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
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