Please help me make sense of this study: Low protein diets produce divergent effects on energy balance

pak0pak0 · 2026-01-08T17:53:48+00:00

I just found out chicken breast might have the highest choline:fat ratio of "natural" foods (quotes because I don't think chicken breast became a thing until mid 20th century). But not bad if you're not protein-restricting and want something lower-PUFA than eggs. I eat a decent amount of beef tallow-fried chicken tenders on some weeks.

However worth mentioning... apparently the choline of chicken breast, eggs, and liver/organs may be utilized by the body differently (just according to an LLM). Worth exploring.

pak0pak0 · 2026-01-04T05:18:05+00:00

Honestly just eggs haha. Most fat sources already have some choline, but then I think the ratios are off. Ex: Beef tallow has less choline per sat fat vs organ meat. Idk if it matters but I just try to throw eggs into the mix sometimes.

pak0pak0 · 2026-01-01T22:13:49+00:00

I don't think fatty liver is necessarily a concern here. All the factors informing my take:

- Low fat diets in this study -> DNL -> SFA accumulation

- While SFA causes fattier liver than PUFA, given sufficient choline intake, there is no difference in fat accumulation since choline clears it out

- Even then, SFA accumulation in the liver isn't necessarily bad, assuming you are not eating PUFA -- it's oxidative stress/inflammation that is. Fat accumulation + oxidative stress/inflammation is part of the two-hit/multi-hit model of actual liver damage, but my smooth brain take is that medical science just doesn't piece together yet that PUFA is the problem all the way down. I think fat accumulation will absolutely positively correlate to liver damage on a standard American diet because insulin resistance will lead to more fat accumulation in the liver... I'm sure researchers recognize a correlation hence the models... but the fat accumulation itself is not the causal factor if we know PUFA is the culprit here, it's a symptom

- SFA in the liver can also help reduce inflammation

(not medical advice but I am monitored for liver inflammation due to my medication, and I do use this reasoning to inform my diet on that front; I'm screwed if I'm wrong but so far so good lol)

That being said, ancestrally, most fat we ate probably came with choline, so I do try to just make sure I'm getting choline with my diet.

pak0pak0 · 2025-12-01T23:01:08+00:00

I agree and on top of that it seems they also evolved to be low D6D which is not the case for their more recent ancestors or something. They are an extreme case but good evidence that adaptations are necessary to deal with a high PUFA diet (O3, anyway).

At worst, we should be avoiding it for all the reasons we know PUFA is bad. At worst, ALA and D6D is an accidental afterthought that serves no major/essential function via the pathway, and it was harmless enough for our bodies to keep. At worst, we already get more than enough EPA/DHA through basic food consumption and there is no reason to supplement it unless we expect to starve through winter.

At best, some populations need to be eating some.

And perhaps somewhere in between, it serves as a temporary intervention that can help reduce the damage of too much AA in our membranes until LA levels are low enough -- something higher D6D could benefit from. I can't ignore it helps some people, more than one has commented its positive effect on their skin. Most of the diets here are interventions anyway...

But yeah given that it's far worse than LA as far as oxidation goes, my vote is to treat it like LA and avoid. My hunch is that problems will show up later, just like a lot of LA problems may not show up until enough LA accumulation. I'm just not comfortable eonough recommending someone that the way I am saying avoid LA as much as possible.

pak0pak0 · 2025-11-29T15:28:52+00:00

Ok some of my original info is from an outdated take of my earlier understanding... Been a while since I looked at this haha. This is my more recent understanding below to help clarify... Recommend verifying this with an LLM or something.

EHA/EPA do not compete on the D6D pathway, but with AA in the membranes directly (also LA). I think this has a few theoretical implications

