Professor Lustig’s Hateful - Grateful 8, follow up Q & A (with slightly improved audio)

Foreign.

So, Rob, it's a pleasure having you here again.

My pleasure.

You were here a few months ago and you had an amazing presentation on the hateful grateful eights. And a bunch of questions came out of that presentation, and the one that I'm really focused on is you mentioned that basically kids used to get type 1 diabetes, type 2 diabetes, and now kids are getting type 2 diabetes all over. Something is going on. They're being exposed to something. We're in a crisis.

Indeed. So, number one, they didn't used to get type 2 diabetes. Okay. I never saw type 2 diabetes before 1990 as a pediatrician. I graduated medical school in 1980. I started practicing at. My first job as an assistant professor was in 1990. I saw my first case of type 2 diabetes in about 1992 in children. Okay. And then they started coming fast and furious after that. Fact of the matter is they didn't get type 2 diabetes. Type 1 we've had since time immemorial. Now, that has picked up as well. It used to be 1 in 600 children, now it's 1 in 400 children. So it's increased by about 50% in terms of prevalence as well, which is part of this whole issue, as also. But type two we never saw. So the question is type two was an old age disease. I remember when I was in medical school, I did a report on type 2 diabetes, and I cared about it a lot because my grandfather had type 2 diabetes. And so I looked at the statistics, and in 1975, only 2.5% of adults over age 65 had type 2 diabetes. And under age 65, it was infinitesimal. Today, 9.4% of all adults over age 20 have type 2 diabetes. And now one third of all diabetes diagnoses in children is type 2. Where is this coming from? Now, we learned in medical school way back when, and we're unfortunately, a lot of physicians in training are still learning this in medical school, that type 2 diabetes is a chronic, progressive, unrelenting genetic disease that has no treatment. And that basically once you develop type 2 diabetes, you need to be on oral hypoglycemics or insulin. That is what doctors are continued to be told and educated. Yeah, Every single thing I just said is wrong, babe. Now, it wasn't wrong in 1976 when I learned it, but we have now since learned that every single statement that I just made is completely false. It is not chronic because you can turn it around. It is not unrelenting because you can turn it around. It is not Genetic. The reason your mother had it and you got it too, is because you eat the same crap she did. And it is occurring in children because children are exposed to the same reasons for getting type 2 as are adults. And so the question is, what's the exposure? Right. And that's where ultra processed food comes in. Now, the main problem in ultra processed food, it's not the only problem, but the main problem is, is sugar, for reasons that we discussed when I was here last time, because sugar is a unique, chronic dose dependent mitochondrial toxin. And we will talk about exactly how that works today. Right. But in addition, there's trans fats, there's branched chain amino acids, and then there are the things that affect the microbiome and increase inflammation. So such as preservatives, emulsifiers, glyphosate, other things that ultimately increase inflammation. You put those two things together, inhibit metabolism, promote inflammation. You have type 2 diabetes. And this is why children get the diseases of adults today, because they're exposed to the same things. Children get the diseases of alcohol. Type 2 diabetes and fatty liver disease were the diseases of alcohol. Well, now five year olds get both of those, they don't drink alcohol. Yeah. Point is, each of these is due to an exposure. And so we have to determine what are the exposures and what can we do about them. Right, right.

You also mentioned metabolically healthy obese versus metabolically unhealthy obese.

Correct.

How can you tell the difference? By, you know, is there any biomarkers, is there a blood test, is there a CT scan that I could say that person is metabolically healthy obese, Leave him alone.

