posted discusses how supplementing with omega-3 s a good thing. I am not going to comment on that as it speaks for itself.
Also, the link contains this language:
"...A study in healthy Japanese men and women aged 55-70 investigated whether ARA supplementation affects clinical parameters involved in cardiovascular, inflammatory, and allergic diseases.[12] Subjects were supplemented with ARA-enriched oil (240 or 720 mg ARA per day) or placebo for 4 weeks, followed by a 4-week washout period. The fatty acid contents of plasma phospholipids, clinical parameters, and AA metabolites were determined at baseline, 2, 4, and 8 weeks. It was found that ARA content in plasma phospholipids in the ARA supplemented groups increased dose-dependently and was almost the same at 2 weeks and at 4 weeks. The elevated ARA content decreased to nearly baseline during a 4-week washout period. Contrary to expectations, during the supplementation and washout periods, no changes were observed in plasma phospholipid EPA and DHA content. There were no changes in clinical blood parameters related to cardiovascular, inflammatory and allergic diseases.[12]"

Increasing the unsaturation of the phospholipids is the last thing you want to do. Things like cardiolipin unsaturation already increase greatly with age and disease. I just posted a study showing the effects of a well known toxin DEHP (a type of plactic similar to BPA, BPS, etc) has the same effect - increases in phospholipid unsaturation. Here is that thread for more info:
https://raypeatforum.com/community/...sol-block-glucose-oxidation.9288/#post-120458
"...Overall distribution of metabolites is shown in the volcano plot (Fig 2A and S1 Table), indicating a general shift towards higher mean values for many lipids and carnitines. We found a clear trend both for lipids and carnitines, that the unsaturated forms are increased, whereas the saturated forms are not changed or even downregulated by DEHP exposure. As an example, the acyl-acyl forms of phosphatidylcholines containing 38 carbon atoms in their fatty acid chain are shown in more detail in Fig 2B. Similar behavior was found for carnitines and acyl-ethyl forms of phospholipids. DEHP treatment led to lowering of aspartate and kynurenine, but not ADMA and ornithine (Fig 2B)."

 

[Soup Lady]

The first study simply showed that ARA is in the blood once you take it as a supplement by itself, yet it was not found to be inflammatory, like people often think. By the way, in the fat from pastured chickens, there is nearly equal ARA and EPA, which is the proper ratio-no need to supplement with anything. Also, bisphenol A, like all estrogens, inhibits the production of arachidonic acid, which may be a major reason why many people are low.

A few other things. The link you posted discusses how supplementing with omega-3 s a good thing. I am not going to comment on that as it speaks for itself.
Also, the link contains this language:
"...A study in healthy Japanese men and women aged 55-70 investigated whether ARA supplementation affects clinical parameters involved in cardiovascular, inflammatory, and allergic diseases.[12] Subjects were supplemented with ARA-enriched oil (240 or 720 mg ARA per day) or placebo for 4 weeks, followed by a 4-week washout period. The fatty acid contents of plasma phospholipids, clinical parameters, and AA metabolites were determined at baseline, 2, 4, and 8 weeks. It was found that ARA content in plasma phospholipids in the ARA supplemented groups increased dose-dependently and was almost the same at 2 weeks and at 4 weeks. The elevated ARA content decreased to nearly baseline during a 4-week washout period. Contrary to expectations, during the supplementation and washout periods, no changes were observed in plasma phospholipid EPA and DHA content. There were no changes in clinical blood parameters related to cardiovascular, inflammatory and allergic diseases.[12]"

Increasing the unsaturation of the phospholipids is the last thing you want to do. Things like cardiolipin unsaturation already increase greatly with age and disease. I just posted a study showing the effects of a well known toxin DEHP (a type of plactic similar to BPA, BPS, etc) has the same effect - increases in phospholipid unsaturation. Here is that thread for more info:
https://raypeatforum.com/community/...sol-block-glucose-oxidation.9288/#post-120458
"...Overall distribution of metabolites is shown in the volcano plot (Fig 2A and S1 Table), indicating a general shift towards higher mean values for many lipids and carnitines. We found a clear trend both for lipids and carnitines, that the unsaturated forms are increased, whereas the saturated forms are not changed or even downregulated by DEHP exposure. As an example, the acyl-acyl forms of phosphatidylcholines containing 38 carbon atoms in their fatty acid chain are shown in more detail in Fig 2B. Similar behavior was found for carnitines and acyl-ethyl forms of phospholipids. DEHP treatment led to lowering of aspartate and kynurenine, but not ADMA and ornithine (Fig 2B)."