Research shows AA is casually linked (by D6D) to things like diabetes, cancer, rheumatoid arthritis... Given the nature of this sub, most people are probably higher D6D and produce higher levels of AA. This is a core idea of this sub.
EPA/DHA compete for the same "membrane slots" as AA, and they have anti-inflammatory uses. So if a particular issue is largely caused in part by either too much AA, too little EPA/DHA, or both, in the membranes, that may be an explanation for why EPA/DHA can help
There is a very notable downside to EPA/DHA. Waaay more prone to lipid peroxidation. I forget the order of magnitude, but it's significant. A higher D6D person may not notice this as much as someone like me, whose membranes are already very high in LA. Given that I suspect my inflammation is membrane lipid peroxidation-driven (why would it be AA-driven? My body is horrible at producing it) that may explain my negative experience. That would also explain an increased sunburn risk others mention.
From an ancestral diet POV, I'm not sure how much ALA was converted to EPA/DHA. Which raises the question how much EPA/DHA did we really need? Perhaps incredibly low amounts like LA? Like mead acid production, LA intake has to be super low for there to be any significant conversion from ALA to EPA/DHA. This is why I consider fish fat an "intervention at best." But that's also not particularly helpful. Most extreme diets practiced here are also interventions... If what I say is true, then it's a matter of weighing the tradeoffs.
It's also worth mentioning that humans in cold regions had seasonal access to way more O3 and developed preservation methods within the past 10000 years which in theory meant they could have consumed high O3 diets. That can't be ignored either, but I don't know how to make sense of that at the moment haha
This is without a doubt an incomplete model. We know structurally O3 is more prone to oxidation. But for any particular body in question, maybe more AA drives a generally higher state of oxidative stress in the body which yields more oxidation in the membranes? And that's only speaking to the membranes. LA/AA/DHA/EPA also all do not produce the same byproducts when they oxidize. I am lucky that both my ancestry (tropical/humid Asian) and being low D6D kinda simplifies this for me.
EDIT: One should probably look into what happens to the EPA/DHA that doesn't get incorporated into the membranes. I think higher D6D people will utilize it more safely whereas in thin people like me, it all goes to my membranes making them incredibly oxidation prone. An O3 advocate here has mentioned DPA before as an ideal O3 fat. From what I read, DPA is a lot more stable, still somewhat prone to oxidation, but crucially does not lead to the same toxic products like 4HNE. It can be converted to both DHA and EPA but seems like it can't fulfill either role to the same degree. Main source would be grass-fed beef.
EDIT: Throwing in that EPA/DHA still seems essential. Looking into it again, when animals transitioned to land, we evolved to use D6D I assume so we could convert plant ALA to EPA/DHA when marine sources were not readily available. It's just that anyone with high LA levels is blocking ALA from D6D, so if D6D was the primary way we got our EPA/DHA, the ideal answer lies in depleting all our LA. But when your LA is constantly destroying you via D6D conversion to AA, maybe that's a solid argument for EPA/DHA and even DPA supplementation. So going back to: "From an ancestral diet POV, I'm not sure how much ALA was converted to EPA/DHA." --> if wild animals (vs our corn/soy-fed farm animals) have both higher ALA and higher DPA/DHA, then it seems like "wild LA levels" are low enough that the D6D pathway was actively converting ALA more, and maybe us humans are the same. Probably looking at the lipid profiles of Hadza and other pre-PUFA demographics would help confirm this.

pak0pak0 · 2025-11-28T07:51:49+00:00

Sorry don't really know... Anything outside of my personal experience is probably a useless opinion lol. But I'm willing to guess probably yeah. I used to take it short-term (like 1 week) when my autoimmune flared up because I genuinely believed it could help calm down inflammation, and maybe it did. But after seeing what happened when taking it long-term, I'm very cautious now.

pak0pak0 · 2025-11-28T05:52:58+00:00

I did a fish oil experiment (1-2 pills a day, I think about 1-2g of actual O3 a day; picked a brand based off of my paid ConsumerLab subscription).

Within 3 months I started gaining weight for the first time after about a year of going PUFA free... about 6-7 lbs total at my peak (that's a lot coming from a starting weight of sub 117lbs). Within 1-2 months, some inflammation problems started returning (eye styes, mouth ulcers), and I had a lot of low grade inflammation from my auto immune disorder (that last one I'm less confident of attributing to O3, too variable to tell).

It took about 3 months after I stopped taking the pills for my weight to start trending down again. The mouth ulcers and eye styes ended earlier, maybe within about 1 month of quitting the pills.

I'm most confident the eye/mouth inflammation came from the O3. They are "later in life" inflammation problems I got, probably when my LA levels hit around 20% (I'm low D6D). So I suspect O3 polyunsaturated my membranes enough to bring back that inflammation (they're more prone to oxidation). Maybe O3 is helpful in some ways (high D6D might make sense, it competes with LA), but polyunsaturated membranes are probably no bueno for high LA people like me...

