Arachidonic Acid Cascade And Peat's Views

Jack Roe

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Peat's thesis is that PUFA are totally unnecessary---not that they're only necessary in small quantities but that they are biologically unnecessary and harmful. Without linoleic acid (LA), arachidonic acid (AA) cannot be formed, but, per Peat, mead acid (MA) can be formed.

AA participates in what the academics, that Peat thinks are in the thrall of vegetable oil pushers, the arachidonic cascade (AC) which leads to the synthesis of prostaglandins and leutrokines. The explanation Peat offers for the scaly dermatitis on rats fed an LA-deficient diet is that their metabolic rate is increased and that extra B6 and zinc (tho I don't think he is very clear on this point) will fix them up and that the reason this has not been trivially demonstrated is that there is something ranging from industry pressure to academic authoritarianism that prevents the truth from being known.

Reading his long, rambling articles, yes, there are lots of citations, but his basic premise seems to be that if there are studies showing that lots of LA is harmful (and there are loads of studies like this) then we can infer that zero LA is better than any LA. Of course, we cannot apply this principle generally: B6 from purified sources (let's take seed oils as "purified sources" of LA) can induce nerve damage, but this does not mean that B6 is a poison and that our biological need for B6 is zero. What it means is that two conditions are possible: overdose and underdose.

The problem is that he does not really say what it is that deals with scaly dermatitis as effectively as LA. In a quotation re: eczema (scaly dermatitis) he says

"Coeliac disease is one of the causes of both skin disease and Arthritis. Coeliac disease, among other things, will allow endotoxin into your circulation and low thyroid is probably the most common thing associated with just ordinary eczema and that's because when your thyroid is low the circulation to your intestine is poor, the serotonin is high. The combination of endotoxin and the serotonin for example will cause the skin to have abnormal growth patterns." (https://raypeatforum.com/community/threads/chronic-eczema-dry-skin-please-help-me-with-my-plan.7725/)

So, these rats, due to nutritional deficiency, have developed coeliac disease, leading to infiltration with endotoxin and excess serotonin. It's strange that he doesn't repeat here what he says about the rats in the LA study---eczema is basically the same thing as "scaly dermatitis," so why doesn't he mention what he thinks would be trivial in a rat study, to wit, giving them more B6 and other nutrients?

The most current research that I have reviewed suggests that actual LA needs are somewhere around 1% energy, with 0.5% energy coming from alpha-linolenic acid (ALA), for a total of around 1.5% EFA requirement. It may be that even this is higher than necessary, with the total requirement being closer to 1%. This would appear compatible with Peat's view that excess PUFA is damaging, and it would also comport with the research demonstrating that AA is derived from LA which enables the AC to produce various compounds.

For a 2000 calorie diet, this would be about 4g of PUFA a day, as 1% LA and 0.5% ALA.

One article that Pete cites, he mis-cites, making me think that he read an abstract that had a summary and not the article itself. He cites

"J. Physiol. 1920, liv, p. xxx, Proc. Physiol. Soc. Nutrition on diets practically devoid of fats. Drummond, JC."

The proper citation is
"J Physiol. 1921; 54(Suppl)", it is a supplemental journal recording the proceedings of the Physiological Society, which took place in 1920, published in 1921.
PROCEEDINGS OF THE PHYSIOLOGICAL SOCIETY: July 10, 1920

The study concerns an attempt to isolate "Factor A." In the article, the rats are, it is true, maintained on a fat-free diet for a while, but their growth is "subnormal" and "irregular." The rats were 4 weeks old, implying that they had been on standard chow for 4 weeks. Further, the "Factor A" extract was a carrot extract that was not devoid of fat, it was basically an extraction of the carotene and all other fatty substance from carrot, which would include a small amount of LA!

What I can find concerning carrots says that the fat is in the ratio Monounsaturated:Polyunsaturated:Saturated 2:14:5. The study suggested 11mg of "fat" from the carotene extract, which would be approximately 7.3mg of LA per day. This is not a lot of LA, but, again, this was not a fat free diet, that certainly was not the goal of the diet, the diet was designed to test carrot extract as a source of "Factor A," that is, what we now call Vitamin A.

So, Did Peat not read the original proceeding or did he simply mischaracterize it? The article, which is very short, spends much time talking about how it was "practically devoid" of fat, not "totally."

http://www.jbc.org/content/12/1/81.full.pdf is a 1912 article he cites merely says that the topic can be approached, it does not draw definitive conclusions. Further, the animals were maintained prior to the study period on standard diet or by their mothers. A footnote in the study says that the animals were not brought to their maximum growth rate.

So, basically, there is research showing that fat free diets can keep animals alive, but they do not thrive. Further, the contemporary research suggests that LA requirements are very low. It is also possible that these "fat free" diets were not devoid of what the 1912 article calls "lipoids."

