Jay Feldman: 

In the alternative health world, we're told that fructose is a poison that works just like alcohol, but we're never given the full honest picture when it comes to fructose and fructose metabolism. So that's what we'll be going over in today's episode of the Energy Balanced Podcast, a podcast where we explore health and nutrition from the bioenergetic view and teach you how to maximize your cellular energy to maximize your health.

In today's episode, I'll be discussing whether Robert Lustig is right about fructose being a poison. I'll go over what Robert Lustig completely misses when comparing the biochemistry of glucose, fructose, and alcohol. I'll discuss whether a low carb, high fat diet actually causes fatty liver. I'll go over the research on fructose and its toxicity, and whether you should be minimizing fructose intake in the form of fruit, juice, and honey to optimize your liver and metabolic health.

As always to check out the show notes. We're all linked to the studies articles on anything else that I referenced throughout today's episode. You can head over to jay feldman wellness.com/podcast. And with that,  let's jump in.

Alright, so anytime I post podcast episodes or videos discussing carbohydrates and their benefits, or discussing the benefits of fruit or why fructose is not actually harmful to the liver, or some other benefits of different forms of carbohydrates, there are always a ton of comments.

And when it comes to the critical comments, there are always comments as saying that Robert Lustig has shown us that fructose is a poison and that it causes metabolic syndrome and fatty liver disease. And in many ways, Robert Lustig is the father of this idea that fructose is a poison, it's a metabolic toxin.

It works just like alcohol. And not only is this something that I see in the comments all the time on my videos, but it's something that I also see suggested and parroted and repeated by different practitioners, pretty much all of the practitioners in the alternative health space. I think fructose is one of the most widely maligned nutrients, especially in the alternative health world.

And maybe that sentiment is starting to change a little bit. But for the most part, especially in the low carbs spheres, the carnivore spheres, fructose is known as a poison. And this is something that, Robert Lustig has been saying for. More than 15 years in various talks. And in his books, in podcast interviews, he's repeated over and over that fructose is a poison, it's a toxin.

He's shared with us, some biochemistry to supposedly support that, some research to supposedly support that. So we'll be going through that. But we're just gonna start by getting an idea in case you're not familiar with what Dr. Robert Lustig has to say in a broad sense about fructose, and we'll dive into all the details in a little bit.

Robert Lustig:

High fructose corn, serpent sucrose are exactly the same. They're both equally bad, okay? They're both dangerous, they're both poison. Okay? I said it poisoned My charge before the end of tonight is to demonstrate that fructose is a poison and I will do it and you'll tell me if I was successful. Okay? There's good carbohydrate and bad carbohydrate and glucose is good carbohydrate. Glucose is the energy of life. Fructose, okay, is poison. And it turns out mitochondria actually poisoned by fructose. So in fact, fructose is a chronic dose dependent mitochondrial toxin. And this is why we have to eat less of it.

Fructose is a metabolic toxin in the same way alcohol is a metabolic toxin and fructose is a three in one mitochondrial toxin. Poison. It's poison and it actually detracts from metabolic health and it turns out that fructose is a mitochondrial toxin.

Jay Feldman:
Alright, so I was just a little compilation there of us hearing over the years, again, the last 15 years plus from Robert Lustig, that fructose is poison. It's a toxin. He's gonna be convincing us of this. It's the main subject of his books. And, all the. In his books and other talks, he digs into all the reasons why this is the case. And he's one of, one of the big advocates for this. And again, as I was saying, there are a ton of people out there parroting these ideas, even without fully understanding them.

They'll say things like, fructose produces the same byproducts of as alcohol, which is untrue. And we'll discuss that as well. And even Robert Leslie doesn't say that. He does say that they're both equally toxic and poisonous, whereas again, in contrast, glucose is good, it's a good carbohydrate, it's the energy of life.

That's that general narrative we're hearing. So that's really what we're going to be discussing here is how different is fructose from alcohol and from glucose, and what actually is responsible for the differences If. any, We'll be digging into Robert Lustig's claims here surrounding fructose, the physiology he cites suggesting that fructose is a poison.

