 causes of death, 1900 versus 2010. And this is Joan's paper in 2012. And you notice on the left, 1900, the top three causes of death, pneumonia, tuberculosis, gastrointestinal infections, all are infectious. Whereas in 2010, seven of the top ten causes of death are chronic disease, heart disease, cancer, COPD, diabetes, and so on. We'll come back to this. Now, interestingly, also from Joan's paper, this is a list of the causes of death in Boston in 1811, the town of Boston. And if you notice on the lower left, there is none listed for heart disease. And on the far right, 25 sudden death cases. And in the upper left, cancer, five of 942 deaths. Now we'll come back to this as well. So this is the timeline for heart disease over the past couple of hundred years here in the United States. And so, again, 1811, Boston, no heart disease deaths, but 25 sudden deaths, so that's 2.6 percent, right? So even if all of those are heart disease, it's 2.6 percent of cases. The entire 19th century, there's eight worldwide published papers on Heart Attack. Eight. 1897, Sir William Ostler, famed physician, started Johns Hopkins Hospital, reported in his previous 21 years of hospital experience about six cases of angina, chest pain, but not a single MI, not a single heart attack. 1900, we know from Joan's paper, 12.5 percent of deaths were due to heart disease. But that wasn't coronary artery disease cases. Those were valvular disease, rheumatic fever, endocarditis, syphilis, valvular cases. Again, not coronary artery disease. 1912, John Herrick publishes the first known case of myocardial infarction heart attack in the United States with documented autopsy evidence. 1930s, coronary heart disease now becomes the leading cause of death 30 years earlier, virtually unknown. Why? By 2010, 32 percent of deaths in the U.S. due to coronary heart disease, again, nearly one in three. So if you look at the increase, it looks something like that, and I'll show you the real data later. Now, cancer. 1811, Boston, 0.5 percent of deaths, five of 942. That's one in 188 deaths due to cancer. 1900, it's rising 5.8 percent of deaths. That's one in 17. 2010, 31.1 percent of deaths. That's nearly one in three again. So the increase probably looks something like this. Type 2 diabetes. We know that diabetes of any type was rare in the 19th century and for all of history prior. 1935, it's rising 0.37 percent. Notice it continues to rise up to 2015, we're at 9.4 percent. So in a period of 80 years, there's a 25-fold increase in diabetes. Obesity. We know from the 19th century, from studies in prisoners in Nebraska and Texas, obesity was 1.2 percent in men, 18 to 80 years of age. It rises by 1960, we're at 13 percent. 1988, 23 percent. 2015, 39.8 percent. So over a period of roughly 115 years, obesity is up around 33-fold. Macular degeneration. My area of expertise. So Herman von Helmholtz introduces the ophthalmoscope, 1851. That allows ophthalmologists to see the retina. The next 80 years of potential discovery, there's no more than around 50 cases of macular degeneration in all the world's literature. 1940, Duke Elder calls macular degeneration, quote, a common cause of failure in central vision in old people. 1975, 8.8 percent of Americans over age 52 now have AMD. That's 4.5 million people. 1994, 15 million Americans. Today, around 26 million Americans with macular degeneration. Worldwide, 196 million people with macular degeneration and climbing. So if we look at the timeline for macular degeneration, 1851 to 1930, it affected about one in thousands. By 1990, it's nearly one in three, around 29 percent. All right. So what about processed food during this time? So we know from 1822 to 1999, sugar consumption was rising. It went up 17-fold, nutrient-deficient food, right? Cotton seed oil, our first vegetable oil introduced right after the American Civil War, about 1865, 1866. We got roller mill technology, which created refined white wheat flour and nutrient-deficient food in 1880. 1911, Procter & Gamble introduces Crisco, trans fats, right? So that's our four processed foods right there. Put those together and you've got processed food. Weston Price recognizes all this in his epic research and his treatise, nutrition and physical degeneration, publishes this, connecting these four foods essentially to what became diseases of civilization. Nobody listened, right? Or we wouldn't be in this mess. 2009, our own USDA shows 63 percent of the American diet is made up of these four processed foods and diseases of civilization look something like this, right? They're through the roof. But the human food experiment didn't begin in 1980 when we were told to go low-fat, and it didn't begin in the 1950s when saturated fat was vilified. It began right after the American Civil War when the first vegetable oil was introduced. Now, so here's our data, total vegetable oil consumption. You can see from the 1860s up until about 1909, we're around two grams a day. Steadily rises then with the introduction of all the other vegetable oils up to 80 grams a day by 2010. So we went from zero to 80 grams of vegetable oil a day in 145 years. This is an infinite increase in these. We didn't have them before. 