So, 5% of calories as LA is obviously excessive, and bringing ALA into a "1:1" with that is also unnecessary, but a modest 1-1.5% of diet as LA+ALA is likely necessary for stable growth. The fact that the AC produces so many varied compounds suggests a strong presumption that it is not merely a disposal method for unnecessary compounds nor that it is merely leftover machinery from, for example, when we were fish. There seems to be quite a bit of research into the effects of prostaglandins
 

SOMO

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-0 Fat diet for me leads to dry skin.
-Small amounts of Canola or Soybean oil result in acne and itchy dermatitis.
-Large amounts of fish oil and/or daily fish consumption do not result in acne.

Realistically though, achieving ~1% EFA in the diet, if you consume meat/eggs or nuts, is guaranteed.

RP also brings up the point that some of these older fat-free studies were done at a time BEFORE the discovery of all the B-Vitamins. There's loads of anecdotes online of people reversing or improving skin conditions with Biotin or B5, but B3 is also used to "bleach" hyper-pigmented skin.

I also think that the long chain fats stimulate digestion and prevent constipation because of bile production. A zero-fat diet may not be physiologically appropriate for reasons besides skin texture. MCTs are used in hospital settings when the person can't digest fats, which begs the question - why not just omit fats entirely from these people?
Regarding AA, I consumed 2-3 raw egg yolks daily for maybe 3 years with no ill effects and egg yolks are high in AA. I was also consuming a lot of pork and chicken during this time, so I was definitely over the Peat-approved PUFA limit. It's also possible mice are more sensitive to changes in PUFA than humans are.

My point is that the effects of fats is as varied and needs further study.



 
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lvysaur

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I think that human evolution for much of recent history (last 15k years definitely, and probably even longer) was largely insignificant or scattered and incomplete, because our ability to change our environment outpaced our rate of genetic adaptation.

So if you could imagine a frugivorous common ancestor between humans and chimps, it probably went two ways: one evolving into into a tree dweller (good strategy for monopolizing fruit) and one evolving into a big brained cognitively adaptive weakling (good strategy for monopolizing fruit).

The big brained weakling is much more energetically expensive, so human ancestors probably had control of a much larger/much sweeter array of fruit, while the chimps had to deal with what they could get.

Ever since then, humans have been introducing new foods, techs, etc faster than we've been able to "adapt" to them; and I think maybe the lineoleate pathways are a primitive vestige of a life where calories were hard to guarantee (which is the case for literaly every other animal on earth). ALL pufa are beneficial if you're on the brink of starvation.
 
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Jack Roe

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-0 Fat diet for me leads to dry skin.
-Small amounts of Canola or Soybean oil result in acne and itchy dermatitis.
-Large amounts of fish oil and/or daily fish consumption do not result in acne.

Realistically though, achieving ~1% EFA in the diet, if you consume meat/eggs or nuts, is guaranteed.

RP also brings up the point that some of these older fat-free studies were done at a time BEFORE the discovery of all the B-Vitamins. There's loads of anecdotes online of people reversing or improving skin conditions with Biotin or B5, but B3 is also used to "bleach" hyper-pigmented skin.

I also think that the long chain fats stimulate digestion and prevent constipation because of bile production. A zero-fat diet may not be physiologically appropriate for reasons besides skin texture. MCTs are used in hospital settings when the person can't digest fats, which begs the question - why not just omit fats entirely from these people?
Regarding AA, I consumed 2-3 raw egg yolks daily for maybe 3 years with no ill effects and egg yolks are high in AA. I was also consuming a lot of pork and chicken during this time, so I was definitely over the Peat-approved PUFA limit. It's also possible mice are more sensitive to changes in PUFA than humans are.

My point is that the effects of fats is as varied and needs further study.

Well, it seems like it is a fairly well-studied problem, and all this Peat character has to offer is vague and contradictory statements that don't appear to really characterize the historical research properly. He acts like they had some secret fat-free diet that they knew worked and it was covered up rather than that, at least in the two historical papers I've looked at, the diet (a) wasn't fat-free and (b) did not lead to optimum growth, tho it did not _kill_ the little darlings outright.

And even the fruit-eating animals another fellow mentions, the dataset I can find says mandarin oranges have 48mg omega-6 per 100 grams/53 calories. So, even if you got 2000 calories from oranges alone, you'd still get around 1.6g LA, or about 0.65% en from LA.

What I think I am getting at is that if Peat is right, the only diet that is really non-toxic is one that has only become possible in the industrial age, with the capacity to, for example, refine sugar. That's the other thing, if he has it all figured out, why doesn't he suggest subsisting on protein powder + sugar + whatever minerals/vitamins he thinks are necessary? And why is it necessary to take thyroid, etc? There are plenty of vigorous free-living animals that don't take thyroid and other medications, and there are plenty of vigorous animals that don't eat the thyroid glands out of the necks of their kills.

