Why Linoleic Acid: is A Toxic Metabolic Poison?

I became aware of linoleic Acid around 2015 even though I had heard of it and knew it was not exactly good for us, I did not understand the devastating effects it has on our health and until then I always believed sugar was one of the worst food sources that we consume on a daily bases which it is but after many years researching and looking into the literature linoleic acid is considerably more destructive than I would ever of known without looking into the information I examined, without saying our diets or food choices continually change and adjust however anyone being aware even of the basics of  the following will give you a good idea of the damage caused by this toxic metablic poison. 

One of the most exciting developments in helping you achieve your health and prevent the devastation of the epidemic of chronic disease that we’ve encountered over the last century. And it’s a topic that most interested holistic and health care practitioners who focus on natural medicine understand, but only lightly, and didn’t get it. didn’t understand the avoidance of this toxic metabolic poison that virtually everyone doesn’t understand and is completely exposed to, and that toxin is a special fat, an essential fat, called linoleic acid. It’s an omega-6 polyunsaturated fat, which you may or may not have heard about, but you’re going to be stunned, people who value nutritional interventions to optimize health understand that vegetable oils, which are loaded with this poison, are something to be avoided. I don’t think it is unquestionable, but what’s failed to appreciate is even if you eliminate the vegetable oils and you avoid them like the plague, you’re still not hitting the mark, there is a massive possibility that you are taking too much of this dangerous fat,  the focus is on the seed oils and the linoleic acid. 

Balancing of the omega-6 to omega-3 ratio that’s been taught for decades, seed oils which have massive amounts of omega-6. and even to this day, many people think, “Oh, the solution for too much omega-6 increases the omega-3,” while that is a dangerous, dangerous strategy.

The ratio is not really what’s important, what’s important is avoiding the omega-6 fats, there are diseases like age-related macular degeneration, where that’s starting to be clearly understood, and you can find papers saying explicitly that the important intervention there that prevents that disease from progressing is the reduction of omega-6 fats and you can’t prevent it by increasing your omega-3 fats. some papers show in animal models, very nasty outcomes, liver failure with a lower omega-6 to omega-3 ratio, but high absolute levels of both fats still allow pathology to progress. So when you talk about omega-6, it really is synonymous with linoleic acid because that is the bulk of the omega-6.  I’m sure some people are pretty well-informed about this stuff, but there are, broadly speaking, three types of fats, saturated fats, which have a full complement of hydrogen atoms, monounsaturated fats, which are missing a single hydrogen atom, and then the polyunsaturated fats, which are missing multiple hydrogen atoms. What that means is that polyunsaturated fats are very susceptible to oxidation, which means that the fat breaks down into subcomponents and those are what we’re going to spend most of this focusing on because it’s the oxidative breakdown products that have the negative effect on human health.

Over the last 160, 170 years, these have gone from being very rare in the human diet to being introduced as a product of refined seed oils, like originally cottonseed oil, which was introduced in the late 1800s into the human diet. At one point they had to pass laws because lard was so adulterated with cottonseed oil. After all, it was a cheap alternative, not to get too into conspiracy things here, but it was literally a repurposing of an industrial waste product, which is what cottonseed oil was, from the cotton industry into something that they figured out they could detoxify or so they thought and feed it to people which ultimately led to the introduction of Crisco in 1911 as a lard alternative, which really brought consumption of these fats as a marketing department, healthy alternative to animal fats, so over the next hundred years, consumption of these seed oils went up and up and up, promoted in large part by the cardiology profession, which had convinced itself that saturated animal fats were the cause of the heart disease epidemic that had overwhelmed in the UK and the USA. 

A lot of it early on was just that it was a cheaper alternative to butter. that’s how margarine was originally invented. It was made from beef fat and refined into something that looked like butter, ultimately they started using vegetable oils, seed oils to produce that same product and it was always promoted as a healthier alternative to animal fats because there was a widespread, after World War II, it was explicitly promoted as the healthy alternative to animal fats and the that it would reduce heart disease. This is regarded as the most catastrophic, devastating impact on human health in the history of the human race, to make that radical change in the exact opposite direction of what is needed to optimize human health. It has killed millions, probably hundreds of millions of people prematurely and still continues to because people don’t understand this.

People don’t understand it, even the medical professionals, there’s a vast literature to discuss a tiny little portion of out there. Everything that we’re going to cover today is based on studies that have been done in the medical literature or uncontroversial history of the alteration of the diet over the last 100, 150 years. So this is the mainstream explanation of what is causing our chronic diseases. What I have done that’s distinct is just, I’m an inveterate reader, I’m a speed reader, I like to reading some of the medical journals, everybody needs a hobby, this one’s turned into mine, but what nobody’s really done is gone through and connect all the dots. There are a lot of people who understand little sections of it, but they haven’t gone on to coalesce everything into a common explanation for these pathologies across different disease states and different species even and I think that’s what’s been able to do and which I think that’s kind of the key insight that makes this message really compelling.

