Everyone carries personal biases based on their beliefs and history. Layne Norton argues that these internal convictions are often more powerful drivers of behavior than financial incentives. While many people point to funding as a source of bias, the way people argue online for free shows how deeply individuals hold onto their views without any money involved.

I think that personal beliefs are actually just as powerful, if not more powerful. I mean, look at how many people spend hours online arguing over politics that get zero money from arguing about politics.

Layne shares that his own history should technically lean toward a bias against seed oils. His past research was funded by the National Dairy Council and the National Cattlemen's Beef Association. He spent years in a lab that supported low carb diets and questioned the impact of saturated fat. However, he changed his mind as the evidence evolved. He stresses that the scientific method is perfect, but it is performed by imperfect people. To find the truth, one must look at the overall consensus and converging lines of evidence rather than searching for a single study that supports a specific wish.

There are four primary arguments often raised to suggest that seed oils may be harmful. The first involves mortality data from large randomized controlled trials. During the period when researchers realized saturated fat raised cholesterol, they attempted to substitute it with seed oils. While this substitution, such as choosing margarine over butter, successfully lowered cholesterol, it did not always result in lower mortality rates.

When we go back and look at the literature, particularly in the era when people began to appreciate that saturated fat raised LDL cholesterol, the question became if we can substitute something else. These studies, while lowering cholesterol, did not lower mortality.

The second argument focuses on the biochemistry of LDL particles and the process of oxidation. This perspective looks at what specifically happens to a particle to make it pathologic. The third argument questions the industrial refining process. It asks whether the commercial methods used to create seed oils introduce harmful byproducts. Finally, an evolutionary perspective suggests that because seed oils did not exist a century ago when people were generally healthier, their introduction might be problematic.

The Minnesota Heart Study is a unique piece of nutritional research from the 1960s because it was conducted in a highly controlled environment with institutionalized patients. Researchers divided subjects into two groups to test the effects of fat substitution. One group consumed a diet high in saturated fats like butter and meat. The other group replaced those fats with polyunsaturated options, primarily corn oil and margarine. While the study found that total cholesterol dropped significantly in the polyunsaturated group, the results regarding mortality were unexpected and remained unpublished for over a decade.

The biggest thing that really confounds all these outcomes is the inclusion of trans fats. The polyunsaturated fat group was getting quite a bit of their polyunsaturated fats from margarine. Margarine at the time was around 25 to 40 percent trans fats. We know that trans fats are absolutely atherogenic.

Layne explains that for every 30 milligram per deciliter decrease in total cholesterol, there was a 22 percent increase in mortality. This outcome often leads people to argue that polyunsaturated fats are harmful. However, the high concentration of trans fats in the margarine used at the time likely skewed the data. Trans fats are a specific subset of polyunsaturated fats that do not occur naturally in the same way. In a typical unsaturated fat, a double bond creates a physical kink in the fatty acid tail. This kink is essential because it maintains the fluidity of cell membranes and lipoproteins.

Saturated fats have no double bonds and are more likely to be solid at room temperature. In contrast, natural unsaturated fats have what are called cis double bonds. These force the structure to bend. Trans fats are problematic because even though they have a double bond, they remain straight and look structurally similar to a saturated fat. This structural difference affects how these fats aggregate and interact with LDL receptors, which is a key factor in the progression of cardiovascular disease.

Trans fats are unique in the research literature because they show a very clear link to heart disease. This effect was so significant that the FDA eventually banned them. Historically, these fats emerged as a substitute when saturated fats were being demonized. Food manufacturers wanted a product that was not saturated but behaved like it. Butter is a prime example of a saturated product that is popular because it stays solid at room temperature. To mimic this, makers created margarine, which initially contained high amounts of trans fats.

In an effort to create something that looked, felt, tasted, and behaved like butter, and we were gonna deprive you of saturated fat, we had to put in something that at least behaved like saturated fat. Initially thought that was a win because you got the benefit of solid at room temperature. It was only after a few years, we realized actually this was creating far more heart disease than we were seeing, even with saturated fat.

The problem lies in how trans fats interact with cell membranes. Saturated and trans fats have tails that pack together tightly, making the membrane very rigid. In contrast, mono and polyunsaturated fats have kinks in their structure that create space. This space is essential for how the body recognizes particles through LDL receptors. Layne notes that trans fats create a dangerous combination. They pack together like saturated fats but also have double bonds that can be oxidized. This makes them more harmful than the ingredients they were meant to replace.