As for the unknown quantity of B Vitamins, this is true, but it appears to me that in most of the old papers they used Brewer's Yeast which contains all of the necessary B Vitamins.

It seems like Peat's advice would make more sense if he were truly some technocrat who thought we could subsist on refined sugar, protein powder, vitamins and minerals, and if he stated which ones, but he doesn't, he has this vague artsy-fartsy "it's like a paintaing, there are no straight lines" view that seems pseudoscientific to me. If the body can produce its own fats from protein and sugar, why would you need any fat? And why would these rat studies he cites as "evidence of a fat free diet" all talk about sub-optimal growth? I guess Peat is not a "team player" enough to have attracted a lab or teaching position w/ lab space sufficient to do it, this would be my guess, but wouldn't it be a fun experiment to have some rats, give them sugar + protein + vitamins + minerals with zero added fat and see what happens?

And of course some people will have skin problems due to B vitamin deficiencies, or mineral deficiencies, or protein deficiencies, but Peat makes very specific claims, although, again, they're not specific-specific, they're hand-wavey bluff-the-laypeople specific. Which is it, Doctor, Zinc or B6? What seems to me more likely is that plenty of experiments, like the ones he's cited that I bothered to read, have shown problems with fat-free diets, and the goal was to figure out what corrected these problems. The correction of the scaly dermatitis used as proxy for LA deficiency has been repeated until modern times, tho it seems that it may be AA deficiency.

What both of the posters above me say seems reasonable, but it is not what Peat says---Peat acts like PUFA are basically like radioactive substances, that they are biologically unnecessary and that they are going to have bad effects, so, if they're unnecessary and have bad effects, why not eliminate them? But it seems he hasn't really taken this to its logical conclusion---protein powder that is well and truly nearly totally devoid of fat is available, so are vitamin and mineral supplements.
 

Travis

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Peat's thesis is that PUFA are totally unnecessary---not that they're only necessary in small quantities but that they are biologically unnecessary and harmful. Without linoleic acid (LA), arachidonic acid (AA) cannot be formed, but, per Peat, mead acid (MA) can be formed.
This has been proven many times, and Mead acid is now the diagnostic biomarker of 'fatty acid deficiency.' Mead acid can be synthesized de novo entirely from glucose through stearic and oleic acid intermediates, yet this process only occurs in the absence of ω-6 fatty acids.
AA participates in what the academics, that Peat thinks are in the thrall of vegetable oil pushers, the arachidonic cascade (AC) which leads to the synthesis of prostaglandins and leutrokines. The explanation Peat offers for the scaly dermatitis on rats fed an LA-deficient diet is that their metabolic rate is increased and that extra B6 and zinc (tho I don't think he is very clear on this point) will fix them up...
At least one study disproves that by feeding that rats extra B-vitamins, but there could have been more. Something also overlooked by Ray Peat had been the 50% increase in water consumption in 'essential fatty acid-deficient' rats. Since the degree of unsaturation on a cell's membrane is correlated with water affinity and permeability, I am convinced the scaly dermatitis had essentially been 'dry skin.'
The most current research that I have reviewed suggests that actual LA needs are somewhere around 1% energy, with 0.5% energy coming from alpha-linolenic acid (ALA), for a total of around 1.5% EFA requirement. It may be that even this is higher than necessary, with the total requirement being closer to 1%.
This appears correct based on that rat feeding study I'd read. Alpha linolenic acid is an omega−3 fatty acid that can be elongated to DHA for cell membranes. As far as I am concerned, α-linolenic acid is the only essential fatty acid. Alpha-linolenic will be elongated to provide the degree of unsaturation that is needed for high brain glucose flux, and omega−6 fatty acids inhibit the process through enzymatic competition for elongation & desaturation. The omega−6 membrane product most similar to DHA is osbond acid, yet this does not function as well as DHA. The scientific facts are in accord with humans having evolved in the tropics, a location where omega−6 fatty acids are relatively rare. With increasing latitude comes increasing desaturation in seed lipids, as can be seen by comparing macadamia and coconuts with the nontropical ones. Ray Peat doesn't talk much about docosahexaenoic acid, but here's a good review article on that one.
One article that Pete cites, he mis-cites, making me think that he read an abstract that had a summary and not the article itself.
I too had got that impression once.
So, basically, there is research showing that fat free diets can keep animals alive, but they do not thrive.
These diets necessarily must be highly refined, with essentially all lipids being chloroform-extracted prior to the reconstruction of food under contemporaneous assumptions of what constitutes 'adequate nutrition.' I think you could only make realistic assumptions about such studies when control groups had been fed the same refined diet + fatty acids. This should of course be done in every case, yet experiments are sometimes flawed in this way.
So, 5% of calories as LA is obviously excessive, and bringing ALA into a "1:1" with that is also unnecessary, but a modest 1-1.5% of diet as LA+ALA is likely necessary for stable growth. The fact that the AC produces so many varied compounds suggests a strong presumption that it is not merely a disposal method for unnecessary compounds nor that it is merely leftover machinery from, for example, when we were fish. There seems to be quite a bit of research into the effects of prostaglandins
All 1- and 2-series prostaglandins derived from omega−6 fatty acids are directly-analogous to 3-series prostaglandins. The 3-series prostaglandins tend to be less-active, and for that reason most prostaglandin research is devoted to 2-series prostaglandins. All prostaglandins in each class are created by cyclooxygenase from one of three fatty acids: dihomo-γ-linolenic (20∶3ω−6), arachidonic (20∶4ω−6), and eicosapentaenoic (20∶5ω−3). Cyclooxygenase is not known to cyclicize any other lipid, including Mead acid (20∶3ω−9). Mead acid does, however, become the chemotactic leukotriene B₃. Since all prostaglandins appear to work on the same receptors as their class counterparts—i.e. prostaglandin E₂ and E₃ both activate EP₁—the assumption that omega−6 fatty acids are essential based merely on prostaglandin necessity is faulty logic.
 
