[davebrown10]

Actually, excessive omega-6 arachidonic acid intake is far more problematic than saturated fats. Dr. Gregor knows about the arachidonic acid problem but doesn't seem to understand it. https://nutritionfacts.org/topics/arachidonic-acid/ Compare what Gregor says to this comment by Norwegian animal science researchers. "Chicken meat is commonly regarded as a healthy type of meat; it is popular, and hence the consumption has increased. Chicken meat is lean, protein-rich and rich also in other important nutrients. However, the fatty acid composition is strongly dependent on the diet fed to the birds. A typical modern poultry diet is rich in cereals having a high ratio between omega-6 and omega-3 fatty acids. This diet is very different from the natural diet for the same species containing more green leaves that are rich in the omega-3 fatty acid alpha-linolenic acid (ALA). It has been shown that a diet rich in ALA gives increased concentrations of ALA, eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA) and docosahexaenoic acid (DHA) in broiler muscle and improved, i.e. reduced ratio between total omega-6 and total omega-3 fatty acids. The utilisation of ALA and linoleic acid (LA) for synthesizing EPA and arachidonic acid (AA) depends on feed concentrations of ALA and LA as well as on other factors. Much AA in the diet may contribute to prostaglandin overproduction in disease situations in humans, but some AA is necessary for virtually every body function. Dietary sources of AA are especially meat, eggs and offal, with smaller amounts coming from milk and fish. https://pmc.ncbi.nlm.nih.gov/articles/PMC2875212/ It's likely that the global increase in obesity and diabetes is largely due to increased consumption of grain-fed monogastrics such as poultry and swine. A 2021 paper by Australian zoologist Anthony Hulbert, PhD entitled 'The under-appreciated fats of life' concludes, "As a final comment, I note that we are only beginning to understand the implications of the balance between omega-3 and omega-6 fats in the human diet. Although most animals have a relatively constant diet, we humans are especially diverse (both between individuals and over time) in the types of food we consume. Over the last half-century, the modern human food chain has emphasised omega-6 and diminished omega-3 intake, largely because of: (i) a shift from animal fats to vegetable oils, (ii) an increase in grain-fed meat and dairy, and (iii) a decline in full-fat dairy products from grass-fed livestock (an important source of omega-3). In the opinion of the current author and others, these diet trends are likely to be responsible for the increased incidence of obesity and other modern epidemics of chronic disease, but that is a story for another time." https://journals.biologists.com/jeb/article/224/8/jeb232538/...

[KempyKolibri]

This is just mechanistic speculation based on animal studies. There is no good evidence that I’m aware of showing harms from high n6 consumption in humans, outside of their contribution to caloric excess.

The n3:n6 ratio was a hypothesis that never panned out. If you look at the studies that “support” it, the “bad ratio” is brought about by reducing n3 levels below sufficiency, not by keeping n3 levels at the RDA or higher and then boosting n6 further.

So it’s no more evidence that n6 is harmful than taking a cohort of people, reducing half of the group’s iron intake to a minuscule amount and claiming that because that group’s “iron:magnesium” ratio is wrong, then consuming more magnesium is clearly harmful. It just doesn’t add up.

[davebrown10]

Actually, there is human research. Below is a message Olaf Adam sent to myself and several others on September 5, 2021.

    I refer to the very readable review by Philip Calder “A systematic review of the effects of increasing arachidonic acid intake on PUFA status, metabolism and health-related outcomes in humans.” His final statement is that an increase in arachidonic acid intake up to 1.5 grams per day does not significantly change the parameters associated with inflammation, blood clotting or atherogenesis. In this very interesting observation, I was astonished by the fact that the background diet was not taken into account. Although the intake of arachidonic acid with the background diet is reported several times, the resulting metabolic consequences are not discussed.
    From the data provided, it can be concluded that the background diet in all studies included in the review was a Western diet, the proportion of arachidonic acid being estimated at 200 to 400 mg per day. Our studies on healthy volunteers were carried out with formula diets and allowed a precisely defined supply of arachidonic acid over a period of 6 weeks. These studies have shown that the exclusion of arachidonic acid from the diet (vegan diet) causes a progressive decrease of this fatty acid from 11 + 3% of the total fatty acids in the cholesterol esters of the plasma to 8 + 2% after 6 weeks. The later studies on patients with rheumatoid arthritis have shown that an intake of arachidonic acid amounting to not more than 80 mg/day does not increase the concentration of arachidonic acid in the phospholipids of the plasma and in the erythrocyte lipids. From these findings I have concluded that the body's own production of arachidonic acid is around 80 mg per day. This means that the Western Diet provides approximately 2.5 to 5 times the estimated need for arachidonic acid.
    This intake that is higher than the requirement primarily has no negative consequences. We know from many studies that the "silent inflammation" characteristic for the prevalent diseases of western societies has a latency period of more than 10 years before the consequences such as arteriosclerosis and myocardial infarction become apparent. The body is evidently able to avert the consequences of an unfavorable diet for a long time. To do this, there are numerous regulatory options, such as substrate or product inhibition in the case of enzymes or the inhibition of transport to or incorporation into cells. Arachidonic acid has a very special metabolic pathway that offers possibilities for regulating absorption from the intestine, transport in the chylomicrons, metabolism via the enzymes involved and also for incorporation into the cells. For example, we have found a completely different efficiency for the uptake of arachidonic acid into the cell membrane for platelets compared to erythrocytes or granulocytes. It is therefore very likely that regulation options on the metabolic pathway of arachidonic acid can, to a certain extent, compensate for changes in intake.
    Only when too much arachidonic acid is present in the food for a prolonged time do these protective mechanisms apparently fail and inflammation and the manifestation of lifestyle diseases is seen. This explains the long latency period with which the diseases of civilization occur. It is documented in the literature that unhealthy supplementation, such as megadoses of vitamin E, has no deleterious effects on health-related outcomes for humans in the short term. Only long-term observations and meta-analyzes have been able to prove the increased overall mortality. These protective functions with which our body is endowed are very important, because our body is often confronted with megadoses of vitamins or other food stuff or unreasonable diets. Otherwise humans would already be extinct.
    In summary, I would like to note that the human metabolism has many opportunities to compensate for unreasonable interventions for a limited time. The studies available so far relate to arachidonic acid intake with the Western Diet. This condition may already have provoked defense mechanisms that delay the occurrence of Western Diet diseases. We all agree that the Western Diet is too meat-based. The studies included in the review gave me the impression that an attempt had been made to further aggravate an already bad situation, present in Western civilizations. The negative result of these studies is reassuring for me, but does not mean that this supplementation has to be harmless and without long-term effects.
    From my point of view, it would have been more productive from the experimental approach if vegans had been given the doses of arachidonic acid employed in the studies that are included in the review. This would come closer to the desired goal of the effects of arachidonic acid on PUFA status, metabolism and health-related outcomes in humans. Then one could also come to a result for the desirable intake of arachidonic acid, which I estimate for patients with inflammatory rheumatic diseases at 80 mg per day, corresponding to 560 mg per week. This corresponds to a diet with 5 vegan days and 2 days with consumption of animal products per week.