And we're going  to be pulling this from Clipse, mostly from his talk. That was, I think around 10 or 11 years ago titled Fat Chance Fructose 2.0. He, of course, has a lot of different places that we can pull information from and there's a number of different arguments he makes, but these are really the main ones that he and most people rely on.

So that's why we're going to focus on these and we'll discuss some other things that he suggested on other podcasts as well. But we're gonna start with the glucose section from his talk Fat Chance Fructose 2.0. We're going to hear what he has to say about glucose and its metabolism specifically at the liver, since that's his central concern when it comes to fructose and alcohol, is that they're toxic to the liver.

So let's hear what he has to say about glucose and whether this is actually what happens physiologically.

Robert Lustig:

When you consume glucose, say rice, white bread, starch, 80% of the glucose goes to all the organs of the body. Only 20% hits the liver. And where does it go? It goes to this  guy over here, glycogen.

Glycogen is liver starch and liver starch, for lack of a better word, is good because that's your energy store for a rainy day. That's the first energy that's used when you fast. Okay? That's what, why marathoners? Carload before a marathon race is to try to build up their glycogen stores because glycogen is non-toxic. So if you can, alright,

Jay Feldman: so just pause there. We have two main points that are being made. One is that when glucose is consumed, only about 20% of it goes to the liver. The other 80% goes elsewhere. And of the glucose that goes to the liver, a good portion of it goes to glycogen, which he's saying here is non-toxic.

That glycogen is fine. It's fine if we're producing glycogen in the liver. It is also interesting that we've heard, we heard in that compilation that he was saying glucose isn't toxic either. Glucose is a good carbohydrate. It's the, the energy of life. So it is, he's almost making a dichotomy here between glycogen and glucose.

But in any case, we're generally getting the picture that glucose is okay, glycogen is okay, and we get less glucose going to the liver when we consume it because a good portion of it goes elsewhere in the body. So that's what we have so far up.

Robert Lustig:

Your glycogen stores, your liver has more energy in reserve and that's a good thing. Now, a little of it will sneak down here and get metabolized by the mitochondria and throw off a little of this stuff called citrate and that will then get turned into liver fat. This process here in orange is called de novo lipogenesis new fat making. This is how your liver turns carbohydrate into fat is through this process here, but you're not dealing with very much carbohydrate here because it all went to glycogen and most of it actually got metabolized elsewhere. Anyway. So your liver's protected.

Jay Feldman: Alright, so these next points here, the central one is that he's saying some portion of the glucose will be going down to the mitochondria in the liver, which is where it gets metabolized to produce energy. He skipped over that part and that's really important.

We'll come back to it. But the liver uses a massive amount of energy. So it's needs for a TP are very high and the carbohydrate that goes there will be used to produce energy. He then mentioned that some amount will end up leaving as citrate and that'll be used to be converted into fat through a process called de novo lipogenesis.

And that's where you can get liver fat and it can also leave the liver in lipoproteins. So there's truth there, but it's just really important to emphasize that it's not a situation where just any extra glucose that doesn't go to glycogen goes straight into fat. A large portion will be metabolized into energy because liver has a really significant capacity for producing energy and a significant need for energy production. So that's really the central place that it'll go. But if there's excess beyond what can be stored in glycogen, beyond what can be used in the mitochondria there, some portion of that will end up getting converted to fat.

So that is what we have up to this point. And as he mentioned, and his real central piece here is that only a small portion of the glucose actually goes to the liver. So there's less there to be used and therefore less that will become that. Now, just as a starting place here, we will get into some details, but. This is really no different than any fuel in any other tissue in the body, or even looking at the body as a whole. If you're consuming massive amounts of a fuel beyond what can be stored and beyond what can be used, it will then get stored as body fat. It could be converted into body fat. The reality is actually, while we're consuming a diet containing carbohydrates, the conversion of carbohydrate to fat is pretty inefficient.

So we actually store the fat as fat since that's much more efficient as opposed to converting the carbohydrates to fat. And instead we just use those carbohydrates for energy. But yes, if we consume far more than we're capable of utilizing, then we'll put into storage. If that glycogen store is full, then we'll convert some of it to fat.

And of course, there's always some amount of substrate, glucose, amino acids, fat being stored as fat, and that's some amount being released. That's something that happens, if anytime there's excess and there's constant flux in there. But that's the general picture we have here from [00:10:00] glucose, and we're given the idea that it's not toxic.