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Jack Roe

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Interesting, but I dunno if ALA is the only EFA.

Essential function of linoleic acid esterified in acylglucosylceramide and acylceramide in maintaining the epidermal water permeability barrier. Ev... - PubMed - NCBI
Essential function of linoleic acid esterified in acylglucosylceramide and acylceramide in maintaining the epidermal water permeability barrier. Evidence from feeding studies with oleate, linoleate, arachidonate, columbinate and alpha-linolenate.
"Essential fatty acid-deficient rats were supplemented with 300 mg per day of pure fatty acid esters: oleate (O), linoleate (L), arachidonate (A), and columbinate (C) for 10 days. During this period, the rats in groups L, A, and C all showed a decrease in their initially high trans-epidermal water loss, a classical essential fatty acid-deficiency symptom, to a level seen in non-deficient rats (group N). The trans-epidermal water loss in rats of group O was unaffected by the supplementation. Fatty acid composition of two epidermal sphingolipids, acylglucosylceramide and acylceramide, from the skin were determined. The results indicate that re-establishment of a low trans-epidermal water loss was associated with incorporation of linolenate into the two epidermal sphingolipids. Supplementation with columbinate resulted in relatively high amounts of this fatty acid in the investigated epidermal sphingolipids. Analysis of pooled skin specimens from a previous study in which weanling rats were fed a fat-free diet and supplemented orally with pure alpha-linolenate for 13 weeks (Hansen, H.S. and Jensen, B. (1983) Lipids 18, 682-690) revealed very little polyunsaturated fatty acid in the two sphingolipids. These rats showed increased evaporation which was comparable to that of essential fatty acid-deficient rats. We interpret these results as strong evidence for a very specific and essential function of linoleic acid in maintaining the integrity of the epidermal water permeability barrier. This function of linoleate is independent of its role as precursor for arachidonate and icosanoids."

AA retroconverts to LA:

Apparent in vivo retroconversion of dietary arachidonic to linoleic acid in essential fatty acid-deficient rats. - PubMed - NCBI
Apparent in vivo retroconversion of dietary arachidonic to linoleic acid in essential fatty acid-deficient rats.
"Essential fatty acid-deficient rats were fed ethyl [U-14C]arachidonate (308 dpm/nmol) and when a decrease in the transepidermal water loss was seen, the epidermal sphingolipids, acylglucosylceramide and acylceramide were isolated. [14C]Linoleic acid (approx. 130 dpm/nmol) was present in both lipid classes, while the substrate was only detected in the former. These results intimate that in vivo retroconversion of arachidonic to linoleic acid can be induced in the rat."

This seems to be a function for LA other than conversion to AA and thence to eicosanoids, so it would seem that LA is also incorporated into the skin, to form a barrier.

The first article talks about an experiment from 1953, where ALA was without effect at restoring the water barrier, so it seems that LA and ALA are both essential, LA for incorporation into skin, and ALA for production of eicosanoids. However, I don't buy the idea that the LA-derived eicosanoids are "bad" and the ALA-derived eicosanoids are "good." Even coconut oil has 1.6g/100g LA and zero ALA.

