Why is Bryan Johnson so obsessed with with supplements?

[D2sage]

Too much Omega-6 is bad. Not sure why anyone would need supplementation of that kind.

Less than 2% of your brains  fatty acid is omega-6 whereas around 35% is omega-3.

Edited September 11, 2023 by D2sage

[Princess Arabia]

54 minutes ago, D2sage said:

Too much Omega-6 is bad. Not sure why anyone would need supplementation of that kind.

Less than 2% of your brains  fatty acid is omega-6 whereas around 35% is omega-3.

This is a good balance of all 3. You're right about excessive Omega 6 intake, that's why this oil is a great balance.

[toasty7718]

11 hours ago, D2sage said:

 

Too much Omega-6 is bad. Not sure why anyone would need supplementation of that kind.

 

Yea, too much of anything can be problematic

[Jason Actualization]

On 9/11/2023 at 5:59 AM, D2sage said:

Too much Omega-6 is bad. Not sure why anyone would need supplementation of that kind.

Less than 2% of your brains  fatty acid is omega-6 whereas around 35% is omega-3.

Indeed, yet our dietary guidelines recommend getting between 11 and 22 grams of omega 6 linoleic acid per day, and that's on a 2,000 calorie diet.

For me, even while closer to 3,000 calories, I'm getting less than 4 grams of omega 6 daily.

The more we eat, the more we store in our body fat.

Increased linoleic acid consumption marks the most significant, detrimental change to the human diet over the last 100 years.

[toasty7718]

9 hours ago, Jason Actualization said:

Increased linoleic acid consumption marks the most significant, detrimental change to the human diet over the last 100 years.

Increased linoleic acid consumptions marks the most significant change in CVD mortality over the last 100 years 

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5268076/

 

[Jason Actualization]

13 hours ago, toasty7718 said:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5268076/

The reason for the recent drop off in CVD deaths is due to surgical interventions such as coronary artery bypass grafting, i.e., the prevalence of heart disease remains sky high, every 33 seconds, on average, an American drops dead due to heart failure.

[toasty7718]

I see,

The seamless logic of ecological associations between the use of surgical interventions, like coronary artery bypass grafting, does explain at an epidemiological level the risk for CVD mortality going down, so we can't rule PUFA intake exclusively because there's an abundance of confounding factors. That's a logical fallacy on my part

So for that reason, the intake of PUFAs and lowering of CVD mortality at a population wide scale isn't robust enough.

I should specify that in terms of large scale RCTs, we don't really have large scale outcome trials on the effects of PUFA intake and CVD risk. Given the bulk of the evidence that has been accumulated over the past century, health experts have ruled that performing such an RCT to be unethical because it would mean upping the intake of SFA. The best evidence we currently have in terms of RCTs are trials that were completed decades ago.

When it comes down to the observational evidence, what we find is that higher intake of PUFAs and MUFAs reduces CVD risk.

This is a prospective cohort study done analyzing the intake of saturated fats, unsaturated fats, and carbs with CVD risk. It has a total of 127,536 participants and their diets were assessed by food frequency questionnaire every four years. It followed them for up to 30 years, and they found that higher intake of PUFAs and unrefined carbohydrates was associated with lower risk of CVD

https://www.sciencedirect.com/science/article/pii/S0735109715046914

"During 24 to 30 years of follow-up, we documented 7,667 incident cases of CHD. Higher intakes of [PUFAs] and carbohydrates from whole grains were significantly associated with a lower risk of CHD [...] Our findings indicate that unsaturated fats, especially PUFAs, and/or high-quality carbohydrates can be used to replace saturated fats to reduce CHD risk."

That's just observational evidence, is it not? How accurate even are FFQs?

In truth, not very accurate. There are a multitude of pitfalls that come with self-reporting, so for that very reason, researches have resorted to measuring biomarkers (more on that later)

Increasing your intake of saturated fat past a certain threshold increases your circulating levels of LDL cholesterol and ApoB.

This is a study from the World Health Organization analyzing the effect of modifying of of SFA intake with MUFAs, PUFAs, and carbs, and here are the results they found:

https://apps.who.int/iris/bitstream/handle/10665/246104/9789241565349-eng.pdf

There was a 0.058 mmol/L change in LDL cholesterol per 1% of energy replaced when you replace calories from PUFAs with calories from SFAs, as compared with 0.019 mmol/L and 0.012 mmol/L with replacement with carbs and MUFAs, respectively.

