Why is the epidemiological literature overwhelmingly in favor of PUFAs?
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@Vapid-Bobcat I'm not implying that.
There can be so many other confounding factors that are not taken into account. I mean, just if you look around, who eats high SFA and who eats PUFA?
Well, from my friends, a lot of them who are overweight are binging cheap cheeses and cheap processed (smoked) meats with all kinds of conservatives together with a good amount of wine.
Do I feel like shit if I eat those processed meats and cheeses? Yes.
Do I think they are healthy? No.I mean certainly those people are having a lot of problems and I don't think the saturated fats is going to protect them from everything.
They would do much better if they incorporate more plant foods in their diet. Such as fresh organic tropical fruits and fruit juices.
But TBH, there microbiome is probably so out of balance, that they need something extra such as carrots and apples. To change their microbiome for the better, and high sugar fruits could even mess them up.
Now is their microbiome and metabolism going to become better from switching from high SFA to high PUFA fake vegan cheeses full of conservatives as well. Well, that is the point Ray Peat is trying to make. It is not.
There is no study that you showed, with an intervention, where they kept the diet EXACTLY the same, but they only switched the content of the fat. That is the only way to show that.
The reason correlation is not considered causation is that you can never confound for all variables. Here are some confounding variables:
- High SFA could be correlated with conservatives
- High SFA is probably correlated with fast food
- High SFA might be correlated with "I don't give a shit about my health" kind of mentality
- High SFA might be correlated with low carb diets, high fat, high protein diets.
- High SFA is probably correlated with high methionine intake (with Ray Peat warned about and why he recommends oxtails and lamb shank over muscle meats)
Etc. etc.
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What you're describing is basically the same as what is called the "healthy user bias", where healthy behaviours or behaviours that are socially percieved as healthy tend to associate to each other, and the same happens with unhealthy behaviours. I agree it is probably the only explanation for the positive results of PUFA in obseravtional studies.
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@Vapid-Bobcat said in Why is the epidemiological literature overwhelmingly in favor of PUFAs?:
In pretty much every retrospective, cohort study or RCT I happen to take a look at, higher PUFA consumption, especially linoleic acid, almost always leads to better outcomes than lower PUFA consumption.
@Vapid-Bobcat I suspect that there are ulterior motives. But then, I've become pretty cynical.
Sometimes animal research performed for the preservation of an industry (and making $) provides better designed studies and interesting results that can be extrapolated to humans in general ways.
Thiamine Deficiency M74 Developed in Salmon (Salmo salar) Stocks in Two Baltic Sea Areas after the Hatching of Large Year-Classes of Two Clupeid Species—Detected by Fatty Acid Signature Analysis
"Fatty fish that feed on fatty marine prey fish are prone to suffer from thiamine deficiency [1,13] because the requirement for thiamine increases with the increase in the diet’s energy content [14] and because thiamine is depleted as a consequence of lipid peroxidation [14,15,16]."
"In fish with a high tissue concentration of n−3 PUFAs, thiamine can be depleted during the pre-spawning fast so that the eggs do not provide enough thiamine for the yolk-sac fry (free embryos or eleutheroembryos [23]) to develop. Thiamine deficiency, therefore, primarily affects yolk-sac fry [8,24,25], which must survive on yolk nutrients from hatching to the alevin stage, i.e., the stage when the hatched fry start external feeding [23]. As THIAM is a reserve form of thiamine, its concentration of the different thiamine components in eggs varies most, depending on the female’s thiamine status [8]. The thiamine deficiency of the offspring of fish can, therefore, be predicted from the THIAM concentration of the eggs [8,26]. At worst, thiamine deficiency can be seen as weakness and loss of equilibrium in brood fish before spawning, and they may die before spawning [8,27,28,29]."also:
Fatty acid signatures connect thiamine deficiency with the diet of the Atlantic salmon (Salmo salar) feeding in the Baltic Sea
"Thiamine is an essential micronutrient, which has a central role in energy metabolism (Lonsdale 2006) and also a linkage to fatty acid (FA) metabolism. Moreover, thiamine serves as an antioxidant (Lukienko et al. 2000; Gibson and Zhang 2002). Fish need to obtain thiamine from their diet (Niimi et al. 1997), and the requirement for it depends on the energy density of the food (Woodward 1994). As the net energy value of lipids is more than double that of proteins (Kriketos et al. 2000), the need for thiamine largely depends on the lipid content of prey fish."
-end pastes-I think that each of these studies confirm Ray Peat's work regarding fats. The added wrinkle is the connection to thiamine deficiency. Thiamine deficiency is implicated in many of today's chronic diseases, including coronary heart disease, diabetes, and the dementias.