Take the banana as the quintessential equatorial fruit: it has 0.03g ALA and 0.05g LA per 100g, according to one source I found. So even with equatorial fruit, LA and ALA are present. As for coconuts, Death By Coconut: A Story Of Food Obsession Gone Too Far is an interesting story about a guy who ate nothing but coconuts. It did not end well.

It seems to me that the problem with anything is excess---for some things, like radioactive materials, any is excess, but even those, I know some people who were grad students who were informed of the quantitative risk of some of the tracers they used and it ended up being less than smoking a single cigarette. Plus nutrition is, if we take the vitamins and minerals and EFAs and amino acids (whether we call the aminos one thing, "protein", or several things is another story), a very big multi-variable problem. Molybdenum, for example, is a very important micronutrient, without it, the body cannot deal with sulfate or aldehydes. As I understand it, one of the concerns about PUFA is degradation to aldehydes. Without sufficient molybdenum, dealing with any aldehyde burden could be difficult. Perhaps at least part of the problem with PUFA is a molybdenum deficiency---there is some research suggesting that regions with molybdenum poor soil have higher rates of cancer.

I like your signature quotation:

"With the institutions of research and education controlled by pharmaceutical, military and industrial interests for their own benefit, fundamental progress in knowledge is a threat to the system." ―Ray Peat

But the fact is that it's PhDs (albeit mostly in law, medicine, architecture, etc.) that control the pharmaceutical, military and industrial interests, through a complex system of regulation and public health. I am always skeptical of academics who like to scapegoat powers beyond the University. The University is the "company store." It produces the physicians, the pharmacists and the lawyers, who control the whole waxworks...
 

lvysaur

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And even the fruit-eating animals another fellow mentions, the dataset I can find says mandarin oranges have 48mg omega-6 per 100 grams/53 calories.

with or without seeds?
 
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Jack Roe

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That's an interesting question! But the data I've found indicate orange juice has LA too, so I don't think it's a matter of eating the seeds.
 

Travis

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Interesting, but I dunno if ALA is the only EFA.
Eicosapentaenoic acid can freely substitute for all hormonal eicosanoids, and the substitution of brain DHA with omega−6 is invariably associated with pathology. The ω-3/ω-6 ratio in the brain is very high, and elongation enzymes have a strong preference for ω−3 fatty acids. I have read the classic experiments that led to the idea of 'essential fatty acids' and in no instance have I seen anything to indicate that ω-6 fatty acids in particular were essential. Back then they had considered 'linolenic acid' essential without discriminating between the α- and γ- forms; between the omega−3 and omega−6 isomers
 

Travis

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I like your signature quotation:

"With the institutions of research and education controlled by pharmaceutical, military and industrial interests for their own benefit, fundamental progress in knowledge is a threat to the system." ―Ray Peat

But the fact is that it's PhDs (albeit mostly in law, medicine, architecture, etc.) that control the pharmaceutical, military and industrial interests, through a complex system of regulation and public health. I am always skeptical of academics who like to scapegoat powers beyond the University. The University is the "company store." It produces the physicians, the pharmacists and the lawyers, who control the whole waxworks...
Well I think that's the best quote by Ray Peat, and also that it's better than anything you've said so far.
 
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Jack Roe

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So what about incorporation of LA into skin tissues, reduction in evaporation? Seems fairly well-established. This would jive with the enzyme preference for ALA > LA, because ALA is preferentially converted to DHA and the eicosanoids where LA is left for incorporation into the skin. Having sufficient ALA would mean LA is either incorporated into skin or turned into the small amounts of necessary AA and derived eicosanoids.

"Additionally, linoleate is present in a subgroup of acylceramides, which anchor adjacent bilayers together into multilayers of broad membrane sheets. In essential fatty acid deficiency, oleate replaces linoleate resulting in an abnormal appearance of the extracellular lipid membranes and perturbed permeability barrier function, indicating that essential fatty acids are required for the formation of a normal stratum corneum"
Redirecting (from article)

Detailed look at mechanism for LA incorporation:

Formation and functions of the corneocyte lipid envelope (CLE)
Redirecting

It seems that there is decent chemistry behind how LA is incorporated into the skin, thus demonstrating LA is essential for normal formation of skin tissue. This is recent research, not old stuff that doesn't distinguish between ALA and LA, etc.

Links won't show properly, not going to fix them, but why is everyone on this forum so salty? I mean, if there is something wrong with how I have read things, why not just say so?
 
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Travis

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The first article talks about an experiment from 1953, where ALA was without effect at restoring the water barrier, so it seems . . .

It seems as though you've misread something. The 1953 Thomasson article not determined the evapotranspiration rates or water consumption, but growth under low-water conditions:

'Thomasson developed an assay for EFA activity based on growth on a regime of water restriction and applied it to the comparison of EFA activities of a variety of fats and oils.' ―Holman

The author of the the newer 1984 study you cite had made the assumption that Thomasson's growth index could be equated with water loss. Ostensibly, this derives from the idea that water was the primary growth factor.