It’s a radical step in the right direction to help shift the consciousness around this issue because it’s so important if we’re going to make a massive impact on cutting down the epidemic of this chronic disease. So the summary is omega-6, primarily linoleic acid, 60% to 90% of the omega-6? If you have an omega-6 reading, you’re probably somewhere 60% to 80% of that as linoleic acid.

Highly susceptible to oxidative damage. You just breathe out the wrong way, it’s going to get oxidized. And then these oxidative byproducts are what devastate your health, and to go into the specifics of why. But here’s the key, 150 years ago, as you alluded to, we had minute amounts and to get into some specifics because  it’s important as we tease out the details, it was like 2 to 3 grams a day, 2 to 3 grams a day and now we’re getting 10, 15 and 20 times that, and now that may not sound like a lot because you can eat that much more sugar and still potentially think you’re not having problems, though I’m not a big fan and you aren’t, and most health care professionals have large amounts of sugar, but compared to this, because sugar doesn’t oxidise like these fats do, it has other metabolic consequences, but it is nowhere near as damaging as these fats. and there’s no question that sugar’s not good for you. people who claim that carbohydrates are healthy even in excess, I say, “Look, any food that rots your face isn’t healthy.” But that said, even avoiding sugar diligently for a couple of decades will not prevent you from getting sick, didn’t prevent weight gain and it didn’t prevent some of the other negative effects that are seen when reversing and fixing your diet.

There’s  a researcher Dr Christopher Ramsden, who looked at the change in the human diet over the 20th century and the single biggest change was the introduction and increase of soybean oil, which is primarily an N6 fat. And it went up a thousandfold over the century.

It’s the single biggest change that happened over the 20th century. and the initial level, was like 1% to 3% of energy in the human diet and now it’s up to 15 to 20% of energy in the human diet. It’s been a massive change and a massive change that was never properly understood before its introduction. It’s not obviously acutely toxic, It’s not like you’re going to go drink a bottle of corn oil and keel over dead.

The parallel best to make is with cigarettes, cigarettes will make you nauseous and ill the first time you smoke them, but they won’t give you lung cancer, which takes time and a constant exposure to it. and it’s that pretty much the best metaphor for excess consumption of seed oils is that it takes exposure over time. It’s not going to happen.

 The problem with medical research is that it’s generally done in the short term and a lot of the medical research that we count like the food-related epidemiology, which was the field largely invented by Ancel Keys, didn’t exist when all of these things were introduced in the diet. So it was a complete blind spot that happened. and then when organisations like the FDA (Food and Drug Administration) came around, this was something that was generally regarded as safe.and if you understand these 3 letter organisations then no need to say no anything more, so a lot of research was never done. there was no malign intent here, they thought that they were doing something good, just like doctors used to recommend smoking because they thought it was healthy. there’s an excellent parallel there, and only as the diseases that are related to it become pandemic do we start to realise, 

So to help people understand what this excess consumption does and how it damages your body at a molecular level you’ve quoted some of the associations that are present.  we view it as probably the single largest variable to this epidemic of disease that we’re having. But at a molecular level, it not only damages your metabolism but your body’s ability to generate energy in your mitochondria. And to help understand that, maybe we’re diving in prematurely it’s probably one of the key elements, there’s a very special fat that’s primarily only located in your mitochondria and most of it’s in the inner mitochondrial membrane called cardiolipin, that has four fatty acids, unlike triglycerides which have three and most of its linoleic acid, a common misunderstanding in the scientific literature and you’ll find a lot of papers that say exactly that. There was a wide variety of different, what is known as, species of cardiolipin, which means it is comprised of various fatty acids. Linoleic acid-but the individual fats can vary. So some cardiolipin can contain oleic linoleic or palmitic acid or the acids that we get through fish oils, DHA (docosahexaenoic acid) and EPA, I think EPA (eicosapentaenoic acid) it can be a wide variety of different fats. they have very different effects on mitochondrial function, which is an area that’s not really well understood, but what is seen for instance in the difference between mitochondria in the brain and mitochondria in the heart. The heart seems to really like linoleic acid and preferentially builds cardiolipin with linoleic acid. The brain really dislikes linoleic acid and preferentially builds mitochondria or cardiolipin in the mitochondria with other fats like DHA, which is one of the reasons – to give you an idea of how important this is, 20% of the fat in your entire body is contained in cardiolipin. anybody who doesn’t understand mitochondria, mitochondria are what distinguish us from bacteria,  It’s what allows us to be a multi-cellular creatures. They are what produce the energy in your body, what’s known as ATP (adenosine triphosphate), which is a chemical carrier of energy. To give you an example of how important it is, cyanide, which we all know is highly toxic, cyanide breaks your mitochondria, and that’s why it kills you so fast. It prevents mitochondrial respiration and therefore your entire body shuts down almost instantly. So this is something we want to take good care of because they’re everywhere, in almost every tissue I think, except for red blood cells perhaps, in your body has mitochondria in it. It depends on thousands of mitochondria and things like muscle cells have huge numbers of mitochondria to generate the energy that allows us to walk around and live and breathe into everything else that we do. Some studies show that cardiolipin is directly controlled by the dietary intake of fats. different tissues build cardiolipin in the mitochondria out of different fats. But they can vary that composition in fairly short order through changing the diet in rat models, like in the order of weeks. So you can see changes pretty quickly. it was happening in days. and some of the things took longer, but you can have an immediate effect on your health in my experience and that of others at this point.

