Why is the epidemiological literature overwhelmingly in favor of PUFAs?
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Thanks for sharing your thoughts. From what I gather, you seem to agree with me on healthy user bias being the main reason for the association.
"The healthy user effect is best described as the propensity for patients who receive one preventive therapy to also seek other preventive services or partake in other healthy behaviors.18 Patients who choose to receive preventive therapy may exercise more, eat a healthier diet, wear a seatbelt when they drive, and avoid tobacco. As a result, an observational study evaluating the effect of a preventive therapy (e.g., statin therapy) on a related outcome (e.g., myocardial infarction) without adjusting for other related preventive behaviors (e.g., healthy diet or exercise) will tend to overstate the effect of the preventive therapy under study. The healthy user effect has been widely cited as a likely source of bias in observational studies of HRT. Studies indicate that women who took HRT were more likely to engage in healthy behaviors such as regular exercise, a healthy diet, abstinence from alcohol, and maintenance of a healthy weight as compared to non-users.2 The apparent protective effect of HRT on cardiovascular disease likely reflects these unmeasured differences in patient characteristics."
In this case, the "preventive therapy" would be eating more PUFAs.
Underreporting alcohol and energy intake could be thought of as an extension of healthy (or in this case unhealthy) user bias
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Based on the two studies you posted that I don't consider "real life", they analyze fat consumption and the occurrence of diseases and draw a conclusion, with absolutely no information other than the type of fat (one of them is based on a questionnaire that the person has to answer, it's not even a follow-up). Did they have any nutritional deficiencies? What was their calorie intake like? Did they exercise? What kind of exercise? Did they sunbathe? How was their social life like? Was work stressful? After that you have studies linking the consumption of PUFAs to a reduction in some marker that they say causes/increases such a disease, like cholesterol, and based on this isolated marker they conclude that PUFA is good, you see this quite often when it comes to omega 6, that's why there's this emphasis on the balance between omega 3 and omega 6 because then the problem isn't omega 6 but the omega3:omega6 ratio...
It's very difficult to have a human study comparing a deficiency of essential fatty acids with a replete of essential fatty acids. The "essential" status makes it unethical to carry out such an experiment on humans, which is another reason why most of them are based on rats, even in super-artificial environments, and in these cases the indication of the relationship between PUFAs and inflammation becomes clearer because you have studies of the resistance of these "EFA-deficient" mice that are practically immune to autoimmune diseases such as type 1 diabetes, glomerulonephritis, resistant to inflammation, endotoxin, etc. ..
In "real life" we can only look for very detailed studies or examples (such as Israel and its high consumption of PUFAs vs. Okinawa before 2000s consuming 4.8g PUFA/day, or Japan consuming around 6g PUFA/day, Tokelau before seed oils/PUFA).
But that's my opinion, of course.
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https://www.bmj.com/content/346/bmj.e8707
https://www.bmj.com/content/353/bmj.i1246
https://pubmed.ncbi.nlm.nih.gov/4100347/
https://www.sciencedaily.com/releases/2020/01/200117080827.htm
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2640413/
https://lipidworld.biomedcentral.com/articles/10.1186/s12944-020-01256-0
https://pubmed.ncbi.nlm.nih.gov/21256145/
https://www.sciencedaily.com/releases/2017/12/171207141624.htm
https://pubmed.ncbi.nlm.nih.gov/18710653/?dopt=AbstractPlus
https://pubmed.ncbi.nlm.nih.gov/20172549/?dopt=AbstractPlus
https://pubmed.ncbi.nlm.nih.gov/18029129/
https://pubmed.ncbi.nlm.nih.gov/12398924/
https://pubmed.ncbi.nlm.nih.gov/8640909/
https://pubmed.ncbi.nlm.nih.gov/17656037/
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Researchers obviously control for relevant variables such as energy intake, socioeconomic status etc. What reason is there to believe work stress or social life would significantly differ between thosa at low vs high PUFA intake?
I agree that looking at biomarkers such as cholesterol is not a reliable way of assessing a persons health. But studies looking at hard outcomes paint the same picture in favor of PUFA.
Ray Peat was against both omega 3 and 6...
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Are high omega-6 seed oil good?
Even Chat GPT considers MUFA-rich fats better for cooking than omega-6 rich fats such as soy oil or sunflower oil. I think the recent scientific consensus is not in favor of high PUFA seed oils, at least not according to Chat GPT.Omega-3/omega-6 balance
The reason they point out is that omega-6 should be balanced out with omega-3. I think this is a valid concern TBH. Ray Peat never admitted that. But I think he never found out the problems of too much omega-6, as he always drank milk, containing omega-3.My girlfriend and I eat basically the same diet. Except that I eat diary and she can not tolerate it. She will get eczema from too much chicken, while I won't. If she supplements krill oil the eczema goes away.