 

[Soup Lady]

"It was the body's load of polyunsaturated fats which made it very susceptible to inflammation, stress, trauma, infection, radiation, hormone imbalance, and other fundamental problems, and drugs like aspirin and cortisone, which limit the activation of the stored “essential fatty acids,” gain their remarkable range of beneficial effects partly by the restraint they impose on those stored toxins." I think this is the essential problem-mixing the problem of linoleic acid, which is ridiculously high in our i\diet and has caused major damage, with arachidonic acid.

prostacyclin receptor-deficient mice fed either diet were similar in this respect, indicating that the prostacyclin signaling contributes to adipose tissue developmen

A high linoleic acid diet, similar to our high vegetable oil diet, blocks the critical D6D enzyme, which makes arachidonic acid our of linoleic acid. This fat then gets stored as adipose tissue, not ARA. In fact, the amount of linoleic acid in adipose tissue has gone steadily up throughout the 1900's. Linoleic acid from oils and seeds is a huge problem. The prostacyclin receptor has perhaps saved the body from the free radicals that linoleic acid produces, called, 9 and 13 HODE, by storing it away.

 

[haidut]

The first study simply showed that ARA is in the blood once you take it as a supplement by itself, yet it was not found to be inflammatory, like people often think. By the way, in the fat from pastured chickens, there is nearly equal ARA and EPA, which is the proper ratio-no need to supplement with anything. Also, bisphenol A, like all estrogens, inhibits the production of arachidonic acid, which may be a major reason why many people are low.

What do you mean by proper ratio of ARA/EPA? Why would anyone need EPA or ARA? Again, the increasing unsaturation of adipose fat and phospholipids is a characteristic of aging and disease. The study from your link lasted only 4 weeks. Also, again, that website pushes supplementation with DHA/EPA which so far has failed every major human clinical trial that looked at it. Unsuprisingly, if you ask me, considering the metabolic effects of omega-3. If you want to ingest a lot of DHA/EPA that's your right but please provide evidence for their benefit if you are suggesting others do the same.
Finally, estrogen does not inhibit ARA synthesis but promotes it due to estrogen enhancing the activities of the delta-5 and delta-6 desaturase enzymes. See below.
http://www.ncbi.nlm.nih.gov/pubmed/8655636
"...The hormones 17 beta-estradiol (17 beta-E2), dexamethasone (a synthetic glucocorticoid), and 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) have been identified as regulators of AA metabolism, at various levels, in several tissues including bone. The possibility that these osteotropic steroids modulate the availability of free AA in bone cells was studied in the human osteoblast-like (hOB) cell model system. Following a 48-h steroid pretreatment, bradykinin or the calcium ionophore A23187 were used as agonists to stimulate hOB cell release of AA. The principal findings from these investigations were that (1) 17 beta-E2 pretreatment potentiated the appearance of free AA following bradykinin stimulation of the cells but, did not alter their response to A23187 stimulation; (2) dexamethasone pretreatment limited bradykinin-induced increases in free AA levels but did not alter cell response to A23187 stimulation; (3) hOB cells derived from different trabecular bone compartments (manubrium of the sternum, femoral head) differed quantitatively in their responses to bradykinin stimulation of AA release; and (4) 1,25(OH)2D3 did not effect AA release stimulated by either agonist. The ability of the steroids to modulate AA release by hOB cells suggests that these hormones may indirectly mediate bone cell responses to other osteotropic hormones that act through eicosanoid-dependent processes."

The study looked at effects on DHA levels but the synthesis pathway for ARA is largely the same.
http://www.ncbi.nlm.nih.gov/pubmed/23764042
"...Progesterone exerted no effect on Δ6-desaturase or DHA. These results indicate that 17β-estradiol increases DHA through increased Δ6-desaturase, possibly explaining sex differences in DHA."

 

[Soup Lady]

NO is given to newborn babies with pulmonary hypertension and destroys their lungs.

Interesting you should mention this. People/babies with pulmonary hypertension are low in ARA and are usually given prostacyclin as a treatment. Babies have a great need for ARA for proper development, yet they are often low, especially preemies, and the complications they suffer is the result of low ARA. In fact, diabetic rats (who would be low in ARA, as all diabetics are-prostacyclin protects the beta cells) were given ARA and it prevented spina bifida, cleft palate and mal-aligned teeth.
People have been eating bird fat since man began to cook. Arachidonic acid itself actually tastes like chicken, so it seems that we evolved eating it.

