Bryan Johnson on Seed Oils

tl;dr: Trying to become immortal is a sign of mental illness.

Snake Oil

So apparently there’s this guy Bryan Johnson. He’s trying to become immortal, or at least to extend his life by some substantial amount.

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You can read about him at Wikipedia, if you choose. Apparently he has some money, and is using it to either extend his life or to make money selling anti-aging supplements. It’s not clear which. I like the name, though.

Source

We’ll get back to snake oil.

Eat Seed Oils For Immortality?

So recently he posted his thoughts on seed oils:

I remember once seeing some ‘longevity expert’ saying that there is no hard-coded limit to how old humans can live.

This is an insane statement. Expand it to animals: if we didn’t have a hard-coded limit, the world would be full of immortal animals and people. At the moment, we don’t have evidence for a single example of any vertebrate that is immortal, including in farms and zoos.

So clearly there’s a limit. Some organs in humans can regenerate, many others can not. You get one chance at life with your brain, heart, eyes, cartilage, teeth, etc., and if you wear them out, you’re done.

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This is rather amusing:

“And the LORD said, My spirit shall not always strive with man, for that he also is flesh: yet his days shall be an hundred and twenty years.”

But somewhat off-topic. There is exactly one example of a human exceeding that limit, she died at 122. Assuming her birth certificate was accurate (Newman, 2020).

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Since I’m not really interested in going through his post point-by-point, let’s just hit the high points. I’m also not going to look at his “initial thread”.

He claims:

1. “Healthy fats matter: plant-based Omega-6 (e.g. seeds) and marine Omega-3 (algal or fish oils) support longevity and health, with Omega-3s being especially powerful.”

2. “Extra Virgin Olive Oil is key: EVOO (rich in MUFAs) is strongly linked to living longer and preventing age-related diseases.”

3. “Choose fats wisely: While higher fat intake can improve health, saturated fats (from butter and fatty meats) are linked to higher mortality and more age-related diseases.”

He continues with a lot of basic info, then:

“Available evidence from humans indicate positive associations between seed oil Omega-6 (Linoleic Acid) and fish derived Omega-3 (EPA and DHA) reduced all-cause mortality.”

And,

“Reliable evidence indicates that seed oil Omega-6 and Omega-3 is associated with decreased risk of heart disease.”

He then goes on about a lot more basic stuff about cell and saturated vs. unsaturated fats. It’s all pretty rudimentary, and doesn’t really advance his argument at all as to why PUFA might be beneficial. It’s just filler.

Lies, Damn Lies, and Epidemiology

FINALLY we get to some meat:

“Total PUFAs uptake (Omega-3&-6) was associated with 19% and 11% reduction of all cause mortality in a prospective cohort study with 25,000 participants and a meta-analysis with 1,164,029 participants, respectively.”

The paper (his ref. 5) is “Association of Types of Dietary Fats and All-Cause and Cause-Specific Mortality: A Prospective Cohort Study and Meta-Analysis of Prospective Studies with 1,164,029 Participants” (Mazidi, 2020)

Johnson has claimed above that Ω-6 fats are associated with reduced all-cause mortality, and reduced heart disease.

His reference doesn’t support this.

“In the meta-analysis of 29 prospective cohorts (n=1,148,117) we found a significant inverse association between total fat (0.89, 0.82-0.97), MUFA (0.93, 0.87-0.99) and PUFA (0.86, 0.80-0.93) consumption and all-cause mortality.” (Mazidi, 2020)

So a small decline.

But for heart disease, nothing.

“Neither MUFA nor PUFA were associated with CVD or CHD mortality.” (Mazidi, 2020)

Did Johnson not read this before including it?

The bigger problem here is that they are using the NHANES dataset, which has long been known to be garbage.

“Across the 39-year history of the NHANES, EI [energy intake] data on the majority of respondents (67.3% of women and 58.7% of men) were not physiologically plausible. Improvements in measurement protocols after NHANES II led to small decreases in underreporting, artifactual increases in rEI, but only trivial increases in validity in subsequent surveys. The confluence of these results and other methodological limitations suggest that the ability to estimate population trends in caloric intake and generate empirically supported public policy relevant to diet-health relationships from U.S. nutritional surveillance is extremely limited.” (Archer, 2013)

This is typical of such enterprises.

“The large, variable misestimation suggests that the USDA LAFA per capita caloric intake estimates lack validity and should not be used to inform public policy.” (Archer, 2016)

And, just the other day:

“We applied the equation to two large datasets (National Diet and Nutrition Survey and [NHANES]) and found that the level of misreporting was >50%. The macronutrient composition from dietary reports in these studies was systematically biased as the level of misreporting increased, leading to potentially spurious associations between diet components and body mass index.” (Bajunaid, 2025)

So we can throw his ref. 5 in the bin. Garbage in, garbage out.

But there’s more.

“Looking at Omega-6 in particular, Linoleic Acid (predominant in some seed oils) was correlated with 12% reduction in all cause mortality, while dietary Arachidonic Acid (obtained from animal food sources) increased all-cause mortality by 10%. (6).”