The Minnesota Coronary Experiment (MCE) began in 1966. At that time, researchers knew saturated fat raised cholesterol. They did not yet realize that trans fats were harmful. The participants in the low saturated fat group likely consumed many trans fats through corn oil and margarine. Layne notes that we do not have the exact numbers for these trans fats. They were just a likely part of the fat intake.

There was also a significant challenge with study adherence. During the trial, laws changed to allow psychiatric patients to check themselves out of wards. This meant researchers could not track what they ate while they were away. Layne explains that while randomization should help distribute this issue across both groups, it remains a notable factor.

We have to remember this study started in 1966. This was very shortly after it was identified and accepted that saturated fat raised cholesterol and that that seemed to have a pretty strong association with heart disease. When it came to doing this study, they had no reason to suspect that these trans fats were going to be uniquely deleterious.

Another major hurdle in research is the duration of the trials. Cardiovascular disease develops over decades rather than a few years. Layne compares heart health to investing. If two people invest at slightly different rates, the difference is small after two years. However, the gap is massive after 40 years. Heart disease risk is a total lifetime exposure risk.

If you and I start investing same time and I get into a mutual fund that gets me a 9% return and you invest in something that gets 8.5%, if we look a couple years out, there is really not going to be that much difference. But if we look 40 years out, there is going to be a major difference.

The study had an average follow-up time of only one to two years. This is a very short period to see real changes in heart disease or to find significant differences in death rates.

The Sydney Heart Study focused on men who had recently suffered a heart attack. This high risk group was divided into two. One group reduced saturated fat and replaced it with polyunsaturated fat from safflower oil and margarine. Surprisingly, the group eating more safflower oil had a higher mortality rate. This finding is often used to argue against the safety of seed oils.

However, Layne explains that this study had a significant flaw. The margarine used by the participants contained 25 to 40 percent trans fats. At the time, researchers did not realize how dangerous trans fats were. This makes it impossible to know if the polyunsaturated fats were the problem or if the trans fats caused the deaths. The small number of total deaths in the study also means the results could be due to sampling error.

The main criticism of the study is the inclusion of trans fats. A large portion of what they consumed was safflower based margarine, which at the time was 25 to 40 percent trans fats. It is really difficult to pick out if this is a polyunsaturated fat problem or specifically a trans fat problem.

Layne also notes the issue of reverse causality. In older or very sick populations, low cholesterol can be a sign of wasting or poor health. It may be an indicator of an existing disease rather than the cause of it. This complicates the data. Low cholesterol in these specific groups might be associated with higher mortality for reasons unrelated to diet.

When looking at all the evidence, the overall impact of replacing saturated fats with polyunsaturated fats appears neutral. Large analyses of human trials show no significant effect one way or the other. If seed oils were uniquely harmful, the combined data from these trials would show a clear trend of increased risk.

If we include all the human randomized control trials looking at substituting polyunsaturated fats for saturated fat, the overall effect is null. There was no effect one way or the other.

The Rose corn oil trial is a prime example of why small sample sizes can lead to misleading conclusions. In this study of only about 70 people, there were six cardiac deaths in the corn oil group compared to only one in the control group. While a sixfold increase sounds alarming, the tiny number of participants means the results were not statistically significant. Even the olive oil group in this trial had three times more deaths than the control, which contradicts most established science. This highlights how small samples are prone to errors that would likely disappear in a larger study.

If you torture the data enough, it will confess what you want it to show. If you just say there was six times the number of deaths in the polyunsaturated group, you are technically correct, but you are leaving out a really big portion of the data.

Layne explains that many studies showing negative effects of seed oils are confounded by trans fats. For instance, the Sydney Heart Study showed a 74 percent increase in risk, but the diets used were comprised of 25 to 50 percent trans fats. When meta-analyses remove these variables and focus on trials where polyunsaturated fats replace saturated fats without trans fats, a clear benefit of around 20 percent reduced mortality risk often emerges.