But do keep in mind that LDL cholesterol is a surrogate marker for atherogenic lipoproteins, and a much better metric would be apolipoprotein B (ApoB). The atherogenic lipoprotein molecules all have one molecule tag of ApoB. This includes:

LDL, VLDL, Lp(a), chylomicron remnant particles, and IDL.

And as such, what this table shows is that replacement of PUFAs with SFA marks a 10.3 mg/dL increase of ApoB particles in the blood.

And as I've already noted before, ApoB increases risk for CVD and shortens life-span:

https://www.thelancet.com/journals/lanhl/article/PIIS2666-7568(21)00086-6/fulltext](https://www.thelancet.com/journals/lanhl/article/PIIS2666-7568(21)00086-6/fulltext

"In conclusion, our evaluation of apoB using outcomes in first-degree relatives identified that higher apoB is detrimental to lifespan and increases the risk of coronary heart disease and type 2 diabetes. Lifestyle and pharmacological approaches to lowering ApoB should have widespread beneficial effects, including preventing common diseases and prolonging life."

But when it comes to self reporting, it is well known that for large groups of people it reasonably helpful. Not so much for small groups of people in an RCT. Therein lies the reason why researchers have started using biomarkers instead of FFQs.

This group of researches sought to evaluate how circulating levels of omega 6 fatty acids relate to the incidence of CVD, and it pooled together thirty studies from across the world. and their results are as follows:

https://www.ahajournals.org/doi/pdf/10.1161/CIRCULATIONAHA.118.038908

"In 30 prospective studies with medians of follow-up ranging
2.5 to 31.9 years, 15,198 incident cardiovascular events occurred among 68,659 participants. Higher levels of [Omega-6] were significantly associated with
lower risks of total CVD, cardiovascular mortality, and ischemic stroke"

So basically to summarize this, the links between increased PUFA consumption, CVD mortality, and the use of surgical interventions to deal with CVD are hypothesis generating pieces of evidence in of themselves, and much more robust evidence is needed to raise certainty in the domain of omega 6 rich seed oils and CVD risk.

The preponderance of the evidence suggests that replacing SFA intake with PUFAs lowers your ApoB and decreases your risk of heart disease.

 

 

Edited September 14, 2023 by toasty7718

[Jason Actualization]

18 hours ago, toasty7718 said:

When it comes down to the observational evidence, what we find is that higher intake of PUFAs and MUFAs reduces CVD risk.

It's not the higher intake of PUFAs or MUFAs, it's the fact that the people following these guidelines are also engaging in other healthy behaviors because all of these studies were conducted after the indoctrination of this erroneous idea. Epidemiology studies performed in Asia arrive at the opposite conclusion, because meat is associated with wealth and virility.

The problem is that all of the people that scientists could study nowadays are already poisoned by PUFA, so even a "low" linoleic acid cohort is already beyond the problematic threshold, so you are merely comparing the degree to which they've followed government-issued "health" guidelines.

This is the misunderstanding of the millennium and it's unfortunate that people are still stuck on what they deem to be the importance of saturated fat in and so far as it relates to health outcomes. Saturated fat has been a forever scapegoat for the doings of seed oils, which, when they came to fruition, precisely precipitated the diseases of modern civilization, the consequences of which spanning far and wide that folks now have to contend with.

Anyone serious about their health ought to eliminate all industrial seed oils from their diet and advice to the contrary will absolutely compromise your health.

[toasty7718]

jason I'm going to ask you again,

 

 What evidence for you have for this proposition? 

[Jason Actualization]

2 hours ago, toasty7718 said:

jason I'm going to ask you again,

 

 What evidence for you have for this proposition? 

This is a deduction derived from thousands of hours of reading and contemplation.

What was once mysterious, became complex, but is now simple.

[toasty7718]

17 minutes ago, Jason Actualization said:

This is a deduction derived from thousands of hours of reading and contemplation.

What was once mysterious, became complex, but is now simple.

That's interesting.

 

what evidence do you have for your proposition about seed oils and heart disease? 

Edited September 15, 2023 by toasty7718

[Jason Actualization]

9 hours ago, toasty7718 said:

That's interesting.

 

what evidence do you have for your proposition about seed oils and heart disease? 

See below.