What’s unique about linoleic acid and cardiolipin is that it is very susceptible to oxidation when it is in the cardiolipin molecule. Two linoleic acids that are adjacent to each other, and as mentioned, that’s what you find in the heart, can oxidize each other. They’re also attached to proteins in the mitochondria that contain iron and that iron can catalyze the oxidation of cardiolipin. This is a pretty fundamental process in the body. Lots of us have heard of autophagy. 

Oxidation of cardiolipin is one of the things that control autophagy. So it’s one of the signals that your body uses to say, “Uh-oh, something’s wrong with this cell. It needs to be torn down and rebuilt,” which is basically what autophagy is. It’s a mechanism for cleaning up broken cells, and the cell knows that it’s broken when it has too many broken mitochondria and the process that controls that is largely the oxidation of omega-6 fats. So by altering the composition of cardiolipin in your mitochondria to one that’s richer in omega-6 fats, you make it far more susceptible to oxidative damage. there are neat studies where they’ve gone and replaced the linoleic acid in cardiolipin molecules with oleic acid, the fat that is in olive oil, and they find that it makes the cardiolipin molecules extremely resistant to oxidative damage, that is basically what we need to go back to. That’s the model that we evolved with, is low levels of linoleic acid in our diet and therefore in our cardiolipin.

one paper showed that encapsulated this whole model took rats they fed them either a regular rat chow high-carbohydrate diet, or they added polyunsaturated N6 fats to their diet. Just adding the omega-6 fats to the diet caused the mice to become diabetic. They became insulin-resistant, leptin-resistant and obese, and the differences are pretty stark between the fat mice and the skinny mice on the high-carbohydrate rat diet. But rat diabetes is different from human diabetes. Rats don’t get high blood sugar when they get diabetic. So they gave half the rats a poison to make them diabetic bakes them Type 1 diabetic by killing the beta cells in the pancreas. So they killed half their beta cells. All of a sudden they became hypoglycemic. Now, just the high-PUFA diet caused a breakdown in the cardiolipin content in the mitochondria in their hearts. So just adding seed oils caused heart damage through a change in the cardiolipin composition. Adding hyperglycemia on top of that caused necrosis of the heart. They induced heart failure in these rats. Heart failure is one of the biggest health crises that are going on in the industrial world and is going up every year. we now have an animal model of how to induce heart failure in a very short period of time which is “Feed him omega-6 fats and make him hyperglycemic” and boom, you get it almost instantly. in people, it takes a lot longer, but this is one of the cleanest models of how to induce an epidemic disease that there’s not much other explanation for why it’s happening in humans.

This would be a good time to tangent and explain what they find. Because the seed oils, caused it, but the seed oil by itself isn’t the issue. It’s the oxidized by-product.

One of the ones we’re most commonly familiar with is 4HNE, and there are others, but this is the one that’s relatively easy to measure. There’s just a complete, absolute correlation between the elevated levels of 4HNE and heart failure.

Studies are looking at HNE in humans. Now, HNE is the primary breakdown product of linoleic acid after it gets oxidized. Why is this important? It’s highly toxic. Linoleic acid breaks down to HNE, even just in storage. This is well-demonstrated in literature. If you add heat, it breaks down even faster. One of the amusing things about the cardiology profession and polyunsaturated fatty acids is on the one hand, they tell you to eat lots of them because they’re “heart healthy.” On the other hand, they tell you, “Don’t eat fried foods.” Well, what are foods fried in? They’re overwhelmingly fried in vegetable fats nowadays and the problem with that, is that the reason that cardiologists after telling you to eat them tell you not to eat them is because these fats break down into HNE when they’re cooked. Again, this is one of these things where the best source for reading about that is to go read the industrial literature from the oil industry, where you find papers looking at what happens to French fries when they’re fried in vegetable oils and how they become full of this toxic product. And the industry is saying, “Maybe this is a problem, guys. We shouldn’t be eating this stuff.”

It’s an interesting tangent, that there’s an organization extensively designed or whose purpose is to protect public health. It’s called CSPI, Consumers for Science in the Public Interest. and they took out full-page ads in the ‘80s, I think, encouraging McDonald’s to stop cooking their French fries in beef tallow, which is primarily saturated fat and switch to vegetable oils. They are probably responsible for killing prematurely tens of millions of people. even now you can go find papers and literature. Let’s just go through three of them really quickly, which will kind of lead us into the, what diseases are we talking about here. But they’re in cancer, in fatty liver disease, in two different cancer models, in fatty liver disease, You can’t induce those diseases without linoleic acid in the animal models that they use in laboratories. So if you feed a rat beef tallow, you can give it 30% of its calories as alcohol, and it won’t get alcoholic liver disease. You must give them seed oils to induce cancer in animal models of cancer. 