The VA study provides a more robust look at the data with 850 participants followed for nine years. This study did not include trans fats and showed an 18 percent reduction in overall risk. While this specific result did not reach statistical significance because it was likely underpowered, it points toward a trend of benefit rather than harm. Larger meta-analyses are necessary because single trials often lack the power to provide definitive answers on hard endpoints like mortality.

Crossover designs in research provide significant statistical power by having participants follow both the experimental and control diets. This approach allows every person to act as their own control. It reduces the risk that baseline differences or lifestyle factors like stress will skew the results. While some studies fail to randomize individuals, researchers often manage logistical challenges by switching entire groups between treatments after several years.

The largest benefit is that each person is their own control. When you cross over, you are very confident that inherent baseline characteristics are no longer a confounding variable. It is likely that the people's overall lifestyles are going to be similar throughout the course of the experiment.

The Finnish Heart Study used this design over twelve years. One group cut saturated fat intake from 18 percent to 9 percent and increased polyunsaturated fats. This shift resulted in a 41 percent reduction in the risk of cardiovascular disease. This study highlights why long term, well controlled trials often show different results than older studies that may have been confounded by trans fats. Layne notes that the net effect on health is more important than focusing on a single biological pathway.

Mechanisms are like single stocks, and an outcome like a cardiovascular disease event is like a mutual fund. I could take a mutual fund that is doing really well, but I could find a few stocks in it that are down 50 percent. What matters more is that the overall mutual fund is killing it.

This perspective helps explain why some nutrients might activate seemingly negative pathways while still producing positive health outcomes. For example, smoking consistently appears to decrease the risk of Parkinson's disease due to the nicotine. However, the overall health impact of smoking remains overwhelmingly negative. In nutrition, it is essential to look at the total outcome rather than isolated markers.

Nutrition science relies heavily on substitution. When saturated fat is removed from a diet, it must be replaced with something else. Research shows that replacing saturated fats with polyunsaturated fats leads to a net positive for heart health. This effect is similar to how aspirin acts as an anticoagulant overall even though it also activates some pathways that promote clotting. On balance, the evidence suggests that polyunsaturated fats are cardio-protective when they replace saturated fats.

If I just wanted to pick out and say, look, it activates these pathways. Not that it doesn't matter, but on balance, it is a net positive for anticoagulation. And so when it comes to looking at polyunsaturated fats versus saturated fats, there are mechanisms that suggest that polyunsaturated fats can have a negative effect. But on balance, there are more mechanisms that show saturated fat to be a negative.

The outcomes vary depending on what replaces the saturated fat. Swapping saturated fat for simple carbohydrates often results in no real change in risk. However, using fiber-dense carbohydrates or monounsaturated fats generally shows a reduction in cardiovascular risk. Polyunsaturated fats appear to be the most powerful option for improving health outcomes in cohort studies. Layne points out that it is nearly impossible to separate whether polyunsaturated fats are inherently beneficial or if saturated fats are inherently negative because the two are linked through substitution.

Even if there was no net, if polyunsaturated fats didn't do anything cardio-protective, it's still cardio-protective in that when you put them in in place of saturated fat, you have improvements in outcomes.

Meta-analyses provide further clarity when they control for specific variables. The 2017 Cochrane analysis specifically excluded studies involving trans fats. It found a significant benefit to heart health with a risk reduction of roughly 30 percent. Other analyses that included trans fats showed a null effect. This highlights the importance of distinguishing between different types of fats when evaluating health research.

Clinical research often involves a trade-off between the significance of an outcome and the ease of measuring it. All-cause mortality is the most definitive measuring stick, but it is a high bar for any single study to clear. Because of this, researchers use a hierarchy of endpoints. They might look at disease-specific mortality, then major adverse cardiac events like strokes, and finally more granular data like the actual progression of plaque in the arteries.

Mortality and cardiovascular disease events are big blunt instruments. You could have somebody get right up to the point where they have a 99 percent blockage but no heart attack in the time where they were measuring it. In reality, they had disease progression.

Measuring disease progression allows for a more detailed look at the disease process compared to waiting for a major health event. This is why studies that track plaque growth are useful even if they do not show a change in death rates. Additionally, nutritional studies must be careful with how they categorize nutrients. For example, Layne points out that plant-based omega-3s do not convert efficiently into the EPA and DHA found in marine sources, which can complicate the results if researchers do not distinguish between them.