Yes, absolutely. So metabolically healthy obese means that that individual has increased subcutaneous fat. Right. But not increased visceral fat and not increased liver fat. Turns out the subcutaneous fat is protective against metabolic disease. Cosmetically unsightly, metabolically protective. So there are plenty of people who have, shall we say, an extra layer of fat. Okay. And that fat is actually protecting them from disease, not contributing to it. Now, may not look great in a swimsuit, but it is not going to put them six feet under. Conversely, there are plenty of people, 60% of normal weight people, who have that visceral fat or liver fat. So, yeah, they can fit in a swimsuit, but they are just as susceptible to chronic disease and mortality as the unhealthy obese are. So it's not the fat you can see that matters, it's the fat you can't. Now, if you can't see it, how can you Know it's there. Right? That's the question you're asking. What are the biomarkers? So there are a couple. The cheap one, the sensitive but not specific one, is free. It's your waist circumference. So if you have an increased waist circumference, the chances are the reason for the increased waist circumference is visceral fat and possibly liver fat as well. The problem, of course, is standards. And the standards are different for men and women, and the standards are different based on age, and the standards are different based on race. So it gets hard to know who you're standardizing against. True. How about lab tests? So fasting insulin is the cheapest, easiest lab test to determine whether you have a metabolic problem. Your fasting insulin should be less than 10 and optimally should be less than 5. If your fasting insulin is 15 or greater, you've got a problem. Just that simple. Now, why doesn't everyone get a fasting insulin? I think they should. I've promoted that idea. The American Diabetes association says, don't draw a fasting insulin. So how come? They say don't draw it, and I say it's the most important test you can get. Yeah, what's that about? Well, the American Diabetes association says don't draw fasting insulin for two reasons. And both of them are specious. Both of them are wrong. The first reason they say is, well, insulin assays across the country are not standardized. That is true. I agree. They are not standardized. Cheap assays will pick up pro insulin, a precursor molecule to insulin. When your beta cells in your pancreas are under a lot of duress, they're going to put out whatever they've got, fast as they can. And so the pro insulin levels in the blood will go up. Pro insulin is only 5% as active as insulin. You have to cleave the C peptide out of the pro insulin molecule to get the mature insulin. And pancreas is under duress, don't have time to be able to do that. So pro insulin will get picked up. So really what you have is hyper proinsulinemia masquerading as hyperinsulinemia. And so they say don't draw because you're not measuring, because it's not accurate. Yeah. And I say, so what? It's high. That's what matters. Okay. For that patient, if it's high, you got a problem and you should know it. Right. Second reason, the ADA says don't draw fasting insulin. They say fasting insulin levels don't correlate with obesity. That's right. They don't. They correlate with metabolic health. Right. And I just told you that there are plenty of obese people who are metabolically healthy and plenty of thin people who are not. Right. In fact, fasting insulin is the single most important determinant of metabolic health. Now, are there others? Yes, Uric acid. And many people have now written about uric acid. David Perlmutter wrote a book called drop acid. Rick Johnson Johnson at Uber Colorado, very excited about uric acid. And he put that in his book, Nature Wants us to be fat. Okay. Uric acid is a mitochondrial toxin. So measuring uric acid is really important. A third one, alt. Alanine aminotransferase. So this is a liver function test. This is done on a standard chem panel. And ALT will tell you if you have liver fat, the upper limit of normal is 25. Now, when you look at the lab slip, it says the upper limit of normal is 40. I say 25, they say 40. How come? The answer is because when I went to medical school, it was 25, and today it's 40. Because the entire curve has shifted to the right. Because everyone has fatty liver disease and.

They think they're okay and.

Right. It's the silent killer, just like hypertension was. Okay. And because the entire population has shifted to the right, the two standard deviations from the mean have shifted as well. And so now the upper limit is 40. No, no, the upper limit is 25. So you have to be able to interpret the lab test properly.

Right.

So those are the tests that really get to the core of metabolic response dysfunction. Right.

The X rays that you showed or CT scan you showed, were they contrasted or were they just.

Well, I showed.

Can someone do an X ray or CT scan?

Well, so you can do a CT scan of the abdomen, but then you need specific software to be able to differentiate the sub Q from the visceral fat from the organs. And so, you know, it's not for the faint of heart. You sort of need a.

Not an everyday thing.

Not an everyday thing to be able to do CT scans. MRI will also give you that information.

But again, not for the pretty expensive.

You know, and it's expensive. Exactly. So there are ways to do it. There's fiber scans, there's pancreatic elastography. There are numerous imaging techniques that can be used. But better to do it with lab tests. Right. Cheaper.

My next question is, you talked about statin. The fact that everybody and their mother is on statins for. For prevention of cardiovascular diseases. Etc. Etc. And you were saying that it really doesn't work. The data doesn't show it's very beneficial.