80 grams a day of oil, that's 720 calories, that's 32 percent of U.S. caloric intake. That makes this the single greatest change to nutrition in all of history. I don't think anything else can even begin to compare, and we haven't even talked about the toxicity here. Now, 1900, 99 percent of our added fats came from animal fat. By the way, this is all published data. I'll tell you the one time that it's not published data. Everything here is published. 2005, 86 percent of added fats came from vegetable oils. So the vegetable oils almost completely supplanted animal fats, lard, butter, and beef tallow. Now, I think it didn't happen worldwide. Just in the period between 1963 and 2003, they're in developed countries, vegetable oil consumption doubled. Developing countries, it tripled. Japan, for example, four and a half fold increase. China, in this period of time, almost an eight-fold increase. And Asians are getting sick as we are. So here's Pufa consumption, omega-6 and omega-3 together, from our own USDA, 13 grams a day in 1909, rising to 45 grams a day by 2008. So that's a more than tripling of our Pufas right there. All right. What does this do to us? So these omega-6s, they accumulate in our fat tissue. And this is a study from Stephen Guine, put together. He compiled 37 studies that looked at Linnolake acid, the omega-6 in our adipose tissue and human adipose tissue from 1959 to 2008. Look where it was in 1959, 9.1 percent. Look where we ended up in 2008, 21.5 percent. Now, let me let me let you know that 9.1 percent in 1959 was far too high. I think this number should be more like 4 percent, but we don't have any good data to tell us for sure. All right. So when we consume Linnolake acid, we tend to accumulate it. We just can't burn all these for fuel. All right. So here's what we should be eating. This is from Spethenspielmann in 1983. These are wild ungulates, wild-hoved animals. And look at their Linnolake acid consumption. If you can see it there, highlighted in the green. It ranges from trace to 3.85 percent with an average Linnolake acid of 2 percent. So this is the sort of level of Linnolake acid we should be getting in our diet, around 2 percent. Don't believe it? Here's grass-fed beef, 2.01 percent and 3.41 percent. So this is where we should be getting our Linnolake acid primarily, our omega-6. But instead, here's what the fats look like today. So now the top four on this list, coconut oil, butter, palm, and lard, these are great fats. All the red is the saturated fat. That's what we want. All the blue is the omega-6. And if you look from cotton seed oil down, that's all the vegetable oils that have been added since 1866-ish. All right? And that's all the omega-6 we're getting today, right there. Now, transplant yourself back to 1865 and for all of history prior, this is what we would have gotten. So we would have gotten butter, lard, and beef tallow. This would have been our sources of omega-6 and their approximate amount, concentration, based on grass-fed animals. So butter, about 3 percent. Lard and beef tallow, about 2 percent. So that's what we, that's what we should be getting. Here's what we're getting today. Look at all the blue. And here's what we should be getting. So what did this do to us? This is published data for 1909 and 1999. So the omega-6 in 1909, 4.84 grams a day. Confirmed. This is data from ourselves and from Tonya Blaseball at the NIH. 1999. We're at 18 grams a day. All right? Now, I went back and calculated what we should be getting in 1865 had we been consuming a typical diet then. 2,000 calories, 40 percent of it coming from pastured animal fat, two and a half percent of that coming from linoleic acid, which is what we should be getting. And that gives us 2.2 grams of omega-6 per day. 2.2 grams. So over this period of time, 135 years, this elevated about eight fold. Right. So Barry Popkin's paper says the world is shifting rapidly towards a diet linked with noncommunicable disease. Well, absolutely. And the question is why? So we're going to talk about weight gain first, obesity. This is a very interesting study where there's three groups of rats on isochloric diets that was done back in 1993. And this is a three week study. So these rats got identical amounts of calories, protein, fat, carbs, and omega-3 fats. One variable, omega-6. All right. Three different diets. Beef tallow group, omega-6, 4.4 percent. Olive oil, omega-6, 7.7 percent. And a safflower oil group, the high poofa group, omega-6, 36.6 percent. Okay. So here's the table. So you've got the fat source on the left, beef, olive, and safflower oil. Calories, all the same. Fat. It's a high fat diet, 59 percent. Look at the omega-6. And I'm going to highlight these. So we get 4.4 percent in the beef fat, 36.6 percent in the safflower oil group. Look what it does to their body fat on the far right. 