Most of it goes to glycogen, otherwise it'll go to the mitochondria. Some amount can be converted to fat, but we're not going to have that much going to the liver in the first place. So we shouldn't have that much fat being produced. Now, one caveat here that we will be digging into is that if the mitochondria in the liver are not working well, if the liver is stressed, there's a lot of oxidative stress going on there.

If there's a lot of inflammation going on there, and we'll talk about things that can cause that's going to interfere with the utilization of any fuel there and will increase the conversion to fat as well as the activation of various inflammatory pathways. Now that is, again, not dependent on the substrate, the glucose fructose, amino acids fat, but rather dependent on the state of the liver and its general health and.

The healthier the liver. The liver is, the more fuel it'll be able to effectively use versus storing it. So that's our general picture here when it comes to glucose. Now, in a moment here we'll be discussing the metabolism of alcohol and then a fructose, and we'll be discussing why fructose isn't actually a poison at all.

But with that in mind, we don't actually need to be avoiding healthy sources of fructose to improve our metabolic health and reverse fatty liver disease. But there are some foods that we do wanna make sure that we avoid that are actually culprit here now. That's why I've created the Energy Balanced Food Guide to help you determine exactly what to eat, to optimize, support your metabolism, and help you lose weight, improve your digestion, get amazing sleep, boost your energy, and so much more.

The Energy Balance Food Guide is a one page infographic that organizes foods on a spectrum based on how effectively they support your metabolism. And it also has a separate spectrum that adjusts the scale for you in the case that you're dealing with various digestive issues. The food guide makes it extremely easy to get started with a bioenergetic approach to optimizing your health.So head over to jay feldman wellness.com/guide to download your free energy balanced food guide.

All right, so let's dig into what Robert Lustig has to say here in regard to alcohol or ethanol. 

Robert Lustig: So let's consume  the same number of calories of alcohol. Now, most of them go to the liver instead of going to the periphery.

And what happens to it? Glycogen anywhere? No glycogen. It bypasses. Glycogen and goes down to the mitochondria. And since there's so much of it, you get big time fat making and some of it won't make it out. Now you got that lipid droplet, that's alcoholic steatohepatitis and you're gonna make lots of triglycerides.

And so you're gonna have hypertriglyceridemia and that's gonna end up in the muscle. And now you've got muscle insulin resistance and it serves as a substrate for weight gain as well.

Jay Feldman:

Alright, so a couple points here. First one is that alcohol, all of it will go to the liver. It has to be metabolized there.And then the second point is that because it doesn't get converted to glycogen, all of it is going to go to the mitochondria. So those are our two differences between that he's pointed out so far between alcohol and glucose and it, again, it's an amount issue. And then the fact that the ethanol won't be stored as glycogen.

Now we're missing a really important part here that is shown on the diagram, but he's at least not touching on it [00:13:00] here. And that's the fact that ethanol itself and the acetaldehyde that it produces, which are totally different from glucose and fructose as we'll get to. Cause problems inherently, they drive oxidative stress.

They drive inflammation. We'll talk about this in a minute, but acetaldehyde is, it's a highly reactive toxic aldehyde. So it, when it interacts with proteins, DNA fats, it damages them, causes lip bi peroxidation, it damages the mitochondria, impairs mitochondrial function. So these are major problems and are totally unique to ethanol.

As is shown here in the diagram, they do drive inflammation and that also contributes to the fat production from this fuel. So it's not just that there's large amount going there to the liver and that all of it's going to the mitochondria 'cause it's not getting stored as glycogen. But there are these two really important pieces here, especially centering on the acetaldehyde that are going to drive an inflammatory state here, cause inflammation at the liver and also cause excess fat production and accumulation.

So that's not touched on here, but is a really central point that will be discussing. Then he explains a little bit further here.

Robert Lustig: So here's a problem, because this is toxic and abused, and so we regulate it.

Jay Feldman: So he is just pointing out here, concluding ethanol is toxic, alcohol is toxic. We're gonna then talk about fructose and it's toxicity.