So this is a fundamental process and this is in the animal cancer models from 0% up to 4% or 10%, depending on which model you’re looking at of energy as seed oils increase cancer incidents up until you get to a threshold. So in the breast cancer model, cancer incidents increase up to 4% of calories as seed oils, and then additional seed oils don’t cause any more cancer. Now, what’s the relevance to us? Most people in the are at 8%. So we’re way over what these thresholds in the lab would suggest is a safe level of these fats based on the laboratory work in animals.

Which, it’s important to note, is how toxicology is done. We don’t give things that are suspected to be toxic to people first, generally, outside of the food system, of course. We give it to animals. And then, I can’t think of any product that if you gave it to animals, increased their rate of cancer, gave them fatty liver disease and caused obesity, would make it into the food supply. But that’s where we are right now. We’ve got this huge disconnect between what the lab science tells us we should be doing with this and what our dietary guidelines tell us we should be doing. The scientists are saying, “Oh, look, it’s poison. It causes all the chronic diseases.” And the government’s saying, “Eat it. Eat lots of it.” That’s not a good thing.

So, cancer, HNE is a mutagen. A mutagen is a toxin that causes DNA damage. One of the primary genes that HNE damages are the P53 anti-cancer gene. This is the most common mutation in cancers. It’s found in 15% of cancers. It’s preferentially mutated by HNA, which can explain a lot of the increase in cancer over the last 120 odd years. P53 is literally a cancer prevention gene. It’s how your body regulates cancer. You can all draw your own conclusions about the wisdom of eating something that can cause that to break.

It has been demonstrated in animal models as the cause of obesity. There’s an animal model of obesity, a lab diet called D12492, which was named the Cookie Dough Diet by Stephan Guyenet. Rats love to eat it. It’s like eating cookie dough. It makes them obese. It gives them diabetes. This is the standard diet that’s used by scientists to make rats sick like humans get sick, and that’s an important point is a lot of these studies are going to be fairly recent, that’s why a lot of this is new information to people because a lot of this work has come out recently. So in this 2012 study, Ramsden, the scientist, mentioned before, who looked at the increase in soybean, looked at a mouse model of the increase in linoleic acid in the diet over the 20th century and found out that that is exactly what causes obesity in this mouse model. If you feed the mice lots of saturated fat, they don’t get fat and they don’t get sick. It’s only when you increase the linoleic acid in the diet from 1% to 8% that they become obese.

Now this standard mouse model of fat to induce obesity typically has like 20% of the energy in the diet is N6 seed oils, other people have come along and confirmed that finding and they’ve looked at – now what’s interesting, again, how do we take this from animals to people? Because people aren’t mice and rats in labs. What  Anita R.Alvheim and Ramsden were observing is that back in 2006, I think, there was a drug introduced called Rimonabant, which was an anti-obesity drug. It was a bit of a “miracle drug.”  it’s so important to understand the effects that this drug had on humans. “Large randomized trials with Rimonabant have demonstrated efficacy in the treatment of overweight and obese individuals with weight loss significantly greater than a reduced-calorie diet alone. In addition, multiple other cardio-metabolic parameters were improved in the treatment groups, including increased levels of HDL, reduced triglycerides, reduced weight circumference, improved insulin sensitivity, decreased insulin levels, and in diabetic patients, improvements in HBA1C.” This paper was released in 2007. Unfortunately, Rimonabant had a side effect that caused people to want to kill themselves. So it was withdrawn from the market and it largely killed research for several years into that area.

But what Alvheim did in 2012 was demonstrate that the mechanism behind Rimonabant is to block the metabolism of seed oils into the chemicals in your body and the endocannabinoid system that cause overeating. Now, I had mentioned my experience when I stopped eating seed oils was that I forgot to eat carbohydrates. The effect of Rimonabant in these mouse models is to make them crave carbohydrates and to stimulate them to eat sweet foods and carbohydrates. everybody’s familiar with this effect. Well, not everybody’s familiar with this effect in humans, but everybody’s heard of this effect in humans. It’s called the munchies. And it’s what you get after you smoke pot. Because the endocannabinoid system is the system that marijuana effects and the chemical that Rimonabant blocks is your body’s homologue to the THC (tetrahydrocannabinol) in marijuana.

So essentially what we’ve done to ourselves is given ourselves a chronic case of the munchies, which is blocked by this, unfortunately, a very harmful drug to people. This is as open and closed a case for causation as you’re going to find in the medical literature. We have a human drug that treats this, and as I just read, it treats all these different aspects of this disease. And it works through this one pathway that we have a clear demonstration of in animal models, and that would be great if we could use a drug, but as learned from many decades, the fact that drugs rarely, if ever, if ever are the solution for disease and even when they effectively treat the mechanism, they almost invariably have some side effect that in many, if not most cases, is far worse than the disease they’re designed to treat. In this case suicide, and in this case, the drug is completely pointless because the dietary fix is well-known and is simple.

what’s going on with high linoleic acid content and how does it contributes to the physiology and the anatomical disruption within the intima and the inside of the blood vessels that leads to these plaque formations causing heart disease