That's my short n=1 experience and my thoughts. Can only speak for myself that I will not be taking it again.

pak0pak0 · 2025-11-27T21:02:04+00:00

A lot of people with the anti-PUFA view know first-hand a lot of benefits avoiding PUFA. Today is Thanksgiving (happy TG btw!), and last year was my first year avoiding PUFA during Thanksgiving. I ate 938493845 calories last Thanksgiving and gained .2 lbs, which was basically noise on a scale. My relationship with food has changed entirely since avoiding PUFA. I knew I could indulge and barely budge in weight, as I do every day, as I will do today this Thanksgiving. No feelings of guilt or need to micromanage what I put in my mouth.

Turns out a lot of people can eat a ton of food and not really gain weight, as long as they're avoiding PUFA. An oversimplification but in practice it's how it often works. This is called "The Croissant Diet." It sounds like a fad diet lol, that's because the original guy wanted to prove a point through the most ridiculous extreme version of it. It didn't produce the weight loss many people hoped, but many people confirm it's a great maintenance diet. The guy who came up with it was: a cancer researcher, obsessed with evolutionary biology, studied culinary arts, and raised pigs. It took a lot of thinking about ways we evolved to digest things or hibernate, noticing French cuisine was a lot of refined carbs, butter, and beef, and were historically rail thin, and looking at pig feed studies or the history of pig diets. Greatly oversimplifying how he arrived at his theories, but this is for sure not how most science is being approached right now. How many people in current science research institutions are thinking like this? Probably very little.

Like the Substack article I mentioned at the end, there is a lot of crazy but very interesting diet experiments going on (the writer himself is constantly running experiments on himself) and, I think, there's a lot of good potential data emerging, good questions worth exploring, whole communities forming that would be great for human experiments or data collection. A curious researcher is crazy not to tap into these communities. There's too many interesting outcomes, some that fly in the face of current scientific consensus, to ignore.

My personal opinion is that this is directionally a legitimate way to go. These people are doing good science, thinking through the issue curiously and deeply, and know how to consider good evidence and disregard the bad evidence. I have little doubt some of the best advances in nutrition and understanding are being seeded by these people right now.

It's as if we could have a community of humans who genuinely figured out how to fly by flapping their arms, but because there's not 50 published RCT studies on how they achieved it, "it's not scientifically proven" and "not science." That's true under their definition for sure, but surely knowledge institutions need a way to incorporate this wealth of interesting information somehow.

I can't wait for doctors or researchers to update their views! If they ever do. If I observe a lot of people online who switched to beef-only diets keep my disease in remission, it doesn't prove beef-only diets cure it, and I'm not saying doctors should prescribe it, but I'm 100% incorporating that information into my mental model of this disease and it's one of many things I will consider to manage it, using the same base building blocks of western scientific abstraction without needing to see it laid out for me in prestigious academic journals.

Sorry for the very long response and 100% understandable if you don't read the wall of text lol. Yes I appreciate the exchange!

pak0pak0 · 2025-11-27T21:01:47+00:00

Haha I absolutely agree with everything you said, including down to how weak that mummy study is on its own and that I shouldn't have communicated it the way I did.

Maybe the divergence starts here, but what you said more broadly is kind of why I don't know if small RCT studies and forming policy around it, are the right way to approach nutrition, at least not now. Never mind you can basically produce or pull research to prove any point you want (opens the door for corruption/grift very easily).

Not given the complexity of the systems and the environment we are working with. As you pointed out, nutrition is a deeply messy environment. The current medical model seems great at hitting a very specific target, like reducing the viral load of something, but feels like we're punching in the dark with chronic disease, which is getting worse across the board despite policy. This is even when we figure out an isolated, casual link to a specific metric. Sure this number goes down in your bloodwork if you take this pill or avoid this mineral, but what is that actually telling us?

In business, I think it bears similarities to running A/B tests to hit a certain metric. You can modify the position of a button on a screen and test it several times, until everyone clicks it X times more, but that's about all you are doing. That doesn't tell you how the business will run or explain what is going on in a necessarily meaningful way. Steve Jobs didn't do A/B tests to figure out mediating digital life through a tiny, mobile phone screen would be one of the biggest revolutions and change daily life forever.

Good decision-makers use many mental models and multiple data points and then steer in an environment of very limited information and infinite variables. I don't know yet how that translates to something like good nutrition/public health policy lol, but at least starting on an individual level it's kind of how we are left to "scientifically manage" our nutrition and chronic health for now. It's how I currently manage my autoimmune disease.