[Leo Gura]

Supplement is the easy way to make a lot of $$$.

[toasty7718]

14 hours ago, Jason Actualization said:

See below.

I see you've provided me with over 60 sources cited by authors of a paper entitled "Omega-6 vegetable oils as a driver of coronary heart disease: the oxidized linoleic acid hypothesis"

This is a screen-snip from a paper by James J DiNicolantonio and James H O'Keefe.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6196963/

For starters, let's just examine the competing interests of the authors:
"Competing interests: JD is the author of The Salt Fix and Superfuel and operates the website thesaltfix.com. JHO has an ownership interest in CardioTabs, a nutraceutical company"

@Leo Gura so I suppose supplement is the easy way to make $$$, especially if you have mechanistic outcome data to back up your claims

interesting ...

I appreciate the evidence that you've given me from these two authors to support your proposition, but on first glance what I notice is an over abundance of mechanistic speculation. Why need mechanistic speculation when we have meta-analyses of prospective cohort studies showing that those with higher intakes or blood levels of linoleic acid have lower all-cause mortality, CVD incidence and mortality, stroke, and cancer mortality?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6582360/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6582360/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7326588/

Let's examine some of the sources these unbiased authors cite, shall we

Source (2) states:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4334131/
"Our findings suggest that adipose tissue LA has increased substantially in the United States over the last half century, and, to our knowledge, for the first time demonstrate that this increase is highly correlated with increased dietary LA intake over the same period ... Because LA is in involved in numerous physiologic and pathophysiologic processes, these changes have potentially significant implications for public health. These findings call for further research into the consequences, positive or negative, of such a major shift in the adipose tissue concentration of a single bioactive FA occurring over a relatively short period of time in the United States."

Even the authors of that paper conclude that based purely on the increase of linoleic acid in adipose tissue requires further research to see if it has positive or negative health effects. Given the meta-analysis and epidemiologic studies that I've provided, all this paper does is prove my point even further

They say with source (4) Linoleic acid serum concentrations (as opposed to per cent of fatty acids) are higher in patients with CAD

https://pubmed.ncbi.nlm.nih.gov/8472362/

An interesting finding for sure, but how do we link it as being causal? What we need is an RCT that shows that increasing linoleic acid serum concentrations increased CAD compared to a control group, not looking at CAD and seeing that they have higher concentrations of it, you know? That's much better at determining causality.

For source (3) they state linoleic acid in adipose tissue and platelets positively associates with CAD, whereas EPA and DHA in platelets are inversely correlated with CAD

Another interesting finding. Again - correlation does not equate to causation. Also - this is a small sample size of 226 patients. Preferably, we want to have a large group of people to see if the effects are repeatable.

Let's examine more robust studies - more specifically, meta-analyses preferably

Just a side note: when it comes to correlation not equating to causation, an example I like to use is the fact that countries that smoke more live longer, or the fact that those who own lighters are more likely to have lung cancer, or the fact that some foods raise blood pressure so therefore they're bad. You know what else raises blood pressure? Exercise! Having sex! So we can't rule out something raising blood pressure short-term as being bad.

https://www.sciencedirect.com/science/article/pii/S000291652200778X

This is a systematic review and meta-analysis of prospective cohort studies to examine associations between LA intake and mortality (including, but not limited to CVD)

It pooled together 38 studies with 44 prospective cohorts and included 811,069 participants (a far-cry from the 226 you mentioned earlier)

To summarize, the authors finish the article by saying "In prospective cohort studies, higher LA intake, assessed by dietary surveys or biomarkers, was associated with a modestly lower risk of mortality from all causes, CVD, and cancer. These data support the potential long-term benefits of PUFA intake in lowering the risk of CVD and premature death."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6582360/

This study was written by a whopping 59 PhD holding authors (I counted it, by the way)

This is a harmonized, de nova, individual-level analyses in a global consortium of 30 prospective observational studies from 13 countries that looked at the circulating and adipose tissue LA biomarkers with total CVD and subtypes. Heterogeneity was explored by age, sex, race, diabetes, stain use, aspirin use, omega-3 levels, among others.

In the prospective cohort studies ranging from 2.5 to 31.9 years, 15,198 incident cardiovascular events occurred among 68,659, and higher levels of LA were significantly associated with lower risks of total CVD and its subtypes

They conclude by saying higher in vivo circulating and tissue levels of LA were associated with lower risk of major cardiovascular events.