There’s a great – all of us hear about good cholesterol, bad cholesterol, and LDL, right? Back in the 1980s, there were a pair of doctors who were also scientists, Dr Brown and Dr Goldstein, who got a Nobel Prize for discovering the LDL receptor. So Brown and Goldstein discovered the LDL receptor. And the next thing that they tried to do, one of the first things that happen in atherosclerosis is your white blood cells, your macrophage, another type of leukocyte, turns into what they call a foam cell and the thought was that this happened because they take up an excessive amount of LDL full of cholesterol and fats, and they become stuffed with it and turn into this foam cell, which is a macrophage often stuffed with fat and cholesterol. That’s what the core of an atherosclerotic plaque is, is dead macrophages and other types of cells that are stuffed with cholesterol and fat. That’s why they blame it on cholesterol and fat, Because that’s what you find. And there’s certainly a certain logic to that. So Brown and Goldstein took some LDL and they took some macrophages and they put them in a vial together, and they waited for the macrophages to turn into foam cells, but they didn’t. It didn’t work. The experiment failed. Shortly after they discovered that they had to modify the LDL, and they didn’t exactly know what the modification was that was happening in the body. But if you modify the LDL, the macrophages will hoover it up and turn into foam cells, which is what’s happening in the body. But the modification they used wasn’t what you see in the body. It was purely a lab-based thing. But what it made clear was that LDL does not initiate atherosclerosis on its own. That’s an important thing to understand. Then two other doctors came along, Dr Steinberg and Dr Witztum. Very brilliant guys. They figured out what kind of modification happens to LDL. It turns out – and then they did some animal experiments, and then they did some human experiments to confirm that this was actually the mechanism that happened in people. So what were these experiments that they did? They first took rabbits and then humans, and they fed them either soybean oil or seed oils and then they measured how fast and how susceptible their LDL was to this modification, which is now called oxidized LDL. And it turns out that olive oil is protective because it doesn’t contain linoleic acid. It turns out that what’s happening in linoleic acid is almost the exact same-Olive oil has linoleic acid,  let’s get into olive oil, We should talk about olive oil separately because olive oil has one unique trait that other fats don’t seem to have in regards to coronary disease. So let’s come back to the olive oil topic. What they discovered is that this oxidized LDL is what is getting hoovered up by the LDL to form foam cells and the LDL’s susceptibility to this process is controlled by the linoleic acid content of the diet in animals and in humans. And that’s a result that’s been repeated several times, so subsequently, that literally, the definition of an atherogenic lipid in your blood is one that contains oxidized omega-6 fats. That’s it. That’s the definition. what they’re saying here is mainstream medicine, but they just don’t understand the consequences of what they’re looking at. They’re not connecting the dots well enough across these different areas of disease and research. So the standard explanation of why you get heart disease and why it progresses the way it does is because the omega-6 fats in your blood get oxidized and become toxic, and progress you through atherosclerosis until it finally kills you. That’s the standard explanation for what causes heart disease. how many cardiologists don’t understand that that’s what the medical literature says is causing this disease, Now, it’s worse if you’re on a high-carbohydrate diet and why a ketogenic diet is somewhat protective against the negative effects of this. But I can’t stress enough that this is the standard explanation for cardiovascular disease in the medical literature. That seed oils oxidize and that’s what causes the pathology.

Now, unfortunately, after  this research, Daniel Steinberg convinced Merck to bring a drug to market called a statin, which some of you may have heard of and statins were found to reduce LDL. And the hypothesis was that that would reduce your susceptibility to cardiovascular disease, which they do to some small extent. But all of a sudden, you’re doing what we talked about prior. You’re fixing the cause of the problem by taking a drug, to put a Band-Aid on the problem. It’s not a good approach. A drug, in this case, has severe metabolic mitochondrial implications. statins are mitochondrial toxins. We talked earlier about how important your mitochondria on. I would definitely want to avoid taking a mitochondrial toxin.

Now, you can compensate for it by taking CoQ10, but still, you’re not treating the cause. You’ve got to treat the cause if you want to get successful. and that’s the engineering approach to things. You don’t keep putting Band-Aids on things. At some point, you have to just stop and say, “Okay, we went down the wrong path, and back it out.”

Cardiovascular disease has gone down a lot since the middle of the 20th century, but it hasn’t been because of statins. I’m sure you know that it’s because of smoking, because it started well before statins were introduced. But statins is a side topic. Let’s not go down that road. But people are curious, why did these guys abandon this line of research, It’s because they decided that applying this Band-Aid of statins was the way to treat the problem. Research, of course, has continued and you can find countless papers talking about the oxidative stress model of cardiovascular disease. And as far as I’m aware, all the mechanisms of why it progresses centre around the oxidation of omega-6 fats. And there are lots of other players in that. Smoking, for instance. Why is smoking so bad for you? Because it kicks off the oxidation of omega-6 fats in your body through these highly toxic chemicals.