Well, yeah, let me, let me qualify that. There are two reasons for being on a statin. Right. One is primary prevention, one is secondary prevention. Prime prevention means your LDL is high. Put you on a statin basically before you get a heart attack. Secondary prevention is you already had a heart attack, your LDL is high, let's put you on a statin before you have a second heart attack. Turns out, for secondary prevention, the data are actually quite good because you've already declared yourself. Right. You're already at risk because you already had one. Right. And there. The statin data is actually quite good. And I espouse using statins for secondary. Secondary for the right patients, absolutely. Because those patients have declared themselves. The question is whether or not statins are good for primary prevention, because that's what all of the task forces are telling us to do. If your LDL is high, use a statin. Yeah. So the question you have to ask is, is LDL the atherogenic particle? That's the first question. The second question you have to ask is, is there another particle that's more atherogenic than ldl? And then the third question you have to ask is, does a statin alter that risk? Yes, it alters your LDL level, but does it alter that risk in primary prevention? So. So let's take each of those questions. First, is LDL the atherogenic particle? The answer is half of it. Actually less than half of it. Because there is not one ldl. There are two. Two. There's one called large buoyant ldl, and there's one called small dense ldl. You pick both of them up in the LDL assay. Turns out large, buoyant LDL is not large. The atherogenic particle, it's large. It doesn't get under the surface of the endothelial cells to start the foam cell formation process. And it's buoyant. It gets carried along by laminar flow through the arteries and arterioles. So it doesn't have a chance to sink and end up being incorporated into a plaque. Right. Small, dense LDL does the opposite. It's small. It can get under the surface of the endothelial cells to do the plaque formation. And it's dense. It sinks and so it falls out of laminar flow. And so. And it's more easily oxidized. Oxidized ldl. Small dense ldl. All of these are the same. So when you're measuring ldl, you're measuring both. Now, how can you tell which one you have? Large, buoyant or small dense. And the answer is you have to look at the triglyceride level. Now, turns out the hazard risk ratio for LDL and heart disease is 1.3. The hazard risk ratio for triglyceride and heart disease is 1.8 50% more specific for heart disease than LDL is. So triglyceride turns out to actually be a much better indicator of your atherogenic risk. Right.

You mentioning that statin is mitochondrial toxin. It's mitochondrial toxic. You know, there are assays to test whether a drug is mitochondrial. They're pharmacoh.

Well, there are ways to evaluate the different cytochromes that are in mitochondria, but they're not clinically useful at the moment, unfortunately. They're research based. They're science based. There. You have to get muscle biopsies to look at this. It's, it's not like there's a blood test for it.

Right.

Right. Now, that's part of the problem. But it is true that statins, they, they inhibit a mitochondrial enzyme. Right? 3 beta hydroxyglute coa reductase is a mitochondrial enzyme. And so it shouldn't be surprising to people that when you inhibit a mitochondrial enzyme, you get glucose dynamic problems for just that reason. And so you shouldn't be surprised that in fact, people who use statins have a 20% increased rate of diabetes. Now, is that a good thing? Well, if you're going to keel over from a second heart attack, maybe.

Maybe.

Okay, but if you're not, then no, it's not really. Okay, so I am for statins for the right patient for the right reason. I am not for statins for everybody.

For everybody.

Yeah. And that, unfortunately, is what the task force are telling people, and that's what medical schools are telling people, and that's what the pharma industry is telling people. That's what we have to fix.

Is there anywhere, any way we can consume sugar safely? You know, you've been talking about processed food, processed sugar, processed, you know, fructose, high, you know, corn, you know, basically fructose, corn syrup, all of that. Is there a safe sugar?

Okay, so first of all, fructose is fructose and sucrose is sucrose, and high fructose corn syrup is high fructose. They all contain a molecule of fructose, and fructose is the bad guy in the story. Let me make it easy for your audience. I am for dessert.

Eat your dessert first.

I am for dessert for dessert. I am not for dessert. For breakfast, lunch, snacks, and dinner. Okay? So when you say eat your dessert first, Breakfast cereal is dessert. Dessert. Okay. Chinese chicken salad is dessert. Yogurt is dessert. Okay. Pretty much Trader Joe's beef with broccoli is dessert. So the way I feel about it is if you're going to have dessert, make it a good one, Right? Make it a phenomenal one. Make it a fabulous one. Make it one that is absolutely irresistible. And make it rare, right. So that it's something to look forward to.

Maybe once a day.

No. Maybe once a week.

Once a week.

Okay. So that's how I think dessert should be consumed.

But you can't avoid sugar, you know, so what you do.

Well, you can avoid it if you make your own food. Okay. You can't avoid it if you eat the food in the supermarket. That's true. That. And that's the problem. That's why I've been working diligently to try to get the government to understand that sugar is actually not a food. It's a food additive. And it is not generally recognized as safe. Think of trans fats. Trans fats were in our food supply from 1911, with the advent of Crisco until 2013. Okay. When finally the US Health and Human Services, the FDA banned them from food because they recognize their toxicity. They used to be generally recognized as safe. Now they're not even allowed in our food supply. Right. It took 100 years to get from one to the other. Right. All right. Now, trans fats were thought to be food. They were nine calories per gram, but we learned that they were toxic. Turns out added sugar is 4 calories per gram. But it also does not belong in our food supply, and it is also toxic. So we need added sugar.