So - let's leave the reader with a choice. A study pool of hundreds of patients undergoing coronary angiography without heterogeneity taken into account vs. two meta-analyses of close to a million participants with sex, age, weight, habits, omega-3 intake, etc., taken into account and still finding that higher intake of PUFA contributes to lower risk of CVD.

Your evidence is weak, suffice to say

Source (5) doesn't contribute to your proposition either because it shows benefit of going on a weight loss high carb low fat diet, and one group high in MUFAs with beneficial effects of weight loss to lower risk factors of CVD

https://pubmed.ncbi.nlm.nih.gov/9538963/

"MUFA-enriched hypocaloric diets potentiate the beneficial effects of weight loss to ameliorate cardiovascular risk factors in obese patients with type 2 diabetes."

https://pubmed.ncbi.nlm.nih.gov/14739118/

From what I've seen, none of the studies they cited about oxidized LDL even make the slightest hint that oxidized LDL is caused by increased intake of PUFA, like seed oils. Also - measuring oxidized LDL is something that no cardiologist does because it's a meaningless metric. None of the studies they mentioned were adjusted against ApoB either because if it did, it would have no meaning.

This paper touches on that and says that oxLDL should be compared with ApoB

Viita, H., Närvänen, O., & Ylä-Herttuala, S. (1999). Different apolipoprotein B breakdown patterns in models of oxidized low density lipoprotein.. Life sciences, 65 8,
          783-93
        . https://doi.org/10.1016/S0024-3205(99)00305-7.
"We suggest that in order to improve interpretation and comparison of results, data obtained with various models of oxidized LDL should be compared to the simplest and most reproducible models of 3 h and 18 h copper-oxidized LDL (apoB breakdown) and MDA-LDL (apoB aggregation) since different models of oxidized LDL have significant differences in apoB breakdown and aggregation patterns which may affect immunological and biological properties of oxidized LDL."

To name some more of the studies they cited and the inconsistencies I see

Sources (6), (53), (54), and (56) and models done on rodents, so I don't see any relevancy there in terms of human health-outcome data.

Source 57 is funded by the National Cattleman's Beef Association, so it's best taken with a grain of salt.
https://www.metabolismjournal.com/article/S0026-0495(00)97008-2/pdf

I'm absolutely certain that more are sponsored by that, but...

I don't feel like going through and picking out weak pieces of evidence.

One of the sources concludes
https://academic.oup.com/ajcn/article-abstract/75/2/221/4689295

"Increased ALA intakes decrease the estimated IHD risk to an extent similar to that found with increased LA intakes. Group nutritional education can effectively increase fish intake."

This doesn't support their proposition either.

RCTs like the LA Veterans study where they measured levels of linoleic acid in adipose tissue and the intervention group saw levels increase on the vegetable oil diet and a statistically significant reduction in heart disease.

There's many more sources, but I don't really see a point in dismantling them all given the fact that

a) the authors have a conflicting bias for their own supplement companies

b) the first of the studies I mentioned were weak evidence

c) the narrative just doesn't suddenly flip one day with nutrition science and foods are bad all of a sudden, you have to look at the totality of the evidence, and the totality of the evidence has leaned towards replacing SFA intake with PUFA intake to decrease risk of CVD

d) correlation does not equate to causation

e) the oxidized LDL hypothesis has no real bearing given the fact that the studies never compare it to ApoB (because if they did, it would expose it as a meaningless metric), and therefore no cardiologists use it

f) there is much more robust evidence than mechanistic outcome data speculation

g) the better evidence is in the form of a systematic review and meta-analysis of prospective cohort studies and / or RCTs with very large sample sizes (tens or hundreds of thousands of participants) of people with heterogeneity taken into account, written by authors with nuance and (preferably) without bias

h) "USDA: moderate saturated fat
AHA: moderate sat fat
Canada: moderate sat fat
UK: moderate sat fat
Spain: moderate sat fat
Australia: moderate sat fat
China: moderate sat fat
South Africa:moderate sat fat
WHO:moderate sat fat"

g) I'm getting tired of this

TL,DR: the paper you took a screen snip of was written by two authors with conflicting biases for their own supplement companies and they rely mostly on mechanistic outcome data and speculation for their claims (and some of the sources even contradict their proposition). Why focus on that singular paper there is much more robust evidence in the form of a systematic reviews, meta-analysis, and prospective cohort studies which have hundreds of thousands of participants each? They examine the link between CVD  with the intake of omega-6 and find that higher intake of linoleic acid decreases risk of CVD.