Acrolein is thought to be the chemical in cigarette smoke –  acrolein. Biocide is what they call it, meaning it is so toxic it kills anything it comes in contact with. This is why you shouldn’t smoke, because you are sucking a biocide into your lungs. What’s another way to make acrolein? Well, you can take physiological levels of glucose and linoleic acid and mix them in water, and they will generate acrolein on their own. Just let them sit there and they will generate toxins. And that seems to be exactly, as that rodent model mentioned about before where they induced heart disease in a couple of days, that’s exactly what they did. They gave them PUFA and hyperglycemia and boom, they got heart failure in a couple of days. or you could heat vegetable oil and get high levels, so much so that an order of French fries would be equal to several packs of smoking cigarettes with respect to their acrolein concentration.

So it turns out in China, they have a big problem with lung cancer in women who don’t smoke. It’s a big problem over there. Turns out it’s caused by cooking with seed oils. It’s a carcinogen. So oops, that’s a problem. It took them a while to figure this out. But if you cook – they fry with seed oils in, say, a wok, and they are breathing in the fumes and if you don’t have enough adequate ventilation, it gives you lung cancer. It’s odd they don’t put a warning on the Wesson corn oil that you can go buy at the supermarket. Known carcinogen in humans. Please don’t cook with this.

Back to the olive oil because it’s an important one. explaining how to fractionally distil the olive oil separate the dangerous linoleic acid and remove it from that for essentially just an investment of time. There are no other costs involved. The main fat in olive oil is oleic acid. Oleic acid is your body’s favourite fat. Your body makes hoards of oleic acid every day, which is why it’s not considered an essential fat. Oleic acid is much more resistant to oxidation than linoleic acid is, which is why olive oil’s a pretty decent cooking oil. The problem with olive oil is that it does have a fair amount of linoleic acid. The percentages range from 2%, which is awesome, to 22%, which is not good. The other problem is the olive oil market is hugely corrupt and what they often do is they cut olive oil with cheaper seed oils, like soybean oil, they add other chemicals to make it look and smell like olive oil and then they sell it. It’s fraud. It’s food adulteration. But 80% to 90% of the olive oil market is adulterated with seed oils. So you can get better olive oils. Mostly what I do is just buy California olive oils, which typically come out as the top-rated in terms of not being adulterated. But you can’t tell how much linoleic acid it has. The fractionation test is something that thought worked for years, which is that you put your olive oil in the fridge and if it solidifies, that means it’s good fat. The problem is it turns out that neither the healthy or the unhealthy fat solidifies in the fridge. So what that test tells you is how much-saturated fat your olive oil contains, which can be quite a lot. people have had jars of olive oil that turned pretty much solid in the fridge, and some other ones that were what I thought were good brands that didn’t solidify at all in the fridge. The Olive Oil Council of California went and did some research. They hired a guy to do the research and it doesn’t work. 

Why you want to seriously consider avoiding or limiting, severely restricting linoleic acid, a simple strategy. Replicate what our ancestors did. Approach the historical standards of a mere 150 years ago, which is 2 to 3 grams per day. the concern is you could probably go above that without too much harm, but what’s the threshold? Is it 5 grams? Is it 10? anything over 10 has got to be too much. what threshold should we limit our linoleic acid too? How many grams per day?

There’s a tribe of Indians in the Amazon jungle in Bolivia, called the Tsimané. the Tsimané are the poster children for the cardiologists of late because they don’t get heart disease. That’s really cool, and they’re not unique. Americans didn’t get heart disease 150 years ago. The British didn’t get heart disease 150 years ago. But these people still don’t get heart disease. So they’ve been down there for many years studying them. they noticed that as they were getting more exposure to what they call “market foods,” they started getting obese. 

So what do we take away from that? If you don’t want to get heart disease, eat like the Tsimané. That’s a pretty cool thing. They have other health issues, like they don’t often get enough food to eat. But that’s awesome. So let’s look at what they ate. The ancestral model used to be called the paleo model, They were eating as much animal meat and fat as they could get. We talked about oleic acid, how it’s a healthy acid. It’s your body’s favourite fat. Most animal fats, I think beef tallow is 46% oleic acid, lard is 36% oleic acid. Depending on the lard that you get, lard has the same fatty acid profile as olive oil does. So it’s the other healthy fat,

So what should you be eating? What is the Tsimané eating? Well, they eat a fair amount of carbohydrates because they’re very poor people. They live in the jungle and they grow yams and things like that and bananas. They eat as much animal protein and fat as they can get their hands on, and their biggest complaint in life is that they can’t eat as much meat as they want, and they eat lots of vegetables and they don’t eat any seed oils up until recently, which is why they’re starting to get sick. the difference between the paleo diet, lots of anthropologists criticize the whole ancestral health concept because they say we don’t know what these people ate, and they ate all sorts of different things because they lived all over the world. But the point is we do know exactly what they weren’t eating. All of them weren’t eating industrial seed oils because they didn’t exist up until recently. They weren’t eating super high amounts of carbohydrates with some exceptions, and you can track those exceptions through their dental health in the literature. So they weren’t eating lots of refined foods. So the caveat here is that what you eat is not just what you ate, but it’s also what your food ate.