But again, there are some very unique things about ethanol here that he isn't touching on verbally. They are in the diagram, but they're really important to highlight because as I am mentioning, they don't happen with glucose or fructose. You don't have the acetaldehyde production. And again, that's extremely concerning.

Now, as you pointed out in the diagram, the acetaldehyde can then get converted to acetate, which can enter the mitochondria, get converted to acetyl-CoA, and then enter the kreb cycle and be used to produce energy. And then at that point, if the mitochondria is overwhelmed or if it's if there's inflammation and the mitochondrial function is directly impaired in this case due to the aldehyde  itself.

Then you're going to have problems with producing energy. You will have the excess citrate and you will be producing more fat here. But again, this isn't just because it's all going right to the mitochondria, it's because you also have a highly inflamed state in the liver in a situation like this.

And it's also not just those two components, it's not just the ethanol and acetaldehyde itself, but there are some other negative effects of alcohol that are primary drivers of this issue. The central one is that ethanol causes major issues in the gut. It increases the production of endotoxin lipo polysaccharide, and it increases intestinal permeability, which also causes increased absorption of endotoxin.

Now, when endotoxin goes to the liver, it causes major inflammation. It interferes with mitochondrial function, and so that's another way that you're getting this massive concerning problem when it comes to alcohol, which is unique relative to glucose and fructose, which we'll get to in a little bit. Now, again, this is just a clip from one of his talks in his other talk,  or the, one of his other main ones sugar, the bigger bitter truth.

He does touch on the toxicity of acetaldehyde he does seem aware of this, but he's just not highlighting it, at least in this presentation as a central issue here. And I think it's absolutely central. It's very important to discuss here along with the endotoxin that are really both responsible for the problems here with ethanol.

But in Robert Lustig's view, more than anything, it's just the amount of. The substrate that's going to the liver and the amount that's then going to be hitting the mitochondria. That's really the concern, but that's really not the case. So let's move on here to hear what he has to say regarding fructose.

Robert Lustig: Now let's do fructose. So we're gonna consume sugar. Now we're gonna consume orange juice, same number of calories. The glucose does the same. 2080 split. It did before 12 and 48. But all the calories from fructose are gonna go to the liver because only the liver has the transporter for fructose called glute five.

Jay Feldman: Alright, so we've pointed out the first  difference here, which you mentioned this with ethanol as well. That in contrast to glucose, where only 20% goes to the liver, give or take with fructose, pretty much all of it is going to be going to the liver. So you're going to have more substrate, more fuel heading to the liver. There's our first difference.

Robert Lustig: And glycogen anywhere? No glycogen goes straight down to the mitochondria just like alcohol did.

Jay Feldman: Okay, so we're going to dig into this in, in, in a lot of detail because it's a really important point that he not only conveniently leaves out. It's not like he's just omitting, omitting it, but he's actually suggesting that fructose will not be converted to glycogen here.

That's blatantly false. Blatantly false. We're gonna be talking through some studies here that show very obviously that this is the case. There's no reason or evidence to suggest that this doesn't happen. We know that fructose gets converted to glycogen as well as other substrates, aside from glycogen in the liver, which then gets sent out.

So we'll be coming back to these in a moment, but. [00:18:00] This is what all of Robert Lustig's argument is relying on here. The fact that the fructose doesn't, you have a larger fructose load and it doesn't go anywhere except the mitochondria, so you're going to be overwhelming the mitochondria and it's blatantly untrue.

He's conveniently leaving out these other pathways that the majority of fructose goes to as much as 90% of fr of the fructose is going to pathways that he is not describing Here. He's actually saying it doesn't go to at all and instead he's saying, it all goes to the mitochondria. So 90% of the fructose is going to be going elsewhere.

At least we'll be talking about that in a moment, but it's hard to understand how someone who is a researcher on this topic has been talking about it for 15 plus years, is obviously a medical doctor, has written books on it. Is not describing this aspect of fructose metabolism, this major aspect of fructose metabolism.

If we wanna be generous, we could call it a massive error. But I think honestly, that's giving way too much latitude to someone who, again, is writing research papers on this topic, writing books on this topic, giving talks like this, on this topic that millions of people are seeing and is then making money on these talks and on, on these books that he sells.