 

[haidut]

Interesting you should mention this. People/babies with pulmonary hypertension are low in ARA and are usually given prostacyclin as a treatment. Babies have a great need for ARA for proper development, yet they are often low, especially preemies, and the complications they suffer is the result of low ARA. In fact, diabetic rats (who would be low in ARA, as all diabetics are-prostacyclin protects the beta cells) were given ARA and it prevented spina bifida, cleft palate and mal-aligned teeth.
People have been eating bird fat since man began to cook. Arachidonic acid itself actually tastes like chicken, so it seems that we evolved eating it.

Studies please?
As I mentioned before, just because something is used in clinical practice does not mean it is beneficial. NO is also "helpful" in pulmonary hypertension and also essential hypertension but it really sets the stage for cancer. Prostacyclin is a potent angiogenic molecule (VEGF enhancer) and as such promotes the cascade of unrestricted growth and de-differentiation.
http://journal.publications.chestnet.org/article.aspx?articleid=1084145
"...In this small group of patients, prostacyclin therapy did not protect the patient from the development of metastatic cancer. Possible explanations include observations in which the intermittent administration of cicaprost was protective in rats from metastases while continuous administration was not. Additionally, prostacyclin has been shown to induce vascular endothelial growth factor expression, which plays an important role in the growth of tumors and metastases. Interestingly, all patients are women and half of have ovarian cancer. Further studies are necessary to determine whether continuously infused prostacyclin may increase the metastatic rate and/or the potential for the growth of tumors, or the development of specific tumors."

Also, prostacycline is a potential thyroid "receptor" antagonist and has a direct mutually causative relationship with TSH.
http://www.ncbi.nlm.nih.gov/pubmed/26686607
http://www.ncbi.nlm.nih.gov/pubmed/7016591

 

[Soup Lady]

Studies please?
As I mentioned before, just because something is used in clinical practice does not mean it is beneficial. NO is also "helpful" in pulmonary hypertension and also essential hypertension but it really sets the stage for cancer. Prostacyclin is a potent angiogenic molecule (VEGF enhancer) and as such promotes the cascade of unrestricted growth and de-differentiation.
http://journal.publications.chestnet.org/article.aspx?articleid=1084145
"...In this small group of patients, prostacyclin therapy did not protect the patient from the development of metastatic cancer. Possible explanations include observations in which the intermittent administration of cicaprost was protective in rats from metastases while continuous administration was not. Additionally, prostacyclin has been shown to induce vascular endothelial growth factor expression, which plays an important role in the growth of tumors and metastases. Interestingly, all patients are women and half of have ovarian cancer. Further studies are necessary to determine whether continuously infused prostacyclin may increase the metastatic rate and/or the potential for the growth of tumors, or the development of specific tumors."

Also, prostacycline is a potential thyroid "receptor" antagonist and has a direct mutually causative relationship with TSH.
http://www.ncbi.nlm.nih.gov/pubmed/26686607
http://www.ncbi.nlm.nih.gov/pubmed/7016591

Something seems to have happened to my posts-I just tried to fix one and they disappeared. Anyway, why do you keep mentioning NO, which is a problem for a lot of people because of the high arginine nuts and seeds they eat, nothing to do with ARA, and seem so determined to find bad things about ARA? Everyone with a chronic illness is low in ARA, both mental and physical. I was a vegetarian for 30 years, plus I'm N. European so I couldn't make ARA from nuts and seeds, and I was so hyper (low ARA causes anxiety), along with food sensitivities like gluten intolerance (again, from low prostacyclin). I'm just glad I discovered ARA. You might want to try a rich chicken soup, with pastured chicken, and see what happens-you'll probably feel more relaxed, and digest food a lot more fully (if that happens to be a problem).

 

[Giraffe]

Something seems to have happened to my posts-I just tried to fix one and they disappeared.

I separated the discussion from the other thread because it was off-topic there.

 

[haidut]

Something seems to have happened to my posts-I just tried to fix one and they disappeared. Anyway, why do you keep mentioning NO, which is a problem for a lot of people because of the high arginine nuts and seeds they eat, nothing to do with ARA, and seem so determined to find bad things about ARA? Everyone with a chronic illness is low in ARA, both mental and physical. I was a vegetarian for 30 years, plus I'm N. European so I couldn't make ARA from nuts and seeds, and I was so hyper (low ARA causes anxiety), along with food sensitivities like gluten intolerance (again, from low prostacyclin). I'm just glad I discovered ARA. You might want to try a rich chicken soup, with pastured chicken, and see what happens-you'll probably feel more relaxed, and digest food a lot more fully (if that happens to be a problem).