'In 1953 Thomasson developed a biological standardization method for measuring essential fatty acid activity of different polyunsaturated fatty acids. In this method, rats were fed a fat-free diet and allowed only restricted water intake. The increase in growth when such rats, still under water restriction, were supplemented with fatty acids was used as a measure of the essential fatty acid activity of the acids. Since an increased water consumption (a classical essential fatty acid-deficiency symptom) is mainly due to an increased trans-epidermal water loss, the method of Thomasson indirectly measured primarily the reestablishment of the water permeability barrier. In this test essential fatty acid-activity was confined mainly to linoleate (18 : 2( n - 6)) and arachidonate (20 : 4(n - 6)) while a-linolenate (18 : 3(n - 3)) was without effect.'' ―Hansen

The sentence is bold is flawed. Thomasson's rats had been under water restriction, and since Hansen had said as much he should've known that 'an increased water consumption' would be impossible. It would appear as though Hansen had merely glanced at the chart below and had assumed it that it reflects water loss when it's actually an index of growth under fixed-water conditions.

thomasson.png


Linoleic, γ-linolenic, and arachidonic acid have a pronounced ability to induce growth. Thomasson's activity index had been normalized to some of the heaviest rats:

'The weight gain produced by 10 mg. linoleic acid was taken as the unit of biological activity.' ―Thomasson

Arachidonic acid has a score 39% higher than linoleic under the Thomasson Biopotency Index. This could have more to do with prostaglandins than with the physicochemical properties of the membrane. Prostaglandin E₂ has a roughly fourfold-increased potency over E₃, and omega−6 fatty acids have been correlated with obesity.


Simopoulos, A.P. "An Increase in the Omega-6/Omega-3 Fatty Acid Ratio Increases the Risk for Obesity." Nutrients (2016)
Thomasson, H. J. "Biological standardization of essential fatty acids (a new method)." Internationale Zeitschrift fur Vitaminforschung (1953)

Holman, R.T. "Biological activities of and requirements for polyunsaturated acids." Progress in the Chemistry of Fats and other Lipids (1971)
Hansen, H.S. "Essential function of linoleic acid esterified in acylglucosylceramide and acylceramide in maintaining the epidermal water permeability barrier. Evidence from feeding studies with oleate, linoleate, arachidonate, columbinate and α-linolenate." Biochimica et Biophysica Acta (BBA)-Lipids and Lipid Metabolism (1985)
 
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Jack Roe

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What about the two other articles, one where oleic acid fails to fix the evaporation problem, but LA does, along with the subsequent article suggesting a chemical mechanism for the incorporation of LA into skin?

"Together, these studies clearly demonstrate that oxidation of the omega-esterified linoleic acid moiety is a prerequisite for CLE formation"
Redirecting (from the article)
 

Kartoffel

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At least one study disproves that by feeding that rats extra B-vitamins, but there could have been more. Something also overlooked by Ray Peat had been the 50% increase in water consumption in 'essential fatty acid-deficient' rats. Since the degree of unsaturation on a cell's membrane is correlated with water affinity and permeability, I am convinced the scaly dermatitis had essentially been 'dry skin.'

I don't think he overlooked that. He mentioned it several times, and it is perfectly in line with his argument that EFA deficiency greatly increases the metabolic rate. If you have a higher metabolic rate, and burn more calories, you evaporate more water.
Peat often refers to this study when he claims that providing vitamin B6 cured EFA deficiency.

"When researchers at the Clayton Foundation Biochemical Institute at the University of Texas demonstrated that “Burr’s disease” was actually a vitamin B6 deficiency, rather than a fatty acid deficiency, the issue was settled"
Unfortunately, it seems that no one has been able to find this particular paper. Peat doesn't provide a reference in his article, and when I asked him for it personally a few years ago, he said he didn't have a copy. Maybe I'll ask him again, if he can at least provide the full title of the study. Vitamin B6 seems to be important for the production of Mead Acid, and rats on a very low EFA diet have much higher levels of 20:3n9 when they receive B6. Vitamin B6 also prevents growth retardation.

upload_2018-8-2_13-48-38.png


Interaction between vitamin B6 deficiency and low EFA dietary intake on kidney phospholipids and PGE2 in the rat. - PubMed - NCBI
 
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Jack Roe

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Once Ray Peat warned me about molybdenum in one of his emails. So he basically suggested to avoid food sources of it. I will try to find his email if anyone is interested.

I would be interested, tho I am betting he has some random study suggesting it does something bad for the thyroid and, therefore, it's bad, sort of like omega6.
 