So this is a key point. I presume most of us remember DDT, the anti-mosquito toxin that was banned back, in the ‘70s. The problem with DDT was that DDT concentrated up the food chain. So a mosquito would eat a tiny little bit of it and sick and get eaten by a frog, and so on and so on and so on, until you got to a bald eagle who got this huge bolus of DDT from the foods that it was eating and it died, or its eggs would break. So they banned DDT. Seed oils do the exact same thing.

So there’s the pair mentioned before, Alvheim and Ramsden, along with some other co-authors, did a really interesting study where they took salmon, farmed salmon from Norway, where Alvheim was from, and they fed it soybean oil, which is what they feed farmed salmon, is soy meal. So they fed the salmon and they looked at what happened to it, and it got the typical things that you would expect. It got obese. But then they took the salmon and they fed it to mice, and the mice got obese too. So it bio-accumulated into the mice, concentrated up the food chain. What do we feed our animals? We feed them as many grains as we can. That’s what pigs and chickens are fed. Cattle we only feed them a little bit at the end of their lives. Cattle are ruminants, so they’re somewhat protected against this.

But back to the Cookie Dough Diet, D12492, the manufacturer of that had been telling everybody that the fatty acid composition was, it was 9% or 10% linoleic acid and they were basing this off the USDA (U.S. Department of Agriculture) food database, the thing that we all look at if we want to figure out how much of different nutrients are in a food. That’s all aggregated by the USDA. So they got curious, and they went and they tested the lard that they were using in this diet. The fats used in this diet are lard and soybean oil. And what they discovered was that the percentage of N6 fats in the lard they were using was twice what the USDA said it had been because the food the pigs are eating has changed over the years, and they’re accumulating a lot more N6. Same thing with chickens. And since we know it bio-accumulates, you also need to avoid what I call industrially farmed animals. cows have a rumen, and the bacteria in the rumen protects you from this. Cows also get sick from too much green in their diet, but they get sick in a different way. They don’t bio-accumulate these fats to the same level. The same is true for other ruminants like goats or lambs. So you’ve got to not only – and the same is true for chicken eggs, which is why you want to try and get omega-3 chicken eggs, which are fed with flax instead of less healthy grains or ideally, pastured chicken eggs, which is probably the best option for chicken eggs.

Chickens are the largest source of linoleic acid in diets. the bag of the grains that they’re eating, it’s soy and corn primarily. and even if you have your own chickens and feed them mealworm you have to be mindful of what you feed the mealworm.

lots of health organizations say that you should eat seed oils because it’s an essential fatty acid. That is not correct. That was deduced in a paper done back in 1930 and another paper just came out and showed conclusively that linoleic acid is not, in fact, an essential fatty acid, that what’s essential is a DHA and arachidonic acid, which you get from animal foods. this was looked into the materials and the methods and the diet that they were using wasn’t completely free of linoleic acid. So it’s sort of a moot issue though because you need it. It’s almost impossible not to get linoleic acid. If you eat food, it’s in everything almost, so you don’t have to worry about that. In some ways, it shouldn’t be essential because if you eat, you’re going to get it. The only way to become deficient in linoleic acid is to either be in a lab or under the care of a physician.

with glutathione, that’s a pretty good pearl because so many people use glutathione supplements or glutathione precursors without understanding that well, yes it’s nice to have optimal glutathione, but let’s get rid of the need to use it by lowering our linoleic acid, and then so there are some foods that like beef has low linoleic acid, even if it’s grain-finished beef. If it’s grass-finished, it has higher DHA, which is the main difference, which is an awesome way to get your DHA. Although I will tell people that if you can’t afford grass-finished beef, just eat grain-fed and eat some fish every once in a while. But beef is also the primary source of a chemical called carnosine.

So what does carnosine do? It’s been shown to be anti-atherogenic. It’s a mitochondrial stimulant and it’s a dipeptide, two amino acids put together, beta-alanine and histidine. And it’s a sacrificial scavenger of what, they in the literature call, ALEs, advanced lipo- oxidation end products, which is very similar to AGEs, advanced glycation end products, which is another name for HNE and all the other reactive oxygen species to be generated from oxidizing linoleic acid.

A recent study analyzed and compared the ability of several classical carbonyl scavengers, and we won’t worry about what that is, to prevent the carboxylation of proteins and concluded that carnosine is the most effective scavenger for HNE. So we’re back. Carbonylation of proteins is the process through which proteins in your body get damaged and become ineffective.

It’s a huge deal because there was a paper that looked at how many proteins HNE damages in the cell. It damages 24% of your proteins, they looked at this in various – It has seen work on this in various disease processes, In heart failure, Alzheimer’s and age-related macular degeneration, one of the things they see is an inability of the cell to produce enough energy. The mitochondria are getting damaged, right? HNE does that damage. It damages 24% of the proteins in the cell, primarily around energy production, cancer, one of the worst cancers is glioblastoma, which is brain cancer. so to try and figure out why the mitochondria are getting damaged in glioblastoma, what he found was they all have oxidized cardiolipin. Every single cancer cell he looked at had damaged cardiolipin in it,  another part of the cell that gets damaged, one of the ways your cells produce energy is they ferment glucose into pyruvate, right, outside of the mitochondria, this is a perfectly normal part of metabolism and they produce something called pyruvate and then there’s a molecule called pyruvate dehydrogenase that takes pyruvate into the mitochondria so the mitochondria can burn it very efficiently for fuel.