10.3 percent in the beef fat group, 54.5 percent in the high poofa safflower oil group in three weeks. Now I want to point this out. Even the beef fat group, the omega-6 is too high. This should probably be more like two, two and a half percent, which leads me to believe this is KFO raised beef, not grass fed beef. All right. So what is this due to these rats in three weeks? Now, they all gained weight. These are all adult rats. They all gained weight relative to the beef fat group. The olive oil group, seven and a half percent more weight. That's 12.8 pounds human equivalent. The safflower oil group, 12.3 percent more than the beef fat group. That's 21 pounds human equivalent. Steph and G&A also calculated this. So how is this possible? They all consume the same calories. They all consume the same macronutrients. The only difference was the omega-6. Right? So here's the question. How could a high omega-6 poofa diet induce obesity without increasing calories? And the answer is energy dysregulation. And what I mean by that is very, two very simple concepts. One, energy is stored more efficiently. And two, energy utilization expenditure decreases. So when we're gaining weight, getting obese, we have less energy utilization, expenditure, and we store it more easily. Now, I'll show you why. So let me ask you a question. What condition is it that unifies all of these diseases of civilization? Just name it. Meschemic heart disease, heart failure, cancer, aging, obesity, type 2 diabetes, non-alcoholic fatty liver disease, AMD, Parkinson's, Alzheimer's. The list goes on. The answer is mitochondrial dysfunction. Mitochondria are where we produce our energy. Why would all of these diseases share this in common? What's going on in our mitochondria that results in all this disease? So let's go inside the cell and we're going to look at electron transport chain because this is where around 89% of our energy is produced. And I think this is where the answer is. So in order to understand what goes wrong in the mitochondria, we have to understand lipid peroxidation. So when we consume lipids, there's two potential situations. One is they accumulate in our cells and they can undergo peroxidation. They're oxidized. They're damaged. Two, you can burn them for fuel, beta-oxidation. Here's what happens if they accumulate in our cells, lipid peroxidation for one. Now the PUFA is the omega-6 and omega-3. They're very high risk to oxidize. Why? Because of the double bonds. Monoinsaturated and saturated fats have almost zero risk to oxidize, to undergo peroxidation. So as one lipid researcher put it, he said, you want to oxidize the, you know, monounsaturated and saturated fats, throw them in a can of gasoline and light it on fire because that's what it takes. Right? Okay. So if you look at the model, you see the unsaturated lipid in the upper left reacts with a hydroxyl radical. Those are created by the trillions in our bodies every day. That creates a lipid radical which undergoes reaction with oxygen to produce a lipid peroxyl radical. That reacts with yet another unsaturated lipid sitting right next to it. Then that creates propagation. And that propagation creates another lipid radical. So this is a circular reaction. And this entire reaction takes one millisecond. So a thousand molecules a second can be peroxidized. This is very damaging to us. Alright. So keep that in mind. So what this does is this is going to affect a molecule called cardiolipin that is critical to our mitochondrial electron transport chain function. Cardiolipin is a phospholipid that acts like a scaffold upon which our electron transport chain depends. The proteins in the electron transport chain depend entirely on it. And you'll see why. So here's a model. If you look at the cardiolipin molecules I have labeled there on the upper left, they sit next to an electron transport chain carrier protein. And if you'll notice the fatty acid acyl chains fit together neatly, they interdigitate properly. And that's critical. Alright. Now we're going to go down a little bit smaller and we're going to look at these at the molecular level. So this is a cardiolipin molecule on your far left. And you'll notice it has four acyl chains. These acyl chains are fatty acids. And incredibly, they are usually omega six fat. They're usually linoleic acid. But notice what happens. I'll highlight this in the middle picture. If that linoleic acid or whatever fatty acid it is, if it oxidizes, the oxygens are added. This creates a three dimensional conformational change in the molecule. And that makes these not fit together properly. And then on the far right, it can become pathologically remodeled. So interestingly, linoleic acid here is often, there's a substitution of arachidonic acid or docosahexinoic acid. So AA or DHA are substituted for linoleic acid. Alright. And this changes, you can see the chain length now is different. And now you're going to see very simply with this little diagram on the left is how healthy cardiolipin normally looks. But look at it on the far right when it's pathologically remodeled because those fatty acyl chains become oxidized or replaced. That's what happens. And you're going to see how this devastates the electron transport chain. Alright. So cardiolipin normally is a proton trap for oxidative phosphorylation. Oxidative phosphorylation is how we make ATP, the energy currency of the cell. Alright. Now we're inside the cell. And if you notice on the far right of this, what looks like a complicated picture, there's a cardiolipin that's labeled and it's sitting