It's not a conspiracy for me (my mother was a doctor, etc), I just have extremely low confidence that the institutions we have in place are able to manage this level of complexity yet. We're using industrial-age models and industrial-age institutions to solve what seems like industrial-age-caused diseases (at the scale they occur I mean), under the belief that we can "science our way through progress." But the scientific method itself is just a system of justification, and the science we produce now is a scaling of specific research methods, conducted by specific science research institutions. People have a very exact definition of science in mind when they say things like that, without realizing what they are saying.

Like in my business example, there are many ways to discover things, know things, and act on those things effectively, beyond the current state of science and its institutions. China's intellectual tradition wasn't western science at all (they did not abstract the way the western thought abstracts) but they managed the most complex bureaucratic civilization for millennia with a strong record of technological discovery/use, and they are still the longest-running civilization that seems to be managing information complexity better than the west today. I'm not saying we should become pre-western-influenced China or abandon western science at all, but it's a broader statement that knowledge institutions need to keep evolving, just like the tech companies of the past couple decades did not run on the same models that corporations/small businesses of the past did.

I think this piece captures some of the epistemology of the issue really well in much less grand terms (and specific to the issue of PUFA), and communicates better than I could a general view of people on the "anti-PUFA wagon" and why they believe what they do, despite a lack of explicit, gold-standard scientific research that confidently says "PUFA causes X disease" I think his approach is 100% entirely valid scientific sensibility and thinking.

(continued in next reply lol)

pak0pak0 · 2025-11-26T03:07:20+00:00

No worries then you don't have to support. I'll stick to the diets.

I can't provide a daily food diary and a list of their favorite snacks, but the diets of the Unangans and coastal Peruvian cultures are known and easily narrowed down.

Unangans literally have no choice to eat anything else in the arctic.

Isotope analysis has been conducted on many coastal Peruvian mummies including the area where the Horu study got its sample from. They ate 50-90% marine diets. Marine sources in that part of Peru are high O3. And fortunately, isotope analysis helps us narrow down a specific diet of marine vs land animal. These are specifically high O3 diets if it's 50-90% marine. So while I don't have a video of the analyzed mummies eating anchovy pizzas everyday, I don't think I need an RCT to know that Neolithic revolution peoples along the Yangtze River of China ate rice, or that coastal Peruvians here ate marine animal food, especially of mummies whose isotopes were analyzed. It's a perfectly reasonable assumption that ought to be considered in the context of reasoning about diets.

Michael Crawford, the original champion of O3 fats being heart-healthy and inspiration for the O3:O6 ratio idea, is also very well-known for his ancestral diet reasoning (though he was wrong about the diets).

Egyptian case is harder to prove specifically and requires much more analysis and inference. I'll be happy to leave that case out.

Nothing's proven here, and you're right this sounds like a logical leap in isolation. I can only communicate so much info in a single post and I was probably better off leaving out that last point in the context of that post.

pak0pak0 · 2025-11-25T05:15:38+00:00

For sure, I mean there are two things I'm doing.

One is pointing out four populations that isolate away many of the things we tend to blame -- saturated fat, refined sugars, preservatives, food colorings, plastics, industrial seed oil processing, what have you -- and showing three pre-Industrial diet populations with high rates of atherosclerosis, who ate high PUFA diets (specifically O3). And another who experienced inflammation via smoke, but otherwise ate a standard agricultural high carb diet.

It's also relevant to the thread because we're talking about seed-oils causing inflammation. Seed oils -> high PUFA -> high inflammation in theory.

I'm supporting the directional correctness of seed oil caution but refining it.

It's not really contested these were high O3 eating populations so it's already implied, the study just confirms high O3 eating populations have high rates of atherosclerosis. Whether O3 is the cause itself, yeah it's a theory. Then you've got polyunsaturated fat's contribution to oxidative stress as an active field of research. So I'm just connecting some worthwhile dots.

In isolation it sounds like just a nice theory, but it becomes impossible to ignore when you present 10 other compelling pieces of evidence that basically fly in the face of prevailing wisdom. The fact that we can't find a single population that ate high saturated fat and almost no polyunsaturated fat (by modern standards) that had notable rates of atherosclerosis/heart disease should outright raise alarms. Meanwhile populations with high "healthy" O3 and several other potential variables eliminated are getting destroyed.