At this point I really think you should concede on your proposition, but I find that unlikely to happen. I've debunked your pseduoscientific claims more than once and at this point I'm done with this debate. It takes me hours to compile the evidence (which don't get me wrong, I enjoy doing. It gives me an opportunity and reason to read into nutrition, which is something I'm interested in)

I'll state again: misinformation kills people. What you're doing is a disservice to this whole forum.

Edited September 16, 2023 by toasty7718

[Jason Actualization]

17 hours ago, toasty7718 said:

Let's examine some of the sources these unbiased authors cite, shall we

Source (2) states:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4334131/
"Our findings suggest that adipose tissue LA has increased substantially in the United States over the last half century, and, to our knowledge, for the first time demonstrate that this increase is highly correlated with increased dietary LA intake over the same period ... Because LA is in involved in numerous physiologic and pathophysiologic processes, these changes have potentially significant implications for public health. These findings call for further research into the consequences, positive or negative, of such a major shift in the adipose tissue concentration of a single bioactive FA occurring over a relatively short period of time in the United States."

Even the authors of that paper conclude that based purely on the increase of linoleic acid in adipose tissue requires further research to see if it has positive or negative health effects. Given the meta-analysis and epidemiologic studies that I've provided, all this paper does is prove my point even further

Yes, and I have a personal relationship with one of those authors, her name is Susan Carlson and she oversees a laboratory in Kansas City, Missouri. She is going to personally assay a sample of my adipose tissue in November. Care to guess how she personally navigates and advises others to navigate the linoleic acid infested world that we inhabit? She avoids it all cost and I have spoken with her ad nauseum about this matter. She is helping me save the world from seed oils by not only assaying my own adipose tissue (to prove that my dietary intake is both what I preach and practice) but also the phospholipid composition of my erythrocytes for social media purposes, i.e., to faciliate the proliferation of this this life-changing information.

17 hours ago, toasty7718 said:

At this point I really think you should concede on your proposition, but I find that unlikely to happen. I've debunked your pseduoscientific claims more than once and at this point I'm done with this debate. It takes me hours to compile the evidence (which don't get me wrong, I enjoy doing. It gives me an opportunity and reason to read into nutrition, which is something I'm interested in)

I'll state again: misinformation kills people. What you're doing is a disservice to this whole forum.

I'm sorry you feel that way man. In your lifetime, invariably, you are going to be burdened by enduring the same cognitive dissonance that I have in arriving at these conclusions (having been a traditionally trained pharmacist background spanning the past decade). The truth will eventually come to fruition, and I hope you are able to let it land my friend.

[Thought Art]

I find what he is doing silly in a lot of ways. But, I also commend him in doing what he is interested in. The whole caloric deficit thing plus injecting fat into his face is rather strange to me. 

[toasty7718]

I mean it shows that it's possible. I'll grant it's possible that you're right; that's trivially true. What's the evidence that the claim is actually true?

 

The body of the cake is that it doesn't actually demonstrate your claim, it just shows that it's theoretically possible.

 

yeah, take care man, wish you the best. just don't be surprised when you start to develop CVD in your mid to late 30s

Edited September 17, 2023 by toasty7718

[toasty7718]

& sorry if I got a bit heated at times, I'm just passionate about evidence-based nutrition and find it appalling when people give health advice that has been demonstrated time and time again to result in detrimental health outcomes.

[Jason Actualization]

5 hours ago, toasty7718 said:

& sorry if I got a bit heated at times, I'm just passionate about evidence-based nutrition and find it appalling when people give health advice that has been demonstrated time and time again to result in detrimental health outcomes.

No harm, no foul man. I am very passionate as well and so I understand and appreciate your enthusiasm.

5 hours ago, toasty7718 said:

yeah, take care man, wish you the best. just don't be surprised when you start to develop CVD in your mid to late 30s

I wish you equally well. I am so unshakably confident in my position that I have shared my dietary philosophy with all of my close friends and family members. I will share future imaging studies and laboratory tests on this forum, being 100% transparent, displaying the power of my nutritional paradigm that I have full confidence in.