Ref. 6 is actually 6 and 7:

This must be a quirk of X article software or something. 6 is (Zhuang, 2019), and 7 is (Marklund, 2019).

Again, it’s epidemiology.

“Intakes of saturated fatty acids (SFAs), trans-fatty acids, monounsaturated fatty acids (MUFAs), and polyunsaturated fatty acids (PUFAs) were assessed via food frequency questionnaires.” (Zhuang, 2019)

7 is worse than epidemiology. Unilever, a massive producer of ultra-processed foods containing edible oils, and former major producer of seed oils (they sold that business to Bunge) pays Tufts University to produce, effectively, pro–seed-oil research.

“Sources of Funding: Funding for the Fatty acids & Outcomes Research Consortium (FORCE)… Unilever provided Tufts University with a restricted grant… to partly support this analysis.” (Marklund, 2019)

I discussed FORCE in this post:

Thoughts on "Beneficial Effects of Linoleic Acid on Cardiometabolic Health: An Update"

It’s long been recognized that industry-supported research is more likely to find an result that favors the company paying for the research.

“Industry sponsorship is a key source of bias that can affect research at multiple stages. Data from several fields have shown biases in the design, conduct, and publication of research that are related to industry funding sources.” (Fabbri, 2018)

The biggest problem with epidemiology in the area of consumption of fatty acids is finding an appropriate control group. People in industrial countries have been consuming high levels of seed oils for several generations.

(Lee, 2022)

Yet all the diseases Johnson discusses have increased during this period.

How do we resolve this problem?

“However, before such public health measures are adopted, the important near-ubiquitous risk factors must first be identified.” (Pearce, 2011)

For instance:

“…in a society where everyone smokes, smoking will not identify high-risk individuals for lung cancer.” (Pearce, 2011)

So many of the standard tools of epidemiology won’t work.

“So can the role of near-ubiquitous risk factors be studied and their importance for disease causation quantified? Yes they can, but it’s not easy, and they cannot always be studied with our ‘standard’ methods such as randomized controlled trials, cohort studies or case–control studies…. First, it may be possible to identify important risk factors by comparisons between populations or comparisons over time.” (Pearce, 2011)

For a ubiquitous food item such as seed oils, where do you find a group that doesn’t consume them?

But don’t worry, (Marklund, 2019) makes no effort to control for this problem. They are only looking at consumption in advanced, industrial nations, despite clear evidence that in populations with little or no heart disease (for instance), seed oils consumption is absent.

“…The Tsimane, a forager-horticulturalist population of the Bolivian Amazon with few coronary artery disease risk factors, have the lowest reported levels of coronary artery disease of any population recorded to date.” (Kaplan, 2017; Kraft, 2018)

It’s frankly amazing that Johnson, who’s slogan is “Don’t Die”, would ignore populations that don’t suffer from the leading cause of death in industrial nations, heart disease.

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It’s less surprising that Unilever, making a living by selling seed-oil-laden food, would rather ignore this.

He goes through a bit more epidemiological evidence suggesting that high intakes of seed oils are beneficial. Unlike industrial nation, the Tsimane, don’t have obesity, diabetes, neurodegeneration, or any of the other conditions Johnson assures us consuming seed oils will benefit, despite largely not consuming seed oils.

There are long expositions on the problems with relying on such epidemiological data to guide what we should eat. At least, they should be confirmed with human trials, so we can see if the claimed benefits are real (Ramsden, 2016).

And there are many reasons to think that seed oils are not beneficial for longevity.

“PUFA in membrane phospholipids are particularly prone to peroxidation due to their degree of unsaturation, and longer-lived species are often found to have a lower membrane PUFA/monounsaturated fatty acids (MUFA) ratio than shorter-lived ones. Our [long-lived individuals] LLIs group had a distinctively higher level of MUFA, and lower levels of total n-3 and n-6 PUFA than adults and older adults, as well.” (Aiello, 2024)

Olive Oil for Longevity

Then he starts recommended the benefits of mono-unsaturated fats (MUFA), like those in his “Snake Oil” olive oil. Wait, what?

(Johnson, 2025)

Despite what Johnson and Unilever would have you believe, the evidence of the benefits of MUFA—there is no such thing as “plant MUFA”—is that it is not subject to rancidity like the PUFAs, especially the Ω-6 PUFAs. Remember the 122-year-old woman?

“Jeanne reportedly attributed her remarkable longevity to a diet rich in olive oil, which she also rubbed into her skin daily.”

This has been shown in both human randomly-controlled trials, and in and endless stream of in-vitro studies. One study not cited by Johnson is (Guasch-Ferré, 2022).