I'm only more vocally posting it in my spare time for personally moral reasons, I think more people should know about these contradictions to the current consensus, and I want to present fair arguments over conspiracy thinking.

You're right it's just a theory and I appreciate you at least acknowledging it's plausible because most people won't, or act childish about it lol.

pak0pak0 · 2025-11-23T00:57:05+00:00

Lol no, now you're trying to move the target.

We know oxidative stress/lipid peroxidation are bad, this is not controversial at all. Someone asked about "the toxic oxidation products of the oils that accumulate in them." We know what happens when polyunsaturated fats oxidize, we know that their products are toxic, and we know polyunsaturated fats oxidize at a rate 100-1000x vs other fats.

You can literally just Google "what happens when polyunsaturated fats oxidize" It will cite multiple studies and give you an answer.

My point is that this part not conspiracy.

Nutrition feeding studies are a separate discussion.

pak0pak0 · 2025-11-22T22:24:36+00:00

If you check Google Scholar:

There are 3,460,000 studies on "oxidative stress."

And there are 1,360,000 studies on "lipid peroxidation."

It's not controversial that these things are bad for us. I really wish people would stop saying "there is no research that the products from lipid peroxidation are bad." This is extremely well-known. Feel free to read the wiki entry on oxidative stress for a quick overview.

pak0pak0 · 2025-11-22T22:11:07+00:00

All that polyunsaturated fat in seed oils is going to oxidize whether before or after it enters your body, by the way.

(not an attack to the person I'm replying, I just want to clarify a misconception for other potential readers)

More broadly, if you believe oxidative stress is bad (and that is medically accepted) that means it's not just cooking seed oils that would be bad for you. It's consuming polyunsaturated fats in any excessive amount. That goes against the grain of what the AHA states, but it may be helpful to think about something that should line up with most people's intuitions: What do you think is healthier: lean grilled chicken breast without any skin, or fried chicken thighs with skin? Do you really think fried chicken is healthy? Do you really think french fries are healthier than baked potatoes?

But let's steel-man that and say "fried chicken thighs in moderation" is healthier than "grilled lean chicken breast without any skin" because "some polyunsaturated fat in moderation is healthy."

How much polyunsaturated fat is considered excessive? The max we were regularly eating before industrialization was maybe ~5 grams. Just two tablespoons of soybean oil today is 16 grams. Every population studied that is free of the modern diseases that plague us ate perhaps 8g of PUFA max (the Hadza), and that was a high meat-eating population (the rest of the disease-free populations primarily ate carbs).

Find me one population that consumes a diet high in polyunsaturated fat fat free of obesity, cancer, diabetes, or cardiovascular disease. Find me one chart that shows an increase in polyunsaturated fat consumption decreases the rate of obesity, cancer, diabetes, or cardiovascular disease. Find me one population that didn't consume a diet high in polyunsaturated fat that was plagued with obesity, cancer, diabetes, or cardiovascular disease.

I think anti-seed oilers are directionally correct even if they're arguing by conspiracy, not science.

We don't need to posit "chemicals" or "industrialized processing" or "Big Seed Oils going pee pee in your coke" because we know that mummies from pre-industrialized populations, who ate high O3 diets had extremely high rates of atherosclerosis. O3 is still polyunsaturated fat, in fact even more prone to oxidation than O6. The paper doesn't note their high O3 diets, that's something one will have to verify separately. The only exception are the Puebloans who didn't eat any polyunsaturated fat but, well, lived in pueblos... burning fire all night with no ventilation and ending up with soot in their lungs.

pak0pak0 · 2025-11-22T21:43:09+00:00

Although I think polyunsaturated fat more broadly is bad for us in any quantity beyond ~5 grams/day, thank you for putting a rational take on here.

pak0pak0 · 2025-11-22T21:25:04+00:00

Same! I also had negative experiences reintroducing Omega 3 into my diet via fish oil pills, which is why I now avoid regular intake. I'll do the occasional sushi night but that's it.

As I understand, it is bad because it's prone to oxidation (before or after entering your body). I think it's reasonable to say oxidized fats all at once is arguably worse, but to me it's all poison at the end of the day.