[LSD-Rumi]

On 9/9/2023 at 1:36 AM, toasty7718 said:

Okay,

From what it seems to me, you're very passionate about your beliefs and you seem to be dead-set in your personal anecdotes for the diet you're preaching. That's fine.

What I'm mostly worried about is you preaching this diet to the people on the forum and saying that it is the way to best way to eat and that this will reverse their chronic diseases. I understand why you're coming from this place given your own experience, but based on the evidence done on MILLIONS of people, the epidemiology of this diet seems to result in unfavorable health outcomes. Not to mention it demonizes many food groups and will most likely lead to an eating disorder for most people. For someone who isn't very well versed in nutrition, they might see your posts and start eating in a way that will, worst case scenario, have their risk of CVD and cancer increase drastically. Or, they could see the short-term benefits that you've seen, I'm not denying that.

But do remember, misinformation kills people.

Let's start with your claims:

If everyone told you that smoking cigarettes was highly addictive and hazardous to your health yet when you smoked a pack a day you felt happier, more clear, more energized, and well-rounded, would you still continue smoking cigarettes despite what the evidence says?

 

 

This is wrong on so many levels. I don't even know where to begin.

First off, this is just a blatant appeal to nature fallacy. Might I remind you of a little thing called Antagonistic Pleiotropy? This is the biological phenomenon wherein an individual's genes will favor and select for traits that prioritize short-term survival and reproductive success over long-term survival.

As you know, genetics are a tricky and counter-intuitive thing. Many things effect whether genes are turned on and turned off, so you can't just boil things down to genetics, enviornment and diet play a huge part in it. It's very individualized.

Each one of us has a unique biology - even identical twins!

Identical twins who grew up in a different environments will have different genetics. With that in mind, this is the reason behind how eating an ancestral diet will result in long-term detrimental health outcomes.

TLDR: we shouldn't look to the amount of polyunsaturated fat our ancestors ate, we need something more robust. This is where human outcome data comes into the mix of things

I'll link here some meta-analysis studies done regarding polyunsaturated fat intake and oxidation / chronic disease. I'm well aware that me and your views differ drastically when it comes to the hierarchy of evidence, but I'm mostly doing this in case others want to see it for themselves.

On one hand we have close to half a million participants health outcome data (more on that later), and then we have you and your anecdotal experience. I'm not dismissing your own experience by any means, what I'm trying to get across is the fact that the epidemiology of what your preaching seems to be in direct contradiction.

This is also blatantly wrong on so many levels.

Here are the two studies that many people who share your beliefs about saturated fat might cite. It's also why the Time Magazine Issue titled "Eat Butter" came out an generated a media firestorm.

https://pubmed.ncbi.nlm.nih.gov/24723079/[https://pubmed.ncbi.nlm.nih.gov/20071
https://pubmed.ncbi.nlm.nih.gov/20071648/

These studies looked at people who eating varying amounts of saturated fat and they found they had similar rates of CVD. It's hard to see through this type of study because of many confounding factors (the people on the low saturated fat group may have been eating other things that contributed to that outcome).

Here's a study done to clarify the findings of the previous one. Harvard researchers told people to limit their SFA intake and replace it with PUFAs and MUFAs from nuts and seeds, and what they found was that they had lower rates of CHD risk.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4593072/

"Higher intakes of polyunsaturated fatty acids (PUFAs) and carbohydrates from whole grains were significantly associated with lower risk of CHD"

They also had a group that ate refined grains and what they found is that their risk remained the same.

So, we can conclude that the previous two studies linked above weren't robust enough and when SFA is replaced with healthier forms of fat, risk of CVD goes down.

But that's CVD risk, what about oxidative stress?

I'd assume by oxidative stress you're also inferring that this leads to atherosclerosis like you said in previous posts, but there simply isn't enough evidence to say with absolute certainty that this is the case yet. What we need is a multitude of repeated RCTs and human outcome data before we can say something like that for sure.

The best metric we have currently is ApoB, which I will cover later.

Anyways, here are the effects of high polyunsaturated fat diets and CVD risk:

This epidemiological study analyzed 521,120 individuals and here were their findings:

https://pubmed.ncbi.nlm.nih.gov/33853582/

"Consumption of butter and margarine was associated with higher total and cardiometabolic mortality. Replacing butter and margarine with canola oil, corn oil, or olive oil was related to lower total and cardiometabolic mortality. Our findings support shifting the intake from solid fats to non-hydrogenated vegetable oils for cardiometabolic health and longevity."