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Jack Roe

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I don't think he overlooked that. He mentioned it several times, and it is perfectly in line with his argument that EFA deficiency greatly increases the metabolic rate. If you have a higher metabolic rate, and burn more calories, you evaporate more water.
Peat often refers to this study when he claims that providing vitamin B6 cured EFA deficiency.

"When researchers at the Clayton Foundation Biochemical Institute at the University of Texas demonstrated that “Burr’s disease” was actually a vitamin B6 deficiency, rather than a fatty acid deficiency, the issue was settled"
Unfortunately, it seems that no one has been able to find this particular paper. Peat doesn't provide a reference in his article, and when I asked him for it personally a few years ago, he said he didn't have a copy. Maybe I'll ask him again, if he can at least provide the full title of the study. Vitamin B6 seems to be important for the production of Mead Acid, and rats on a very low EFA diet have much higher levels of 20:3n9 when they receive B6. Vitamin B6 also prevents growth retardation.

View attachment 10153

Interaction between vitamin B6 deficiency and low EFA dietary intake on kidney phospholipids and PGE2 in the rat. - PubMed - NCBI

Even if they did find it, I've looked at a couple of his historical papers he cites, and he sort of reads them to suggest what he wants, without taking into consideration that the papers themselves include the downsides. If he believed what he says, it would be really easy, as I said, for him to subsist on protein powder, water, sugar, vitamins and minerals. But the really strange thing is that he doesn't seem to think a natural diet is possible, he seems to think people need exogenous hormones, thyroid, etc. Humans are not obligate carnivores that eat a few throats every once in a while.

Has anyone put this to bed by trying Ray's diet using vitamin and mineral supplements, whey protein isolate and refined sugar? If he's right, one should be able to live just fine on that. What I find most strange about all of his advice, is that he is cagey---he'll say what not to do, "AVOID PUFA!!" but he really doesn't give much good advice about what to do. The idea that genetically healthy people need exogenous steroids/thyroid is absolutely nutty, so unless he is correcting some widespread genetic defect, I think there's enough evidence to say his ideas are wrong, and a good example of the autistic fixation that the University system promotes.

His biography contains this gem,

"A distorted idea of human nature is sold when people are treated as "the market.""

Anyone who was born last century who believes in "human nature" is...well, he might be a decent technician, if he had someone who wasn't crazy supervising him to make sure he didn't get caught in the "human nature" hole. Any talk of "human nature" is about as scientific as talk of our "divine spiritual essence."
 

mangoes

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Has anyone put this to bed by trying Ray's diet using vitamin and mineral supplements, whey protein isolate and refined sugar? If he's right, one should be able to live just fine on that.

Would you mind linking where he recommends subsisting on whey protein, refined sugar and supplements? I’m not even tryna say he didn’t say that but pretty much every supplement I’ve seen him talk about, he’s cautioned about impurities and whatnot and how that can be detrimental.
he is cagey
Guess that depends on how you define cagey. He’s always seemed forthcoming to me and even when I’ve spoken to him privately.
Anyone who was born last century who believes in "human nature" is...
Human nature doesn’t exist?
 

Kartoffel

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Even if they did find it, I've looked at a couple of his historical papers he cites, and he sort of reads them to suggest what he wants, without taking into consideration that the papers themselves include the downsides. If he believed what he says, it would be really easy, as I said, for him to subsist on protein powder, water, sugar, vitamins and minerals. But the really strange thing is that he doesn't seem to think a natural diet is possible, he seems to think people need exogenous hormones, thyroid, etc. Humans are not obligate carnivores that eat a few throats every once in a while.

Has anyone put this to bed by trying Ray's diet using vitamin and mineral supplements, whey protein isolate and refined sugar? If he's right, one should be able to live just fine on that. What I find most strange about all of his advice, is that he is cagey---he'll say what not to do, "AVOID PUFA!!" but he really doesn't give much good advice about what to do. The idea that genetically healthy people need exogenous steroids/thyroid is absolutely nutty, so unless he is correcting some widespread genetic defect, I think there's enough evidence to say his ideas are wrong, and a good example of the autistic fixation that the University system promotes.

His biography contains this gem,

"A distorted idea of human nature is sold when people are treated as "the market.""

Anyone who was born last century who believes in "human nature" is...well, he might be a decent technician, if he had someone who wasn't crazy supervising him to make sure he didn't get caught in the "human nature" hole. Any talk of "human nature" is about as scientific as talk of our "divine spiritual essence."