Added sugar, not sugar in, say, fruit or apple or orange.

Well, the molecule is the same. There's no difference between the fructose molecule in the McDonald's apple pie and in the apple. Fructose molecules the same. The difference is the fiber. Right. The fruit has the fiber, the McDonald's apple pie doesn't. Yeah. Now, the fiber limits the absorption of that fructose from the gut into the bloodstream. So even though you consumed it, you actually didn't absorb it. You never got it right. Your bacteria shoot it up for its own purposes. So when you consume fruit, that sugar is not for you. It's for your microbiome, and you have to feed your microbiome or your microbiome will feed on you. So when you eat your sugar with its inherent fiber, right. You are actually doing a good thing for your intestine without harming yourself. When you take that fiber and either destroy it like in a Vitamix or a Breville or a magic bullet, right. Or you strip the fiber out completely and now have just processed sugar and put it in say an ice cream or frozen yogurt or you know, you know, cake. Okay? Now that is added sugar. It is not buffered by fiber. You will absorb that just as readily as you will every other thing in, in your diet. And now it will go straight to your liver, lead to liver fat. Now you're also the chronic disease races.

Getting a orange or getting an apple, eating it by on its own, or taking the apple and putting it into this blender and chewing it up in micro bullet or juicing it and drinking the juice. Which one is the best? Which one is the worst?

Eating the apple is the best.

Okay, but on its own.

On its own, that's it.

The meat in the media is the micro. That bullet, whatever.

As soon as you destroy the fiber. Yeah. And that's what the blades magic bullet do. They shoot, shear the insoluble fiber to smithereens. It's not there anymore. It doesn't work to act as a barrier.

And the worst is drinking that juice, apple juice, because it's pure, you know, essentially no fiber.

So there was a paper that came out in 2008 asking the question, what does the glucose excursion look like when you consume an apple? Applesauce and apple juice. So when you consume the apple, very little glucose response. When you consume the apple juice, very large glucose response. What about the apple sauce in the middle? Was it more like the apple or was it more like apple juice? Answer was more like apple juice. Interesting. So as soon as you destroy the fiber, it's not there. Right. It doesn't act on, on your behalf. Right.

Okay, you talked about a few months ago here about insulin intolerance and insulin pathway. And you pointed out to a pathway that is cancer causing.

Yeah.

So how can insulin be cancer causing?

Very simple. Yeah. Anything that causes cell growth in the extreme causes cancer. So every cell in your body at one point in its lifetime in its lifespan had to grow and a different point had to burn. Okay. And no cell can do both at the same time. So either grow or you burn. Insulin prevents you from burning. It actually causes you to grow. Insulin is a mitogen, it is a growth promoting agent. IGF1 insulin, like growth factor 1, which causes statural growth in children, is a growth promoting agent, causes cell proliferation and every time a cell divides, the risk for cancer is enhanced. Now, it doesn't mean that if you sell proliferates it's going to cause cancer, but statistically you've increased the risk and so insulin increases that risk. And also insulin is one of the ways that energy gets into cancer cells in order to be able to be used for their growth because insulin increases glucose transport into cells. So insulin is a cancer promoting agent and the higher your insulin, the greater the risk for cancer. And this has been shown 50 ways from Sunday in a host of different types of cancer.

So you don't want to be producing insulin, just you don't want to be triggering your insulin when you don't need to.

Exactly. Right, yeah. Everyone wants the least amount of insulin that will still do the job. Any less than that, you have type 1 diabetes. Any more than that, you have increased risk for obesity, chronic metabolic disease, type 2 diabetes and cancer. Everybody wants to find the insulin sweet spot. Right. The point is that the more ultra processed food you consume, the sweeter your spot. Moving to the right. Right.

More, more insulin is being produced and.

Causing all of these problems.

And of course, you know, when you have you mentioned you take Diet coke while Diet Coke doesn't have, or Diet Pepsi, we don't want to pick on any brand. But when you have these artificial sweeteners, although it's not sugar, you are triggering your insulin.

Exactly. When you put something sweet on the tongue, message goes tongue to brain, sugar's coming, brain to pancreas, sugar's coming, release the insulin. And so even though that diet sweetener did not have calories, even though that diet sweetener did not have fructose, you still trigger an insulin response. And when that happens, you're still going to end up with weight gain. And this is one of the reasons why there are no studies that demonstrate that switching to diet sweeteners leads to weight loss. Right.

Thank you very much.

My pleasure.

Very useful.