So how much total PUFA is best?
Now if you avoid high omega-6 food, you need very little total PUFA too balance it out. Dairy/beef/lamb are already in perfect balance. So even according to mainstream science, you won't need to supplement fish oil or whatever.I talked a bit with Chat GPT and he buys parts of the Ray Peat theory that high PUFA might decrease lifespan:
"Omega-3 fatty acids, found abundantly in fish, are polyunsaturated, meaning they contain multiple double bonds in their chemical structure. This makes them more susceptible to oxidation, a process that can produce reactive oxygen species (ROS) and lead to oxidative stress within cells, including damage to mitochondrial DNA (mtDNA). There's a hypothesis suggesting that species with a higher proportion of saturated fats (which have no double bonds) in their cell membranes may experience less oxidative damage, potentially contributing to increased longevity.
The concern is that a high intake of polyunsaturated fats (PUFAs), by increasing the double bond index, could theoretically increase susceptibility to oxidative damage, affecting cellular aging and potentially impacting longevity across species. This is because PUFAs, including those from omega-3 rich fish, when oxidized, can harm cellular components, including mtDNA.
Despite the theoretical concerns about oxidative stress and longevity, omega-3 fatty acids from fish are well-documented to offer significant health benefits. These include reducing the risk of heart disease, supporting brain health, and providing anti-inflammatory effects. These benefits are largely attributed to their ability to improve lipid profiles, decrease blood pressure, and modulate inflammatory responses.
A key aspect of consuming omega-3 rich foods like fish is to balance the dietary intake of omega-6 and omega-3 fatty acids. Many diets are disproportionately high in omega-6 fatty acids, which can promote inflammation when not balanced by adequate omega-3 intake. Consuming fish 2-3 times a week can help achieve a healthier omega-6/omega-3 ratio, reducing the risk of chronic diseases and supporting overall health.
While omega-3 fatty acids are essential and beneficial, the principle of moderation applies. Consuming fish within recommended amounts (2-3 times a week) is advised to garner the health benefits without the potential risks associated with high levels of PUFAs. This approach ensures adequate intake of omega-3s to balance out omega-6 fatty acids, without necessarily exceeding what is needed for health benefits."
So if too much PUFA is bad, should we eat MUFA or SFA?"
So I think the mainstream science converged slowly to,
"Don't eat too much PUFA seed oils, but use MUFA (olive oil) instead."
Milk is quite high in MUFA as well. And Ray Peat said in some interviews that the main fats in your diet should be some balance between stearic acid, palmitic acid and oleic acid.Personally, I think MUFA can be in some cases more beneficial for treating acute inflammation problems than SFA. But SFA boosts your sex hormones much more. I can imagine that some studies found that health improves by avoiding SFA, but keeping avoiding it will make sure you never reach the next level of health IMO, which is low inflammation + awesome hormones.
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You'd be surprised by the lack of control in studies, sometimes of variables that have a major influence.
"What reason is there to believe work stress or social life would significantly differ between thosa at low vs high PUFA intake?"
The problem is not believing that it differs, the problem is that a study that seeks to elucidate the susceptibility of a group to diseases that only looks at the type of fat is a joke lol. Since one of the biggest contributors to disease and inflammation is chronic stress, and you're analyzing the susceptibility of certain groups to disease, it's a pretty important reason to consider.
There is no "Japan Paradox" due to low consumption of PUFA(at least in the past), there is no "Tokelaun paradox" due to the very high consumption of saturated fat in the past, but there is an "Israeli paradox" and their high consumption of vegetable oils and high incidence of diseases.
"Vascular disease is uncommon in both populations and there is no evidence of the high saturated fat intake having a harmful effect in these populations."
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@Kasper
Is there a reason to believe stress levels would be higher among people consuming less PUFAs? Because that's what you're implying here.If you have a large enough sample, there's no reason to assume stress levels would be significantly different between those at low vs high intakes of PUFA, thus it's pointless to account for chronic stress in such an analysis. The point of these studies is precisely to isolate the effect of PUFA specifically on health outcomes.
Ecological studies like the Israeli or Japanese ones are arguably far more confounded and less relevant than the meta analysis I posted. Is it the lack of PUFA that made Tokelauans healthy or the myriad of other factors that distinguishes them from the average westerner?
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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.