I am mentioning NO because just like prostacyclin is it is used clinically with purportedly good effects. Like I said in my first response, if a specific diet makes you feel good by all means go for it. However, you are stating some things about ARA and prostacyclin as de-facto true, while actually there is strong evidence against them. How do you know your issues were from low ARA and adding ARA fixed it. The chicken soup you mention has a million other good things in it like thyroid, gelatin, steroids, glycogen, etc if it is indeed made from pastured chickens.
Also, how do you know that low ARA levels in these conditions you mentioned are causative? DHA/EPA are low in autism but when a double-blind trial was done with them it was found they worsened the condition in some patients and overall were without effect. So, the association can only suggest a hypothesis which is then tested experimentally. The actual experiments so far on prostacyclin seem to show it is angiogenic, vasodilatory, pro-aging, pro-cancer substance. NO also has these effects and that is why I brought it up b/c it is a good example of a substance that seems to have a beneficial effect but it really isn't if you look closely at the biochemistry and the effects on living organisms.
Anyways, I think we have argued about this enough. The goal is to improve health and not argue, so whatever is working for you go I'd say go for it.

 

[Soup Lady]

I separated the discussion from the other thread because it was off-topic there.

Good idea! Anyway, I think the problem is you shouldn't have too much ARA in your diet, because it is powerful, but your body does use it up, esp. your brain, so you need to replenish it. Theoretically you can get the small amount you need from linoleic acid in nuts and seeds, but the enzyme is often dysfunctional, so my only point, really, is to get it from a little chicken fat-maybe one bowl of soup a day-like they do all over the world.

 

[Soup Lady]

I am mentioning NO because just like prostacyclin is it is used clinically with purportedly good effects. Like I said in my first response, if a specific diet makes you feel good by all means go for it. However, you are stating some things about ARA and prostacyclin as de-facto true, while actually there is strong evidence against them. How do you know your issues were from low ARA and adding ARA fixed it. The chicken soup you mention has a million other good things in it like thyroid, gelatin, steroids, glycogen, etc if it is indeed made from pastured chickens.
Also, how do you know that low ARA levels in these conditions you mentioned are causative? DHA/EPA are low in autism but when a double-blind trial was done with them it was found they worsened the condition in some patients and overall were without effect. So, the association can only suggest a hypothesis which is then tested experimentally. The actual experiments so far on prostacyclin seem to show it is angiogenic, vasodilatory, pro-aging, pro-cancer substance. NO also has these effects and that is why I brought it up b/c it is a good example of a substance that seems to have a beneficial effect but it really isn't if you look closely at the biochemistry and the effects on living organisms.
Anyways, I think we have argued about this enough. The goal is to improve health and not argue, so whatever is working for you go I'd say go for it.

Please see my other post-it's all in proportion. Also, when I said I was more relaxed, I was referring to the cannibinoids that ARA makes-better than smoking pot! So, I hope you do well in your diet :)

 

[mujuro]

AA is a precursor to the endocannabinoid anandamide (arachidonoylethanolamine), which is the natural ligand for the same cannabinoid receptors as THC, purportedly having the same positive effects on mood, anxiety, etc. They just had a trial in France for a novel fatty acid amide hydrolase inhibitor (thus preventing the breakdown of anandamide) and 6 patients ended up with brain damage, one being brain dead and in a vegetative state. God forbid they use cannabis. Nope, can't patent a weed.

 

[Soup Lady]

That's really horrible! they must have tried it on rats first, and should have known the dangers-just outrageous.

 

[Soup Lady]

I know GABA is extremely important, but that's another thing that you normally get when you have enough arachidonic acid in your diet. From a study:
The results showed that administration of ARA improved learning and memory deficit induced by repeated isofluane anesthesia in Morris water maze test and in a dose-dependent manner. Additionally, ARA increased the activities of choline acetyl transferase (ChAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and the levels of acetycholine (Ach) and γ-amino-butyric acid (GABA), whereas decreased the activity of acetylcholine esterase (AchE), the content of glutamate (Glu) and malondialdehyde (MDA), and the radio of Glu/GABA. Arachidonic acid attenuates learning and memory dysfunction induced by repeated isoflurane anesthesia in rats

This study suggests that ARA prevents irritability and irrational thinking, and helps with social adaptability, among many other things. It also shows that ARA is anti-inflammatory, as it lowered MDA, a marker of oxidative damage. This agrees with the National Institute of Health study that showed that, although ARA kills viruses, bacteria, fungi and parasites as part of the inflammatory immune system, dietary ARA is anti-inflammatory. https://www.ncbi.nlm.nih.gov/pubmed/16234304

The way we used to get GABA, and all these other things, was to eat chicken fat, by eating soup and the skin, so that's why I'm promoting doing this again.