Mendelian randomization studies offer a unique way to understand the long term effects of LDL cholesterol. These studies take advantage of the fact that genetic variants are randomly assigned at birth. Because Mother Nature does the randomizing, these studies act like a lifelong randomized control trial. This helps researchers avoid the usual problems with confounding variables found in typical observational studies.

The benefit to Mendelian randomization is that essentially you have a lifelong randomized control trial. Now, Mendelian randomization takes advantage of the fact that at birth, genetic variants are randomly assigned.

For these studies to be valid, the genes must only influence the outcome through the variable of interest. This is known as avoiding pleiotropy. Evidence shows that it does not matter how a genetic variant lowers LDL, whether through better clearance or lower production. The result is always a consistent reduction in heart disease risk. This consistency suggests a strong causal link. For every reduction of about 39 milligrams per deciliter in LDL, there is a 50 to 55 percent reduction in cardiovascular disease risk.

A specific nuance involves ApoB, which is the protein found on every LDL particle. If a genetic variant lowers the total amount of cholesterol but does not lower the number of particles, the risk reduction is much smaller. This shows that the particle count itself is a central part of the heart disease mechanism.

If you lower cholesterol mass, but your APOB doesn't drop that much, you basically have just made each particle smaller. In that particular subset of variants, there is a small risk reduction, but it's basically explained by the small decrease in APOB.

Peter notes that this methodology also helped clear up confusion regarding cancer. Previous data suggested that low cholesterol might cause cancer. However, Mendelian randomization showed there was no causal relationship between LDL levels and cancer development. This allowed researchers to focus on the clear benefits of lowering LDL for heart health.

Mendelian randomization studies show a much larger reduction in heart disease risk than statin trials for the same drop in LDL cholesterol. While genetic studies show a 50 to 55 percent reduction, statin trials typically show about 22 percent. This difference is primarily a result of time. Genetic variants affect a person from the day they are born, whereas most people do not start taking statins until they are middle-aged. By the time someone starts a statin at age 40, their blood vessels have already faced decades of LDL exposure.

The reason you see such a powerful effect is just a time effect. If you start investing from the day you were born, in 70 years, you're going to see a massive difference due to compounding interest. These problems compound over time. When you put someone with high LDL on a statin, you're pumping the brakes, but that truck still started rolling down the hill. Whereas with people who have lifelong low LDL, it never really got started.

Layne explains that even with a healthy diet and good metabolic health, high LDL remains an independent risk factor. The number of particles in the bloodstream matters because any particle under 70 nanometers can penetrate the artery wall and contribute to atherosclerosis. Some skeptics argue that statins work by lowering inflammation rather than lowering LDL. However, the data shows consistent benefits across all methods of lowering LDL, including genetics, drugs, surgery, and dietary changes. This consistency across different mechanisms makes it highly probable that LDL concentration itself is the cause of the risk.

It is a very consistent effect and the dose is also very consistent. It's hard for us to ever actually say something causes something else. We feel very strongly about smoking because of the dose effect and the consistency of the results.

When evidence converges from multiple types of studies, it becomes difficult to argue against a causal link. Just as dietary fiber shows a consistent dose response in reducing disease risk across almost all research, LDL shows a consistent link to cardiovascular mortality. While it is technically possible that other factors are at play, the probability is low based on the sheer consistency of the data.

The theory that seed oils cause heart disease centers on linoleic acid. This polyunsaturated fat can convert into arachidonic acid, which is a precursor to inflammatory compounds called prostaglandins. Because polyunsaturated fats are more prone to oxidation than saturated fats, some argue that substituting them creates unstable lipoproteins. This process would theoretically lead to more oxidized LDL and accelerate atherosclerosis.

If that were true, what we would expect to see is people who eat more linoleic acid have higher rates of heart disease. And what we see is the opposite.

Layne points to large studies involving over a million people showing that those with higher linoleic acid intake actually have lower rates of cardiovascular disease. This trend holds true even when looking at tissue samples rather than just dietary recall. While some suggest a healthy user bias might explain these results, the protective effect is consistent across various lines of evidence. Furthermore, eating more linoleic acid does not actually increase arachidonic acid levels because that conversion process is already saturated. The theoretical pathway to inflammation does not appear to have a feed forward effect in the body.