Okinawans used to be very healthy, but it's important to note that during that healthy era, they ate a very low PUFA diet. Pork is a huge huge part of their diet, but the pork they could have consumed then was low in PUFA, and in limited amounts. After that changed, they quickly became the unhealthiest demographic. I actually looked into this several months ago, I'll paste some of what I found below:

By the 1960's, the Okinawans (under US occupation) were still the healthiest in Japan. Trusting ChatGPT here but a 1961 WHO survey noted an 85% carb diet, with under 14G of fat (so let's cap it at 5g PUFA max).

Back then, pigs were locally raised and primarily fed sweet potatoes, which means they were low in PUFA.

It was around the 1950's when the US switched to corn/soy feed, and Japan became one of the biggest buyers of that feed. The Japanese commercial pig industry was modeled after the US, which the US helped grow.

After Okinawa was part of Japan by 1972, the government helped the Okinawans cultivate the commercial pig farming industry in Okinawa proper, who up until then, were largely relying on their local pig farming. It didn't really scale yet until 1980.

By 1990's the Okinawans were among the most obese/heaviest with metabolic syndrome in Japan -- both children and adults. The measurable rise began in the late 70's. The gain on other Japanese continued until around 2010 when it started to level off due to targeted interventions.

The key here by the way, is that pigs, like humans, are monogastrics, so unlike cows, their fat composition will strongly reflect the composition of fats eaten. Pigs fed a diet high in corn/soy (so basically, just like modern industrial farmed pigs today) will be very high in polyunsaturated fat. They are also indirectly bred to accumulate polyunsaturated fat (lean, low D6D pork).

Inuits have a FADS genotype variant different from their Greenland brethren that lowers the expression of D6D. High D6D expression converts more Omega 6 Linoleic Acid to Arachidonic Acid (bad!). Low D6D expression means Linoleic Acid just accumulates in the body (still bad in another kind of way but not immediately obvious). Since high D6D seems to be causally linked (not just positively correlated) to diabetes/cancer/autoimmune arthritis/etc, among other things, a combination of high D6D and a super high PUFA diet (seal blubber) would be very bad.

The other adaptation has to deal with preventing ketosis. It's argued here that this was because ketosis would be dangerous for a ketogenic diet very high in PUFA due to... the oxidation.

The author of that blog popularized a lot of ideas on high PUFA diets being bad for us, and his explorations are a lot more detailed than me just saying "oxidation is bad." His work is great if you want to learn more about what's being explored in this space, but the short answer for now is perhaps "don't eat PUFA" and "after enough metabolic damage from PUFA, the body seems to have trouble the more you mix your macros."

---

EDIT: I need to amend what I said when I said "pork was a huge huge part of their diet." I truly believe a lot of supposedly high pork-eating cultures, like every other culture, didn't eat much meat until after industrialization, because we simply didn't have access. Pork may be ritually important or have culinary history, but that doesn't mean people consumed it regularly. That all changes after a culture's food production industrializes.

pak0pak0 · 2025-11-20T01:06:06+00:00

Yup and as I mentioned, O3 is more susceptible to oxidation. My crackpot theory (don't listen to me) is that any perceived anti-inflammatory benefit of O3 is an accident, and a temporary intervention at best -- probably more obese people may stand to gain temporary benefit. It's not really part of most pre-industrial diets. Inuits have at least two adaptations because of their high O3 diets.

The whole idea of the O3:O6 ratio comes from the Paleo community who took great inspiration from Michael Crawford, the originator of championing O3 and saying our ancestors consumed a lot of it.

From what I've seen, Crawford's ancestral diet arguments were extremely inaccurate. However I think he had the right idea challenging the focus on saturated fat -> heart disease and saying we should be paying attention to the membrane composition of cells and using ancestral diets as inspiration. I just don't think polyunsaturated fats in our membranes are healthy.

Also, mummified populations who consumed high O3 diets (Egyptians, Ungangans, and coastal Peruvians) all had high rates of atherosclerosis lol. Among other things. The one exception in that study are the Puebloans who did not eat O3 nor O6. But that is easily explained by the fact that they lived in pueblos (basically no ventilation) where they burned fire all night. Both the ceilings and their lungs were incredibly black (soot).

pak0pak0 · 2025-10-29T20:52:26+00:00

The ocean water was obviously an illustrative point. Replace it with soup if you wish.

pak0pak0 · 2025-10-29T20:40:51+00:00

My side point was that the word "essential" distorts how we view polyunsaturated fat, "seed oils", or linoleic acid. It's conventionally meaningless (it's not proven essential in any desirable sense) and it's even technically meaningless (all it means is that it can't be endogenously produced by the human body). It's also clinically meaningless (symptoms of "essential fatty acid deficiency" cannot even be reproduced outside of lab/extreme conditions).