(Guasch-Ferré, 2022)

“Potential mechanisms of these associations include olive oil being less susceptible to oxidation; having anti-inflammatory and antiatherogenic properties; and improving oxidative stress, endothelial function, lipid profile, insulin sensitivity, and blood pressure.” (Guasch-Ferré, 2022)

It has all those benefits because it contains less Ω-6 fats. You can’t have it both ways, either Ω-6 is bad an MUFA is good, or we have to throw out an enormous amount of science on the harms caused by “oxidation” and “oxidative stress”.

I go through some of that evidence in the post mentioned above.

Thoughts on "Beneficial Effects of Linoleic Acid on Cardiometabolic Health: An Update"

But you can’t do what Johnson is doing here: claim that Ω-6, Ω-3, and MUFA are all beneficial. The latter two are beneficial to the extent that they replace the first.

He’s an example:

“It is claimed by some skeptics that the advantages of Linoleic Acid and other PUFAs compared to saturated fats are exclusively due to monosaturated trans-fats that occur more in conjunction with saturated animal fats.

“This ignores much of the molecular evidence of PUFAs (Omega-3 and Omega-6) and their functions in cellular membranes including the increase in LDL uptake by liver cells associated with Linoleic Acid.”

The first paragraph is incoherent, I presume he means that the trans-fats in saturated animal fats are bad, and this is the reason for the claimed benefits of LA. However, the senior author of (Marklund, 2019, Dariush Mozaffarian, actually has a patent on MUFA trans-fats from animal fats, for their beneficial effects:

“Use of Trans-Palmitoleate in Identifying and Treating Metabolic Disease” (Mozaffarian, 2014)

Johnson does note that the negative effects of trans-fats only applies to synthetic, that is, produced from plant-based, trans-fats.

For the second paragraph, the reason PUFAs causes lower LDL is because it goes rancid (or already is rancid), thus reducing the emission of VLDL (ApoB100), which turns into LDL as its fat payload is delivered.

“Surprisingly, the results of the present experiments in vitro and in vivo provide strong evidence that stimulation of ApoB100 degradation by marine Ω-3 fatty acids requires increased generation of lipid peroxidation products. Moreover, other easily peroxidized lipid molecules — Ω-6 and nonmarine Ω-3 polyunsaturated fatty acids (PUFAs) — act similarly.” (Pan, 2004)

The degradation happens as the VLDL particles are being produced in the liver, and before they are emitted into the blood. MUFA, oleic acid, found in olive oil, is not subject to lipid peroxidation, and does not have this effect. Neither does saturated fat (Pan, 2004).

This susceptibility to rancidity of PUFAs explains another effect Johnson and his sources elide: the reduction in LDL caused by seed oil consumption is correlated with higher mortality. Unlike the epidemiology cited above, this is seen in human randomly-controlled trials of seed oil consumption, the highest level of medical evidence (Ramsden, 2016).

Why wouldn’t Johnson mention this?

“Disclaimer”

“All evidence presented here is for natural, pure, clean, well-packaged and preserved plant seed oils, and does not apply to contaminated, poorly stored, or overheated seed oils (this was partially covered in my earlier thread).”

This is an awful big carve-out. What’s wrong with “poorly stored”, or “overheated” seed oils?

They’ve gone rancid, of course, and hence toxic. So the obvious question then becomes, how do you get non-rancid seed oils?

It doesn’t seem like you can. Even newly-produced oils have high levels of lipid peroxidation products, compared to native LDL.

“For example, low density lipoprotein hydroperoxide levels are as low as 0.03 μmol/kg lipid while [1], while hydroperoxides in refined oils typically range from 2 to 20 mmol/kg lipid [2].” (Vieira, 2017)

“While this field of toxic lipid oxidation products is still relatively young, it is obvious that consumption of oxidized lipids could cause health problems and thus it is critical that food oils are protected from oxidation and that diets include antioxidants that could decrease lipid oxidation in vivo.” (Vieira, 2017)

In some countries, peroxide value (PV) is used as a standard to determine when an oil is safe to eat. This is an estimation of the level of hydroperoxides in the oil. Ironically, the expected (and allowed) PV for cold-pressed or virgin oils is 50% higher than for refined oils, as the refining process lowers the PV (FAO, 1999).

Conclusion

I think it’s fair to say that Johnson has a little bit of information, and has been relying on sources with ulterior motives. Even since the National Diet-Heart Trial failed, the cardiology profession has desperately tried to hide the reality that their favorite prescription offered no benefit, but only harm. Similarly with the other chronic diseases discussed, they only worsen with time and exposure to seed oils in the diet.

It’s a shame that’s he’s promoting unfounded solutions to health, but this is unfortunately all too common.

Is Snake Oil Beneficial?

Amusingly, there is actually a paper looking at the fatty acid composition of snake oil. Turns out there may be something to it: it’s high in EPA, an Ω-3 fatty acid that is sold as a prescription treatment for CVD.

“As a concentrated source of EPA, snake oil is a credible anti-inflammatory agent and might indeed confer therapeutic benefits.” (Kunin, 1989)

Sadly, Johnson’s olive oil won’t have any of this essential, healthy fat. Yet another item he’s got wrong.

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References

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