next to complex four in the electron transport chain. Yeah. Assume this is a healthy cardiolipin. Alright. Now on your far left, when we consume food, goes through glycolysis, goes through the Krebs cycle. Now we're inside the mitochondrion. Those processes create NADH and FADH2. NADH and FADH2 are high energy electron carriers. They donate electrons into this electron transport chain. Now if you watch the chain, they're going to donate electrons to complex one, complex two, to ubiquinone, to C3, to cytochrome, to complex four. And then oxygen is the final electron acceptor and that makes water. And that's why, with oxygen there, that's why we need to breathe is because this whole process stops if there's no oxygen there. Now, there's hydrogen. I just put these in the picture. Hydrogen protons all over inside of this, inside these membranes. And when the electrons are transported, they lose a little bit of energy and that energy is used, if you'll watch here, to pump protons, hydrogen protons into this intermembrane space. And so complexes one, three, and four are the ones that pump these hydrogen protons into this space. And this creates a proton gradient. This has electrochemical energy. Okay? And now there's only one place for these protons which want to re-equilibrate. They want to come back through because we've got this gradient. So there's one place they can come back through. And if you look on your friar right, it's complex five, which is ATP synthase. And as these protons come back through, they use that energy to convert ADP to ATP. That's our energy, right there. Okay, this is how the system normally works. All right, now, but what happens when cardiolipin peroxidizes? And I want you to notice that this kind of research is being done in physics labs, physicists, organic chemists and biochemists are working on, this is some of the most complicated in all of science, in my opinion. So here's what happens. So I try to put this together into the simplest model. So we're kind of looking at the same model again, except if you'll notice right away that on the far right, I have a pathologically remodeled cardiolipin. This is a cardiolipin where those fatty acyl chains have been substituted or oxidized. Now it doesn't fit together and there's a membrane pore. There's a gap here. Okay, so here we go. Watch the electrons. They're going to be transported down the electron transport chain. And they're going to eventually end up at complex 4, oxygen's the acceptor. We're going to put the protons into the picture. These hydrogen protons now are going to be pumped through complexes 1, 3 and 4. All right, into the intermembrane space. We're creating our proton gradient in order to try to create energy next, right? Now watch carefully. Watch what happens to the protons. They're going to escape through this remodeled cardiolipin. This pathologically remodeled cardiolipin. So guess what happens? We lose energy. You know, some are going to make energy, some won't. What happens when we can't make energy? The cell gets sick. All right, so this leads to catastrophic cell injury and cell death is what may happen. All right, so I want you to see this study. This is one of the most interesting studies I've ever seen. So this is, this is, this reviews this essentially. So these researchers hypothesized that chronic dietary omega 6 poofa can induce free radical generation predisposing the cardiac mitochondria to oxidative damage. So they had two groups of rats, a normal, a high poofa group with normal lab chow with 20% sunflower oil and a low poofa group with normal lab chow. This is a four week experiment. Here's what happened. So look at the, the, so we've got the low poofa group on the left, the high poofa group on the right. Look at the cardiolipin in the white histograms. So in the high poofa group, the, the cardiolipin is reduced about five fold. It's destroyed. So the high omega 6 destroys the cardiolipin. Look at the linoleic acid. It's reduced about 10 fold. So this is the paradox, which when I first read this, I couldn't understand, but when you consume a whole lot of linoleic acid, it causes this pathological peroxidation cascade and this destroys the, the linoleic acid where you need it in the cardiolipin. So here's lipid hydro peroxides, which is a measure of peroxidation. It's double in the high poofa group. Here's total phospholipids, which are critical to cell membrane function reduced about three fold in the high poofa diet. Now this needs a little bit of explaining. So across the top in the red, 8 OHG and nitrothyrosine staining and the composite. So if you look at the bottom, 8, 8 OHG is 8 hydroxygonazine, which is a measure of mitochondrial and nuclear DNA damage. Nitrothyrosine is a measure of oxidized lipids and proteins. Now if you look at the low poofa and the high poofa group, notice that the low poofa group has no staining. They have no damage to the DNA or lipids or proteins. High poofa group has marked staining, marked damage to their DNA and to their lipids and proteins. There's oxidation everywhere in the high poofa group. So what does this do to them? In four weeks, the rats on the high poofa group have heart failure. Notice they have