The lipid hypothesis suggests that lipoproteins containing an APOB protein can penetrate the lining of blood vessels if they are small enough. Penetrating the lining is not the only factor in heart disease. These particles can often move back out into the bloodstream. Disease progression happens when those particles are modified by enzymes and retained within the vessel wall. This retention causes oxidation and attracts immune cells that engulf the particles. This process creates foam cells and eventually leads to the thickening of the blood vessel.

Layne notes that while polyunsaturated fats are more prone to oxidation, very little of this happens in the plasma. Less than one percent of LDL is oxidized in the bloodstream because it moves through so quickly and is protected by antioxidants like vitamins C and E. The oxidation mostly happens once a particle is trapped inside the vessel wall. Polyunsaturated fats also increase membrane fluidity. This helps the body clear LDL from the blood more efficiently.

Saturated fats make LDL particles more rigid. When enzymes act on these rigid particles inside the vessel wall, they produce ceramides. These ceramides cause the particles to clump together much more easily than particles made with polyunsaturated fats. This clumping, called aggregation, is a major step in the development of heart disease.

Think about the LDL cholesterol in your bloodstream being a bonfire and there is a whole forest around it. The forest around it is your blood vessels. If you start a forest fire, that is cardiovascular disease. Now, bonfires give off sparks. Let us say each spark is an LDL particle. You do not want the forest to catch on fire.

Layne uses this bonfire analogy to explain that saturated fat creates a large fire that throws off many sparks. Polyunsaturated fat creates a much smaller bonfire. Even if each individual spark from a polyunsaturated fire is slightly more flammable, the total number of sparks is much lower. This means the risk of starting a forest fire is significantly reduced.

When you eat high polyunsaturated fats versus saturated fat, your bonfire shrinks quite a bit. The amount of LDL in your bloodstream shrinks quite a bit. You give off way less sparks. Way less sparks hit the forest. Some of those sparks are much more likely to bounce back into the fire compared to staying in the forest where they can start a fire.

The rate of LDL oxidation is significantly higher once a particle enters the arterial wall compared to when it is in the bloodstream. While some studies show that consuming soybean oil can slightly increase oxidized LDL in the periphery, this increase is minimal. Estimates suggest that 30% to 80% of oxidation occurs after the particle enters the intima. If peripheral oxidation were the main driver of heart disease, antioxidant supplements would likely show a benefit in human trials, but they generally do not.

Your biggest lever to actually reduce your overall amount of oxidized LDL is just to prevent as much getting into the intima and retained as possible.

The most effective strategy for heart health is reducing the number of particles that enter and stay in the arterial lining. Even if polyunsaturated fats are technically more prone to oxidation per particle, they are still preferable on balance. Layne explains that they lower the total amount of LDL that enters the intima. They are also less likely to lead to enzymatic modification of ApoB, which is the protein that helps particles stick to the arterial wall.

Saturated fat-enriched particles create more rigid membranes. These rigid particles are more likely to aggregate or clump together, which leads to the formation of fatty streaks and lesions. Polyunsaturated fats improve membrane fluidity and are less likely to cause this clumping. The focus should remain on the total number of particles and their likelihood of being retained rather than just their susceptibility to oxidation.

The production of seed oils like corn oil involves heavy industrial processing. This includes heating, refining, and using solvents such as hexane to extract the oil. These processes raise questions about whether the manufacturing itself contributes to negative health impacts, regardless of the oil fat content.

Food processing is big industrial chemistry. The actual processing of the seed oils removes oxidants and removes some impurities that are maybe negative.

Layne explains that while these methods are industrial, the refining steps are designed to strip away impurities and oxidants. This suggests that the processing might actually improve the stability and purity of the oil rather than just adding harmful residues.

Extracting oil from seeds requires either mechanical or chemical processes. Most producers choose chemical extraction using hexane because it is more efficient and cost-effective. While mechanical extraction is available, the lower yield makes it a more expensive option for consumers. Even if people prefer avoiding chemicals, the reality of production economics often dictates which methods are used at scale.

I think most people would say, well, I'd rather have the mechanical extraction because less chemicals, but it is much more costly, the yield is lower, and economics is a thing.

It may be possible to find oils like safflower oil that were mechanically extracted in certain stores, but shoppers should expect to pay a premium for those products.