Finally, a Cochrane systematic review, a HIGHLY respected medicine journal that pooled together all available randomized clinical trials done on this topic. It had to meet certain criteria of course, like having to be compared with a higher saturated fat intake, intending to reduce SFA intake or include MUFAs or PUFAs, lasting at least 2 years. Here were their results.

https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD011737.pub3/full

"Replacing the energy from saturated fat with polyunsaturated fat or carbohydrate appear to be useful strategies, while effects of replacement with monounsaturated fat are unclear. The reduction in combined cardiovascular events resulting from reducing saturated fat did not alter by study duration, sex or baseline level of cardiovascular risk, but greater reduction in saturated fat caused greater reductions in cardiovascular events."

But this is epidemiology. Isn't this inaccurate?

No.

https://pubmed.ncbi.nlm.nih.gov/34308960/

"Comparing both bodies of evidence from Cohort Studies, the difference in the results was also small (RRR: 0.92; 95% CI: 0.88, 0.96). Our findings suggest that bodies of evidence from randomized control trials and cohort studies are often quantitatively concordant. Prospective systematic reviews in nutrition research should include, whenever possible, bodies of evidence from randomized control trials and cohort studies on dietary intake and biomarkers of intake to provide the whole picture for an investigated diet-disease association."

https://www.ncbi.nlm.nih.gov/pmc/articles/instance/8803500/bin/nmab095fig1.jpg

What about ApoB as a metric for CVD? What is ApoB?

ApoB is a marker of atherogenic lipoprotein particles in our bloodstream.

Here's a study from the lancet that shows high levels of ApoB increases risk for CVD and life-span.

They got their data from the UK Biobank and it has approximately 500,000 participants. To verify their hypothesis, they replicated the estimates from the UK Biobank using mendelian-randomization (a type of study that analyzes the genetic predisposition of participants).

https://www.thelancet.com/journals/lanhl/article/PIIS2666-7568(21)00086-6/fulltext

"In conclusion, our evaluation of apoB using outcomes in first-degree relatives identified that higher apoB is detrimental to lifespan and increases the risk of coronary heart disease and type 2 diabetes. Lifestyle and pharmacological approaches to lowering apoB should have widespread beneficial effects, including preventing common diseases and prolonging life."

So how do PUFAs and MUFAs contribute to the lowering of APoB? This is a review done on eighty-seven studies. Here is what they found

https://pubmed.ncbi.nlm.nih.gov/27821191/

"Replacement of carbohydrate by MUFA, not SFA, decreased plasma apoB. Moreover, dietary enriching with n-3 fatty acids [PUFAS] (FA) (from fish: 1·1-1·7 g/d or supplementation: 3·2-3·4 g/d EPA/DHA or 4 g/d EPA), psyllium (about 8-20 g/d), phytosterols (about 2-4 g/d) or nuts (30-75 g/d) also decreased plasma apoB, mostly in hyperlipidaemic subjects"

I'll leave you with some of principles regarding SFA:
- It's a dose-dependent response, dose matters, there's a threshold effect associated with it
- What you replace it with also matters
- Source matters. Fish, dark chocolate, olive oil are high in SFA and the health outcomes are overwhelmingly positive. The same can't be said for something like margarine or butter.

But even that's not to mention saturated fat is surface level. We want to analyze the health effects of foods over the macros and micro.

My goal here is to give others on this forum a more evidentially-based approach to their health that will, in all likelihoods, result in favorable health outcomes based on the evidence that we have.

This brings us back to your anecdote. I have no doubts about how you feel healthier and happier after removing PUFAs from your diet, but how exactly would you know that that was the ONE and ONLY thing that caused you to reverse your eosinophilic esophagitis? What if you have a microbiome that doesn't respond well to fiber, for example?

Point is, the way you're presenting your argument for everyone changing their diet because you got individual gains in a way that can have a multitude of confounding factors and goes against what the overwhelming majority of the studies say is ignorant at best and fatal at worst.

I really think you should approach this topic with more nuance and less absolute certainty. I'll state again: misinformation kills people my friend. What you're doing isn't a favor, it's a disservice.

Dude, this is awesome, thanks for the effort.