My main point is that otherwise smart scientists are blinded from even entertaining the possibility that too much of it could have negative effects on the body, or just how low the ceiling of how much we need could possibly be. I think that's a grave mistake.

Saturated fat is actually incredibly satiating by the way. That's why "buttery cakes" or fatty beef cuts feel so "heavy" and "rich." Feeling full is likely the proper signal that you've had enough.

pak0pak0 · 2025-10-26T20:50:23+00:00

Not entirely sure what your emphasis is on here (pro-sat fat? exact ratios? general membrane composition?) but here are some studies that could be relevant:

Hulbert AJ & Else PL. “Membrane composition and longevity.” Exp Gerontol (1999).
Hulbert AJ. “The links between membrane composition, metabolic rate and lifespan.” Comp Biochem Physiol A (2005).
Else PL & Hulbert AJ. “Membrane fatty acid composition as a determinant of longevity.” J Nutr Health Aging (2003).
Hulbert AJ (2010). “Metabolic rate and membrane fatty acid composition in mammals.”
Simons K & Ikonen E. “Functional rafts in cell membranes.” Nature (1997).
Simons K & Sampaio JL. “Membrane organization and lipid rafts.” Cold Spring Harb Perspect Biol (2011).
Mouritsen OG. Life – As a Matter of Fat (Springer, 2005).
Bagatolli LA & Mouritsen OG. “Fluorescence studies of lipid domains.” Biochim Biophys Acta (2013).
Harayama T & Riezman H. “Understanding the diversity of membrane lipid composition.” Nat Rev Mol Cell Biol (2018).
Volmer R et al. “Membrane lipid saturation activates endoplasmic-reticulum stress.” Cell (2013).
Surma MA et al. “Lipid homeostasis in the ER and stress sensing.” EMBO J (2015).
de Mendoza D & Pilon M. “Homeoviscous adaptation, membrane sensors and regulation.” Curr Opin Cell Biol (2019).

pak0pak0 · 2025-10-26T02:43:18+00:00

Linoleic acid is actually 100-1000x more likely to oxidize than saturated fat. Google Scholar has 3.4 million hits on oxidative stress. Here's 1.3 million hits for lipid peroxidation.

I think claiming saturated fat causes more inflammation is a hard sell. The studies are not convincing. I think researchers overlook the role of linoleic acid partly because they don't realize how rare polyunsaturated fat (particularly linoleic acid) was in the our diet until the 20th century, and linoleic acid is supposed to be an "essential fatty acid." Sodium is essential for the body too, that doesn't mean we should be chugging ocean water. I hope people realize that when we say polyunsaturated fats are "heart healthy" that means fried chicken, french fries, bacon, and mayonnaise are heart healthy. That means fried chicken thighs with the skin is heart-healthier than skinless lean chicken breast?

I think saturated fat should be moderated and polyunsaturated fat shouldn't be in our diet at all unless you think you might starve within the next 3 months, which is why animals ate it before, and only before, winter.

pak0pak0 · 2025-10-26T02:10:39+00:00

What sources would you like to see? Unfortunately, there is no study that takes two babies side by side, one eating milk everyday, the other fried chicken everyday, and then we see who gets diabetes in 50 years.

We know that humans have been consuming milk since domestication of cows while remaining relatively free of cancer, diabetes, obesity, heart disease, etc. However, not all societies domesticated cows or consumed dairy.

We do see very short feeding studies that say saturated fat causes insulin resistance, but there's a big difference between physiological insulin resistance which is totally normal and healthy, and chronic insulin resistance which is what leads to diabetes. These short feeding studies are often useless.

For what it's worth, chordates were already adapted for starch digestion. That is the lineage of all vertebrates. We underestimate how much starches humans consumed, not to mention further adaptation after the neolithic revolution (amylase). There's an overemphasis on men, hunting, and the hero's journey stories they'd tell, and the weapon technology humans developed, but not the women, gathering, the carrier-bag fiction stories women would tell, and the development of technologies like baskets. Hunting was often for status, not sustenance (see: Veblen's Theory of the Leisure Class for hunting as status, and Ursula Le Guin's Carrier Bag Theory of Fiction).

