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by KempyKolibri 588 days ago
I read those papers and I don’t see any compelling evidence anywhere in there that n6s are toxic. The first one is just discussing burn patients and yes, we consume more n6s than we used to. But that’s not evidence of toxicity.

The COVID one is disappointing. I was expecting a longitudinal study where they perhaps hadn’t adjusted for confounding variables like obesity, etc. Unfortunately, the reality is far worse.

The only human outcome data they seem to have is a cross-sectional analysis where (as far as I can tell, correct me if I’m wrong) they just looked at gross consumption at a national level of different FA types, then saw if there was an association with COVID mortality. This is an insane way to test the hypothesis “consumption of n6 increases Covid mortality.” It just isn’t evidence at all.

I would take evidence to be something that is expected on a given hypothesis and not the negation of that hypothesis. For example, “we see the sun rise in the sky” is not evidence supporting the hypothesis “the sun orbits the earth”, because it would also be expected on the negation of that hypothesis, for example under another hypothesis: “the earth orbits the sun”.

In this case, we can think of any number of hypotheses that negate the hypothesis “n6 consumption increases covid mortality”. For example, “n6 consumption proxies for junk food consumption and population obesity, which increases COVID mortality.” The outcomes of the study are equally expected on both hypotheses. The outcomes they’re seeing could be explained by this alternate hypothesis, for all we know.

Fundamentally, though, there’s actually a much bigger issue here - the data are just cross-sectional. We have no idea if the increased COVID mortality is even taking place in the people that consumed more UFA - the data just don’t tell us!

This leads to an awkward bullet-bite one has to make in order to make a causal inference from data like these: you would also have to affirm that smoking increases lifespan. Unadjusted cross-sectional data shows that countries with greater cigarette consumption have longer lifespan (http://web.archive.org/web/20220325085356/http://www.thefunc...). Now, clearly this is not because of the beneficial effects of smoking. Perhaps it’s because more cigarette consumption occurs in those countries that are wealthier. The point is, cross sectional data is unsuitable for making causal inferences like this.

The rest is just mechanistic speculation and animal studies, not something that can be extrapolated to human outcomes (more about why later). So the study doesn’t actually show any negative health outcomes in humans from n6 consumption.

The next study is literally a study of cheetahs. Might be of interest if you’re a cheetah, or deciding on your pet cheetah’s diet. But we’re talking about human health here.

And then the final paper suffers from the issue of earlier one - trying to make a causal inference based on cross-sectional data. We have zero idea if the individuals suffering from SAP are even the ones consuming more n6s. Again, if we are to find this convincing evidence of n6 toxicity then we also have to grant that cigarette consumption increases lifespan.

A commonality in these studies is that they try to back up the cross sectional data with animal modelling and in vitro studies, but we have to bear in mind that the best data we have on translation of animal studies to human outcomes suggests the success rate is atrocious. The confidence interval for toxicity studies in animal studies translating to human outcomes includes .5, so you may well be better off tossing a coin than you are relying on animal studies to make inferences about human health outcomes: https://translational-medicine.biomedcentral.com/articles/10...

To sum up, this seems to be a collection of data from the lower end of the evidence hierarchy, none of which is even in the category of data suitable to provide information about what is healthful or harmful to humans. I don’t see why we would find this convincing evidence of n6 toxicity on its own, even before we get into all the much higher quality evidence pointing to benefits from n6 consumption.

1 comments

    (1996) "Excessive signaling of arachidonic acid (AA) metabolites has been associated with various chronic degenerative or autoimmune diseases, and intervention with the metabolism of AA is widely employed therapeutically in these afflictions. In essence, AA is the most biologically active unsaturated fatty acid in higher animals. Its concentration in membranes and its magnitude of effects depend on its amount, or that of its precursors and analogues, in the diet. The tendency of the field of nutrition to ignore the role of dietary AA will optimistically be reversed in the future." The article also said, "The underlying rationale for this symposium is that dietary AA is perhaps the single most important nutritional determinant in regulating AA levels in Americans. This may ultimately account in part for the striking differences in chronic diseases between strict vegetarians and the bulk of the omnivorous population." https://pubmed.ncbi.nlm.nih.gov/8642436/
Both animals and humans have endocannabinoid systems that operate identically in terms of physiological outcomes. Consequently, excessive arachidonic acid in cell membranes has pathologically consequences. https://johnditragliamd.substack.com/p/the-other-fat-science
As I said, happy to move onto AA once we’ve closed off the n3:n6 ratio thing. So do you have any evidence that the ratio is an issue in humans, or do you concede there’s no such evidence currently?