Well, one of the things that HNE does is break pyruvate dehydrogenase, and they see this in Alzheimer’s where their cells are no longer able to produce enough energy, this is why your cells are dying in Alzheimer’s. The beta-amyloid plaques in Alzheimer’s disease are induced by HNE. There’s a great model that came out of Harvard a couple of years ago showing that. And in cancer, if you can’t get pyruvate out of the cell, out of the cytosol, the part of the cell surrounding the mitochondria, it has to ferment there and turn it into energy, which is what we call the Warburg effect, where you start shifting over to this damaged primitive fuel system. And the evidence seems to be that that’s because you’ve broken your mitochondria, right? Even the critical, the most important part of the mitochondria, complex 5 ADP synthase, which is what takes all the energy coming from your mitochondria and turns it into ATP, which is what fuels the rest of your body. HNE damages that protein. This is a huge issue. There’s no more fundamental problem in ageing and health than protein damage, one of the paradoxes that just baffled my mind for decades was why people could eat a keto or carnivore diet and do essentially high fat, low carbs and do really well, and the converse that people could eat low fat, high carb, and do very well too. They can both take care of diabetes and it turns out, once I understood this linoleic acid, that was the answer, both of those strategies, typically not always, of course, because you can have high LA foods in a carnivore, theoretically is that they both are typically low LA. they address the fundamental reason, but what they don’t address, if you take the vegetarian approach, is carnosine, because virtually, there’s no carnosine in a vegetarian diet or very little almost.

There’s a paper looking at diet and oxidized LDL, which as we’ve discussed is the definition of oxidized LDL is LDL with oxidized seed oils and they couldn’t figure out what was going on because they put these people on a healthy, low fat, vegetarian diet or vegetarian-like diet and their oxidized LDL went up. 

one of the interesting interplays about this and the reason that they need to eat animal fats is that there are other fats that may be essential fats that we need to eat that you can only get through animal fats. So one of the weirder dietary trivia pieces is if you don’t give dolphins this fat called heptadecanoic acid, which is a 17-chain saturated fat, they get diabetes. Why would a dolphin get diabetes? They don’t eat any carbohydrates. They live in the ocean. But the lack of that fat in their diet causes them to get diabetes and that happens in people too. It turns out that people with low levels of these two animal fats, heptadecanoic and pentadecanoic acid, are more predisposed to get type II diabetes. So I think you need to get those.  is this an essential fatty acid? If you don’t get it, you get sick. That’s the definition of an essential fatty acid. So I think if you look at the healthiest vegetarian culture that I’m aware of, the Jains in India, they’ve been at this for 5,000 years, longer than any other vegetarian culture on earth, they know they have to eat dairy food, that they cannot be healthy without it, dairy is, of course, the richest source of heptadecanoic and pentadecanoic acids so you need to make sure you get enough oleic acid. Well, you can do that easily through the diet as well with animal fats because you want to make sure that you’re protecting yourselves against this oxidative pathway,

a strong agreement that you need to have some high-quality animal fats in your diet because it’s not just the fats, heptadecanoic acid and these other fats, but there are other micronutrients–that are in that fat that we probably have yet to discover the benefits that we need and you don’t have to take a supplement. You just take real food.

there’s vitamin K2, there are all sorts of fat-soluble vitamins. there’s a paper years ago looking at eating vegetables and they said, if you eat vegetables without any fat, you don’t absorb any of the fat-saturable vitamins.” You have to eat vegetables with fat to get the maximum nutrient load out of them. So 2 to 3 grams, 150 years ago. I don’t see any downside for someone who’s metabolically ill to lowering their total dietary intake of linoleic acid to under 10 grams, by the way, there’s an easy, easy, easy way to do it. You don’t have to send all your food out for analysis. You just enter it into Cronometer and they’ve got an assay there that says how many grams of omega 6 to the 10th of a gram and you can just assume that 90% of that’s linoleic acid. So what is the downside to limiting your linoleic acid to 5 

You want to keep it as low as possible. to me, that’s the take-home message. This is what you need to do to reap all the benefits of this incredible amount of knowledge captured over the last decade. I do lots of fasting training. They looked at a ketogenic diet in rodents and they found that they were protected and it was fascinating. The reason that they were protected is that they were able to burn HNE as fuel, if you add a little bit more insulin into the system, then it turns fat-burning off and HNE goes out of the mitochondria and does more damage, That’s a reason to work out in a fasted state. working out in a fasted state is one of the most important health things that you can do without question

The take-home message to apply to implement so that you can change your health is the number one thing that you’ve got to do to stay healthy, is you got to limit linoleic acid, You want to eat like your ancestors ate because your ancestors were healthier and they were not eating industrial seed oils. They were not eating industrially processed carbs in high quantities. They were making sure that they got lots of animal meat and animal fat and they were getting exercise. it doesn’t matter what kind of exercise you’re doing, just as long as you’re doing some.