Hexane is commonly used to extract seed oils because it is a nonpolar solvent. Most biological substances are polar and interact with water, but oils require a different approach. Hexane mixes well with these oils and has a relatively low boiling point, which makes it easy to remove later in the process. Once the oil is extracted, steam vapor is bubbled through it to evaporate the solvent. While critics worry about the heat used in this process causing oxidation, most oils require temperatures over 200 degrees Celsius for several hours to see significant oxidation. The hexane removal process happens quickly and at much lower temperatures.

As anybody who has had basic chemistry knows, no compound you synthesize is 100% pure. You can get 99.999%, but you always have residual atoms in there. So the question becomes how much hexane is in the end product and how much is required to cause harm?

Layne points out that residual hexane levels in oil are usually under one part per million, and often so low they are undetectable. Hexane toxicity is primarily a risk through inhalation rather than ingestion. In animal studies, reaching even mild liver or neurotoxicity requires extremely high doses. Layne calculated that for a human to experience mild side effects from the hexane found in seed oils, they would need to consume 11,340 kilograms of oil at one time. Even when considering lifetime exposure, hexane does not bioaccumulate in the body. The body processes it into harmless substances and clears it out quickly. Given the tiny concentrations and the way our biology handles the compound, the risk of negative health outcomes from residual hexane is virtually nonexistent.

Linoleic acid consumption has seen a massive increase of up to 75 times over the last 150 years. This shift means humans now consume seed oils in quantities far beyond what was available during our evolution. For some people, these oils now account for 10 to 15 percent of their total caloric intake. While it is tempting to view this change as purely negative based on naturalistic arguments, Layne notes that almost nothing in the modern diet is truly ancestral. Even animal products have changed significantly. Modern cows are much different than the wild game our ancestors hunted, meaning a fatty ribeye is not a historical food source.

If you think having a fatty ribeye is an ancestral diet, it is not. Those cows are much different than they used to be. And it is not wild game. These are very different things.

The core objective of biology is the transmission of genetic material to the next generation. Longevity is not a primary focus of evolution because a species only needs to survive long enough to reproduce and perhaps help raise the next generation. Once an individual passes breeding age, the biological pressure to maintain health begins to decline. This explains why many successful species do not live long lives as long as they effectively pass on favorable traits.

The idea of longevity, living a very long life, that is not really something that is essential to a species surviving or even thriving. What matters is that they get to pass on their genetic material.

Cardiovascular disease rates have risen primarily because people are living long enough to develop it. In the past, death often came from viruses, bacteria, or conflict. Even in the 1800s, people did not have the diagnostic tools to understand heart disease. They simply fell over dead, and no one knew why. Layne points out that if you live long enough, almost everyone will develop some form of cardiovascular disease. It is often a matter of time and exposure.

Cardiovascular disease is a 20th century disease, didn't exist before that. No, it existed. People just fell over dead and nobody knew why. And for the most part, people didn't have much chance to get cardiovascular disease.

We often romanticize the past and assume our ancestors were healthier simply because they were more natural. However, what is natural is not always the best indicator of a long life. For example, high LDL cholesterol is not an ancestral trait. The Hadza tribe, who live a lifestyle mostly untouched by modern humanity, have incredibly low LDL levels and almost no heart disease. This suggests that the environment we evolved in was quite different from the one we inhabit today.

Concerns about seed oil processing often focus on chemicals like sodium hydroxide used during manufacturing. These substances exist in the final product in such tiny amounts that they are functionally harmless. The refining process actually reduces oxidation markers in the oil by a factor of five to ten. While some trans fats are formed during processing, the levels are far below the threshold of causing negative effects.

If we have this refined oil with a very small amount of trans fat, but we know it lowers LDL so much, and then we have all the other mechanistic data, the mechanism is clearly elucidated. The cohort trials agree with it, and the studies that are not confounded by massive amounts of trans fats agree.

When saturated fats are replaced with polyunsaturated fats like linoleic acid, health markers generally improve. This includes positive effects on inflammation, liver fat, and insulin sensitivity. If someone argues that these oils are harmful, they must also accept the evidence that saturated fat is significantly worse for metabolic health.