I'm sorry but it seems to me that you don't really understand Peat, at all. To be honest, I can't believe that you have paid attention to anything he says. What you say about him rejecting natural diets, and suggesting that he advocates a synthetic diet with many obligatory supplements is just so wrong. He always stresses that natural foods are best, and that supplements are best avoided. What makes you think that he believes that a natural diet is not possible? Just because he refuses to accept that PUFA have been shown to be essential, doesn't mean that he promotes a diet of pills and powders. He said many times that this isn't a practical debate anyways since creating an EFA deficiency is impossbile outside of a laboratory.
Just because he makes an effort to show how certain supplements can be used for people with diseases or deficiencies doesn't mean that argues in favor of synthetic diets. Please go back and try to understand his work/philosphy again, because the only thing that appears "absolutely nutty" is your perception of him. What you call cagey is just his realization that the world doesn't need another guru that tells a bunch of morons what exactely they should eat and do.

"The attempt to steer a person can make it hard for them to move, because it inactivates their own guidance system." Ray Peat​
 
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J

Jack Roe

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I'm sorry but it seems to me that you don't really understand Peat, at all. To be honest, I can't believe that you have paid attention to anything he says. What you say about him rejecting natural diets, and suggesting that he advocates a synthetic diet with many obligatory supplements is just so wrong. He always stresses that natural foods are best, and that supplements are best avoided. What makes you think that he believes that a natural diet is not possible? Just because he refuses to accept that PUFA have been shown to be essential, doesn't mean that he promotes a diet of pills and powders. He said many times that this isn't a practical debate anyways since creating an EFA deficiency is impossbile outside of a laboratory.
Just because he makes an effort to show how certain supplements can be used for people with diseases or deficiencies doesn't mean that argues in favor of synthetic diets. Please go back and try to understand his work/philosphy again, because the only thing that appears "absolutely nutty" is your perception of him. What you call cagey is just his realization that the world doesn't need another guru that tells a bunch of morons what exactely they should eat and do.

"The attempt to steer a person can make it hard for them to move, because it inactivates their own guidance system." Ray Peat​

I didn't say he promotes this, but if he knows what people should eat, in terms of a collection of single substances: amino acids, glucose, vitamins and minerals should cover every essential substance, according to Peat. There's no need for fats, because there are no essential fats, not even saturated fat is necessary in his opinion, because his view is certainly not that saturated fat is necessary but unsaturated fat isn't, his view is that fat is unnecessary. Further, the body can manufacture fat from glucose.

Presume Peat is wrong, and that PUFA are necessary, albeit in quantities far lower than most people consume. This would mean that his advice would never work properly, except by accident, that is, if someone ended up accidentally consuming enough PUFA but ascribing it to, for example, eating enough liver or oysters or whatever.

What he does say several times over is that a fat-free diet is possible. Blaming trace impurities in supplements, refined protein isolates, etc. seems weird when he says the evidence that a fat free diet is possible is studies using either rodents and purified vitamins and minerals, or humans and purified vitamins and minerals.

His work seems predicated of a view he adopted early on in his career, perhaps before sensitive analytical equipment had characterized just how, for example, LA is incorporated into the skin. His diet of natural foods, containing oysters, liver, etc. is not going to be PUFA free.

His view that vigorous exercise is to be avoided would have been impossible in hunter-gatherer society or in working-class society, tho it is possible if you subsist on doing consultations, selling patented things, etc. People coming to him are going to be having some problem, more than likely, people don't tend to alter their diet if what they're doing is working.

He doesn't even suggest "diet is not really a solved problem, we have no idea about it," he says that for nearly a century now it has been _known_ that fat free diets are healthy, but he has a conspiracy theory for why this view is not accepted. His view is also not that there are minerals and vitamins which are essential that are not declared essential, his entire view is basically that the Institute of Medicine recommendations are correct, with the exception of their declaration of LA and ALA as essential fatty acids.

I am not saying he recommends eating protein isolate, vitamins, minerals and sugar, but there's nothing he says that would explain why this shouldn't work, as long as you got sufficient extra B6 and Zinc to make up for the "increased metabolism."

"The attempt to steer a person can make it hard for them to move, because it inactivates their own guidance system." Ray Peat

So, what, is he telling people PUFA is unnecessary to make them unhealthy, to motivate them to take more interest in their health? And if we talk about guidance systems, the majority of people's guidance system tells them it's fine to have a curry made with vegetable oil, it's fine to eat a salad with some mayo. So they're all wrong? I know loads of healthy people who eat, as I say, pretty much whatever, people tend to go to diets and "advice" because they have some sort of problem, that is, their guidance system has put them down a blind alley and they need help getting back on track.

One would think that if Peat had solved the problem of diet, it would be trivial for him to put out a "30 day Calendar" of meals that one could repeat ad infinitum. I've read his internet works, none of them say what to do, they all say "avoid LA and ALA" and then offer vague advice about a handful of things that would never amount to a sufficient diet mineral wise, let alone EFA wise.
 

charlie

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