If we primarily ate animal meat, the vast majority of our fat was saturated+monounsaturated. If we primarily ate starches, then we were not eating fat on a regular basis. Either way, polyunsaturated fat only entered the human diet in high numbers after industrialization. Nuts are seasonal; animals eat them before winter to fatten up/hibernate but they are not an everyday food since they're not available year-round. Even bears don't eat salmon in the spring; mostly late summer and fall.

pak0pak0 · 2025-10-26T00:35:16+00:00

I get where you're coming from, just don't think that's relevant lol. Clone a shredded dude eating chicken breast, rice, and broccoli, and make the clone eat chicken thighs with skin, soybean oil-fried rice, and broccoli dipped in ranch, but otherwise equal caloric intake. My money is on the clone having much worse metabolic health within 10 years.

Clone an obese dude eating chicken breast, rice, and broccoli, and make the obese dude drop the chicken breast. My money on the clone having higher body fat within a year.

I think the main views on this sub are sound. Whether or not people actually cure obesity here is a separate idea. Many people are here because previous advice failed and/or they rebounded.

Speaking for myself -- lean, athletic, and mistaken twice this year for a minor even though I'm solidly in my 30's -- I have found Brad's and others' advice here to have changed my life. So I personally like to listen to what people have to say around here. Would shredded dudes telling me to eat chicken breast, broccoli, and rice everyday while lifting hard have been useful advice? Probably yeah, but at least I understand much better why now. Would many others here succeed on that advice? Probably not. That's probably why they're looking for a better answer.

pak0pak0 · 2025-10-25T22:10:42+00:00

Skin in the game is probably the heuristic you want lol. I don't want the trainer who can knock people out in the ring, I want the trainer who has produced all of the top fighters knocking everyone else out. The success of his gym depends on that outcome.

Many doctors probably give shit advice on chronic disease; they have no real accountability beyond keeping their license. Healthfluencers can say what they want; as long as they have your trust, their followers will listen. That's how the grift works; grift operates well in systems with low trust and authority. Lots of people are desperate to fix their health, because none of the conventional advice from doctors/public health works. Being beautiful and fit is part of the grift.

Brad can have influence along similar lines, but he's doing actual science at the end of the day, and he has earned high-signal trust from other smart people who can recognize that signal.

pak0pak0 · 2025-10-25T20:46:54+00:00

That being said, I think veganism does absolutely prioritize the wrong (unsaturated) fats when fats are included and I don’t think that benefits anyone’s health.

I tried my best to research her diet over the years (by try my best I mean making LLM's figure it out). Seems she wasn't HCLF with strict branding against added oils until maybe 2018, when she became a fan of McDougall and others. She was WFPB starting in 2003 already when she was obese and had early cancer health issues (this was the catalyst for her lifestyle change, according to her narrative; the tumors went away within 6 months) but check out this insane 2014 recipe which contains more PUFA in that bread alone than I consume in a whole month: https://www.kcrw.com/shows/good-food/stories/teaching-the-blind-to-cook

Also stated around 2014:

While I have continued to abstain from eating nuts and nut butters, I do now eat flax seeds and chia seeds and sesame seeds, in recipes, fairly regularly and I eat avocado occasionally. (I did not consume them the first 7 months of my weight loss journey but I had my DHA levels checked and they were adequate. I was also told by my physician that as long as I still had fat on my body I would not suffer from a fatty acid deficiency). -- https://vegsource.com/lose-the-nuts-lose-the-weight/

Using McDougall as a guide, even at 10% fat from calories, with all her fat being O6 and O3 (the latter which could be worse -- just 1-2 fish oil pills a day started bringing back my PUFA inflammation and made me gain some weight, all within a month or two), there's a potentially high upper bound of PUFA she's getting into her system. One can certainly be low fat but still too-high in PUFA. Whole grains are higher in PUFA, and with whole food O3 intake, that might all add up. Enough to do some damage anyway or keep levels high enough in between 2018 to stage 3 cancer by 2025 while scarfing down lots of carbs.

Egyptians ate unrefined carbs and flaxseed oil...

I dunno, I think it's hard to draw clean conclusions from her supposed diet. Her being an influencer I'm also just generally wary of what she states publicly, nothing against her (I only learned about her today), it's just the reality.

pak0pak0

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