Seed oils have become culturally unpopular, but the scientific evidence suggests they are more cardio protective than saturated fats. If someone chooses to avoid seed oils, they should still try to displace the saturated fat in their diet. Leaner cuts of meat and monounsaturated fats like olive oil or avocado oil are better alternatives. While monounsaturated fats are not as cardio protective as polyunsaturated fats, they still help lower LDL cholesterol when they replace saturated fats.

If you don't want to consume seed oils, fine, but find something to displace the saturated fat in your diet with. Try and find some monounsaturated fats like olive oil or avocado oil. These are still relatively cardio protective or beneficial.

A major concern with oils involves heating and oxidation. In industrial processing, these oils are often heated under a vacuum without oxygen, which prevents oxidation. However, frying at home or in restaurants can be problematic. Using a thin layer of oil or reusing the same oil repeatedly for long periods creates negative products. If you are choosing between French fries cooked in lard versus seed oil, both options are unhealthy because fries are hypercaloric. Layne points out that marketing fries cooked in beef tallow as a health victory is dangerous. It may lead people to believe they can eat more of them.

The danger becomes, this really only becomes a problem if you're consuming French fries pretty regularly. When you are marketing it as some kind of victory because you are using beef tallow instead of seed oils, people are going to interpret that as these are actually healthier and now I can eat more of them.

Communicating these nuances on social media is difficult. A thirty second clip about toxic seed oils gets more attention than a deep discussion. Many people lose trust in science because they see contradicting headlines, but these headlines often ignore the specific design of the study. High quality science depends on converging lines of evidence. Layne explains that while you can never prove anything in science, we can have high confidence when data from different types of trials all point to the same conclusion, such as the link between certain proteins and heart disease.

People often focus on the tiny details of nutrition while ignoring the most significant factors affecting their health. The average person consumes about 3,500 calories a day and spends less than 20 minutes being physically active. Worrying about what oil fries are cooked in while ignoring these metrics is like stepping over hundred dollar bills to pick up pennies. It is vital to focus mind space on the habits that move the health lever the most.

We're stepping over $100 bills, picking up pennies. I'm not saying don't worry about the little stuff, but you have to keep it in context of what really is driving so much disease in developed countries. A lot of it really is an energy toxicity issue.

Layne explains that caloric imbalance and low activity levels contribute far more to declining health than the consumption of seed oils. While every scientific study has limitations, the data on obesity and inactivity is clear. Severe obesity can increase the risk of mortality by 80 to 200 percent. In contrast, focusing on physical strength and cardiovascular fitness is one of the best ways to predict a long life. Metrics like grip strength and VO2 max are enormous indicators of longevity.

While other factors like blood pressure and insulin sensitivity matter, managing markers like APOB and LDL levels remains essential. Lowering LDL is statistically better for health, even if some individuals live long lives with high levels. Layne compares this to smoking. Some smokers live to be old, but the probability of a negative outcome is much higher for the group as a whole.

Everything else being equal, having your LDL lower is better than having it higher. Statistics are just probabilities. These are not hard certainties. Of course you can always find an individual to show a difference, but you want the probabilities in your favor.

Restricting seed oils often leads to a net health benefit because these oils typically appear in low quality, ultra-processed foods. When someone chooses to avoid seed oils, they naturally stop eating items like potato chips, Oreos, and processed sauces. This creates a positive substitution effect where the diet improves simply because junk food is removed.

There is another confounder with seed oils, which is that they tend to show up in low quality foods. And therefore, if you make the decision to restrict your seed oils, you are probably doing a net benefit to yourself because you are simply going to eat less Oreos, less potato chips, less junky salad dressings and crappy sauces and things like that.

Layne compares this phenomenon to how people view sugar. Many people feel better after cutting out sugary junk food, but some take the restriction to an extreme by avoiding fruit. While the sugar itself might be biochemically similar once digested, the context of the food matters. Most negative effects attributed to seed oils likely come from the overall poor quality of the diet rather than the oils themselves.

People cut out sugar and they say, well, it felt better. You cut out a bunch of junk food, but then you have people who get maniacal with it and start cutting out fruit because fruit has sugar. Biochemically, it is basically the same thing once it gets in your body. Now there is a bridge too far.

There is no need to be obsessive about avoiding seed oils in high quality settings. If a good restaurant uses seed oils or if they are used in a home-made salad dressing, the data does not suggest they are harmful. The focus should remain on the overall quality of the ingredients rather than the presence of a specific oil.