a 32% reduction in cardiac output at high afterloads, which is a systolic blood pressure of 135 mmHg. They've got heart failure in four weeks. So now this is just boilerplate stuff. Omega-6 poofa. This is how we get to inflammation. So just notice, I'm going to have to go quick here. So those produce prostaglandin-2 series, which are unfavorable, pro-inflammatory icosanoids, leukotrienes. They're totally pro-inflammatory, pro-thrombogenic, clot-inducing. Omega-3s, on the other hand, anti-inflammatory, create resolvents, protectants, marisans, mostly inflammation-resolving, anti-thrombogenic and anti-arhythmic. So now a third mechanism, toxicity. When we consume Omega-6, they're peroxidized to lipid hydro peroxides. These rapidly degenerate into these toxic aldehydes. This is something that's rarely talked about, but these are chemicals like 4-hydroxy-noneanol, malendialdehyde, oxidized linoleic acid metabolites like 9- and 13-hode, acrylene, carboxyethyl pyrrole, and these, collectively, are cytotoxic, genotoxic, mutagenic, carcinogenic, atherogenic, and thrombogenic. So these collectively lead to all the diseases of civilization. And this is an example of this. So this is Martin Grutfeld and colleagues in the UK. So what they did is they cooked these lipids, and so you see corn oil and sunflower oil versus coconut oil and butter. And what they measured is the number of these toxic aldehydes. So you see that the corn oil and sunflower oil had really high total unsaturated and saturated aldehydes versus the coconut oil and butter, right? And so that's the take home point right there. Now I'm going to show you a histogram, and you look at the bottom there, 20, 40, and 60 minutes worth of cooking, and you'll notice that in the light blue colors, that's the coconut oil and butter, how low the toxic aldehydes are versus the corn and sunflower oil in the sort of pink and purplish colors on the far right. Okay, so here's what we see. Omega-6 linoleic excess plus westernized diet. Throw in your sugar, your refined carbs, make it nutrient deficient, which it will be, right? This leads to a catastrophic lipid peroxidation cascade. What happens? Pathologic cardiolipin remodeling. Out of that, we get electron transport chain and oxidative phosphorylation failure, mitochondrial dysfunction. The first thing that happens out of this is increased reactive oxygen species. That leads to a vicious cycle back creating more lipid peroxidation. Next, we get due to energy loss, nuclear and mitochondrial DNA mutations. Out of that, we get cancers. Over on your left, reduced fatty acid, beta-oxidation. Now because the mitochondria are failing, we're not being, we're not able to burn fats for fuel properly. So we become more glycolysis dependent, which is what happens when people become obese. So what happens out of this? Weight gain, obesity. Back on your right, energy failure leads directly to apoptosis, programmed cell death, or necrosis, toxic cell death. We get neurodegeneration, diseases like macular degeneration, Alzheimer's, Parkinson's, and so on. From the reactive oxygen species, this directly creates insulin resistance. That leads to metabolic syndrome, type 2 diabetes, non-alcoholic fatty liver disease. Over on your left, we've already seen this, mitochondrial dysfunction leads to heart failure. And back up with the lipid peroxidation cascades, toxic aldehydes, contributing to all of the diseases of civilization. So let's look at one of these real quick, acrolein. So acrolein is a major cigarette related lung cancer agent. And it's in both cigarettes and in edible oils, which those both share a lot of toxic aldehydes, in fact. So here's acrolein. It's 18 to 98 micrograms per cigarette. But the acrolein in 154 gram of French fries, Grootfeld's research shows, is 1,000 to 1,500 micrograms. All right. Now, how big is 154 grams? Well, a large French fries at McDonald's is 150 grams. So we're talking, you know, similar amounts. All right. So that means that eating this large French fries could be the equivalent of smoking up to 83 cigarettes. Right? Now, I'll put, this should be the fine print, but I'll make it the big print. Acrolein content in 154 grams of French fries is equivalent to smoking 17 to 26 average cigarettes or 83 cigarettes lowest in acrolein. So that's why I decided I don't eat vegetable oils, so I thought I might take up smoking. You know, I don't see the problem with it. In fact, ladies and gentlemen, thinking about starting a new company. Yeah. I think we're going to call them acrolein lights. And notice they're healthier than vegetable oils. I think we're going to do well. What do you think? All right, folks, I couldn't help it. I'm sorry. All right, I'll move on now. Seriously. This looks like child abuse, does it not? But the question is, is eating processed foods made with vegetable oils even worse? And I will submit to you that it indeed is. Why? Because when this two-year-old boy eats these French fries, he's poisoned for the next two to six years. Why is that? Because the half-life of these oils in cell membranes is 600 to 680 days. Right? Okay, but I'm not picking on just French fries or potato chips. These oils are in hundreds of thousands of