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davebrown10 | 1 year ago
Vijay p. Singh says, "Separately, on analyzing global COVID-19 mortality data and comparing it with 12 risk factors for mortality, they found unsaturated fat intake to be associated with increased mortality. This was based on the dietary fat patterns of 61 countries in the United Nations' Food and Agricultural Organization database. Surprisingly, they found saturated fats to be protective."https://www.medpagetoday.com/reading-room/aga/lower-gi/86940
It's interesting that fasting and exercise furnish some protection from excessive polyunsaturated fatty acid intake. For example, "The increased proportional intake of dietary fat, decrease in feeding frequency and increased physical activity in free-ranging compared to captive cheetahs are all predicted to result in enhanced mitochondrial FA oxidation through the lowering of circulating glucose concentrations and insulin:glucagon ratios. During fasting/refeeding cycles and increased levels of exercise, tissue PUFA concentrations have been shown to deplete rapidly in both humans and rats. These studies show that most PUFAs, including α-linolenic acid (ALA) and linoleic acid (LA), are preferentially oxidized in periods of exercise or fasting. During refeeding, SFAs and monounsaturated fatty acids (MUFAs), such as palmitic acid and oleic acid, are also more rapidly replaced than any of the PUFAs. Similarly, the concentrations of most plasma PUFAs and MUFAs have been shown to be significantly lower in rats fed a high fat ketogenic diet than in controls. The predicted increase in FA oxidation in free-ranging cheetahs is therefore likely to also skew their serum FA profiles toward lower proportional serum concentrations of PUFAs and MUFAs relative to SFA." https://pmc.ncbi.nlm.nih.gov/articles/PMC5167222/
In the final analysis, dietary saturated fats are benign, if not outright beneficial over a wide range of intakes as long as they are consumed in the context of healthy nutrient configuration as in whole foods. https://pmc.ncbi.nlm.nih.gov/articles/PMC7846167/
KempyKolibri|1 year ago
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.
davebrown10|1 year ago