 

[Herbie]

So far I have found studies suggesting arachidonic acid is involved in dermatitis by metabolising Leukotriene B4 (LTB4) and n-9 Eicosatrienoic acid (ETrA), also known as Mead acid, is a minor fatty acid in essential fatty acid (EFA)-sufficient healthy subjects but is found at increased levels in EFA deficiency which has shown to inhibit Leukotriene B4 (LTB4)

This study found that prostaglandin PGE2 is not elevated in dermatitis skin lesions nor is histamine and that Leukotriene B4 (LTB4) is found in higher levels in the lesions compared to healthy skin might explain the therapeutic efficiency of glucocorticosteroids on dermatitis.
Skin levels of arachidonic acid-derived inflammatory mediators and histamine in atopic dermatitis and psoriasis. - PubMed - NCBI
Full article: Skin Levels of Arachidonic Acid-Derived Inflammatory Mediators and Histamine in Atopic Dermatitis and Psoriasis - ScienceDirect

Lipoxygenase (LOXs) is involved in synthesising Leukotriene B4 (LTB4) from arachidonic acid which Haidut has written about here: Blocking PUFA Metabolism May Reverse Alzheimer Disease (AD)

This graph shows why COX inhibitors like Aspirin or antihistamines may not be effective in treating dermatitis if Leukotriene B4 (LTB4) is what is contributing to the dermatitis. IMO

These finding suggests that n-9 EPA eicosatrienoic acid (mead acid) inhibits LTB4
Dietary (n-9) eicosatrienoic acid from a cultured fungus inhibits leukotriene B4 synthesis in rats and the effect is modified by dietary linoleic a... - PubMed - NCBI
Treatment with DHA/EPA ameliorates atopic dermatitis-like skin disease by blocking LTB4 production. - PubMed - NCBI

This was a reference from Rays article Unsaturated fatty acids: Nutritionally essential, or toxic?
Beneficial effects of n-9 eicosatrienoic acid on experimental bowel lesions. Yoshida H, Soh H, Sando K, Wasa M, Takagi Y, Okada A. PURPOSE: Dietary fortification of n-9 polyunsaturated fatty acids (PUFA) or 5,8,11-eicosatrienoic acid (ETrA) as well as n-3 PUFA might contribute to the suppression of leukotriene B4 (LTB4) synthesis and thereby reduce inflammatory bowel lesions. As a result, the effect of an ETrA-enriched diet on experimental bowel lesions was examined in this study. METHODS: In Expt. 1, rats were freely fed either an ETrA-enriched or a standard diet. After 7 days of feeding, acute bowel lesions were induced by the subcutaneous injection of 10 mg/kg indomethacin. In Expt. 2, chronic bowel lesions were made by performing subcutaneous injections of 7.5 mg/kg indomethacin twice. After the first injection, the rats were freely fed either an ETrA-enriched or a standard diet for 7 days. RESULTS: In both experiments, the rats fed an ETrA-enriched diet showed increased levels of ETrA in the plasma and intestinal mucosa, and a decreased inflammation score. However, there was no significant decrease in plasma and intestinal mucosal LTB4 in the ETrA-enriched diet-fed rats. CONCLUSION: These results suggest that the dietary supplementation of ETrA may have both prophylactic and therapeutic effects on experimentally produced bowel lesions. Further investigations are necessary to clarify the effects of ETrA on bowel lesions and its mechanisms. This was a reference from Rays article Unsaturated fatty acids: Nutritionally essential, or toxic?

“The enzyme that produces the Mead fatty acid is strongly inhibited by PUFA seed oils (less strongly by fish oils), and so the presence of the Mead acid in the tissues is taken as evidence that the animal is suffering damage resulting from the absence of PUFA. The Mead acid happens to have some valuable anti-inflammatory effects, and is associated with many biological advantages, but research in that direction is prevented by the lack of funding.” - Ray Peat.


Apparently mead acid is found in high amounts in cartilage and may be why chicken broth made from chicken carcass could help heal dermatitis and not from arachidonic acid IMO. OX tail soup could be another sources of cartilage containing mead acid. IMO

No one knows what causes dermatitis, I am trying to find possible solutions.