foods all around the planet. Right? They're the fat of choice added to these foods, and they're in restaurants everywhere because they're the cheapest oils they cost about a dollar per kilogram. All right, now, Einstein himself said everything should be made as simple as possible, but not simpler. And so taking that to heart, metabolism is fantastically complex, right? But if you plug processed foods, poof of oils, nutrient deficiencies into our system, you know what we end up with is fubar. If you're not familiar with fubar, I believe it's a German term. It means roughly translates to fouled up beyond all recognition. And out of that, we get all the diseases of civilization. That's really the most parsimonious explanation I can give. But now I want to show you just a couple things that I'm through here is this is a list of linoleic acid omega-6 fats from our own NIH. This is the top 15 sources in the American diet. Now, I'm going to highlight all the ones that are high carb, and it's 10 of them. Now, my point here is that although ketogenic low carb diets generally do work, I don't believe they work because they're low carb. I believe they work because when you have no clue what you're doing, when you go low carb, you're usually reducing your edible oil. And that makes you healthier, it makes your mitochondria healthier. Now, just so you've seen it, this is our published data, vegetable oil and saturated fat versus heart disease deaths. Notice the remarkable correlation between vegetable oils and heart disease deaths and virtually no correlation between saturated fat and heart disease deaths, right? So moving on, okay, here's all the high proof of oils right here. So, but they are pro-oxidative, pro-inflammatory, cytotoxic, genotoxic, mutagenic, carcinogenic, thrombogenic, and atherogenic poisons. That's what they are. So why are they not labeled like this? And the answer is because they're chronic toxins. They're not acute toxins. They don't kill us today. It takes months, years, usually decades, and it depends mostly on the dose. So one of the most important things we do in medicine, in nutrition, is pattern recognition. But if we only look back months, a few years, or even a few decades, we're just lost. We might think all this chronic disease is just normal, but it's not. Is it? If we looked back 135 years, we realized that virtually all this disease didn't exist. And so probably everybody here recognizes that it's the man-made, processed, nutrient deficient, toxic foods that drive all the diseases of civilization. But of those, the proof of oils are the only ones that are pro-oxidative, pro-inflammatory, toxic, and are consumed to a scale to cause catastrophic global disease. They're the poisons. Ladies and gentlemen, I represent CureAMD Foundation. We are a nonprofit organization. And our goal is to prevent vision loss due to macular degeneration through ancestral dietary strategies. We're at CureAMD.org. And I want to thank the Ancestral Health Society. And I want to thank all of you. It's an honor and a pleasure. Thank you on the test. Yes, it'll all be on the test. Well, that's a great question. I honestly don't really have an answer for that other than, you know, I would guess that you would have to measure virtually all the studies you would normally measure for signs of metabolic syndrome, given that virtually nobody is going to be measuring the adipose linoleic acid levels. That would tell you a lot right there. But honestly, I would personally, if I were a clinician in this regard, I would be paying attention mostly to the history and just realize that it's going to take months and years for people to bring their linoleic acid levels down in their adipose and get healthier. And in fact, I've seen it in myself. I quit all these in 2011. And I really felt like it took a few years before my health got back to normal. I am not aware of any societies that have significant obesity and don't consume omega-6. I'm not aware of any. And there's some, Stefan Guine gave a presentation way back in 2011 looking at Pacific Islanders that were consuming diets that were 95% approximately carb, but of course, all natural carbs, fruit and root vegetables, I believe it was primarily. And they had virtually zero obesity, and they had no metabolic disease. And they smoked. A lot of the Pacific Islanders, they smoke like crazy. We saw that in our macular degeneration research with the ophthalmologists in Samoa, the Solomon Islands, and Curabody. And down there, the smoking prevalence is extraordinarily high. And yet they had almost no macular degeneration at all. But they don't get any vegetable oils. Do you mean once they've been consumed and your linoleic acid levels in your adipose are high? Is that what you mean? I think we have to, I think there's no other answer than to say we have to pay for our nutritional sins. It's going to take time. There is no way that I'm aware of that you can just remove these. The only way to do that would be to just drop your omega-6 consumption way down to where it should be. And I do believe it should be in the range of omega-6 omega-3, 1 to 1 to 4 to 1, somewhere in that range. And just wait it out. That's all you can do.