So he either totally is incompetent when it comes to fructose metabolism and doesn't know what happens to it, or he is not being honest. He's lying about where fructose goes. I don't know which it is. That's not my job here. But what is my job is to explain where the fructose is actually going aside from just going to the mitochondria.

So we'll start there, and then we will come back to the next steps because. They're all dependent on this initial point that Robert Lustig has made.

So there are other pathways that fructose goes to, and this is, this includes glycogen in addition to  glycogen. Fructose is also converted into glucose, and it's also converted into lactate that the glucose that's produced and the lactate that's produced are then sent out of the liver to other tissues in the body where they can use those as fuel, or they can store 'em as glycogen, for example, the muscles can take up that glucose and store it as glycogen, and this is where the majority of fructose is going.

Those three places, the glu, the glucose, lactate, and glycogen. So we're going to take a look at some studies here showing that in a moment. So before we dig into these studies, let's just hear the rest of what Robert Lustig has to say here about fructose and how it's causing all of these downstream issues because they all hinge on this one point that he's making.

Robert Lustig: Glycogen anywhere. No glycogen, go straight down to the mitochondria, just like alcohol did. And because there's so much of it, your mitochondria have no choice but to turn the excess into liver fat. There's your lipid droplets. So now you've got non-alcoholic steatohepatitis. You've got high triglycerides just like you did  with alcohol. You get the muscle insulin resistance substrate for obesity, and it tells your insulin receptor not to work. So now you've got liver insulin resistance, which makes your pancreas have to make more insulin in order to make the liver do its job. Now the high insulin goes to the brain blocks, leptin, and now you can't see your leptin.

So what does it do? It makes you think you are starving. So what does it make you do? Consume more fructose. So now you've got a positive feedback effect between a compound that's toxic and abused, causing damage to the liver, damage to the pancreas eventually, and damage to the brain.

Jay Feldman: All right. So as we've seen here, all of his arguments are hinging on the fact, on the suggestion, the claim that he's making that fructose does not get converted to glycogen.

Instead, all of it goes to the mitochondria and you already have all this fructose at the liver. It overwhelms it, you get liver fat production, and that leads to all of these other downstream negative effects. There's a number of other pathways he  has here shown on the diagram that he's not actually touching on.

So just wanna touch on those real briefly. And you can see in the yellow that he's showing the fructose one phosphate, fructose one p, that is going to be causing some issues, some in inflammatory effects uric acid production. And then you can also see farther down, he's showing that glyceraldehyde and fructose one six bi phosphate are going to be some of the factors driving the liver fat production.

And then that liver fat production also being something that's causing the inflammation. So we have this, suggestion that all these pathways are converging causing inflammation and causing fat production. Now, I wanna be clear, these metabolites of fructose, the fructose one, phosphate, the glyceraldehyde, the fructose one six bi phosphate, these are only going to build up in the case that they don't have anywhere else to go.

So if the fructose were only going to the mitochondria, there's still no problem there until there's. Too much going to the mitochondria for what the mitochondria can [00:23:00] handle. Maybe the mitochondria are inflamed, maybe there are nutrient deficiencies. Maybe there are things blocking certain complexes that the electron transport chain, certain enzymes in the kreb cycle.

When that happens, then you see these metabolites build up, so it's not inherent to the fact that these metabolites get produced. In fact, the glyceraldehyde and fructose one six bi phosphate are also produced from glucose, so they're the exact same in that regard. It's just a question of how much is staying as those metabolites, and that's only going to be dependent on if the later steps, the next conversions are getting blocked or getting inhibit because the mitochondria get backed up.

And so yes, if that's happening, then you'll see these inflammatory processes going on in the same way that you would with glucose in the same way that you would with any other substrate. But they're all dependent on this idea that fructose has nowhere to go, but the mitochondria, you're getting so much fructose that it's overwhelming the mitochondria.

And then you get all of these downstream negative effects. As I was saying, there's a major problem here, which is that you're not going to see [00:24:00] buildup of those metabolites. You're not going to see buildup of fructose one fo phosphate, glyceraldehyde, three phosphate fructose, six phosphate, because fructose has a lot of other places to go and it favors these other places.

And as I was saying, 90% or more of it is going to these other pathways. These are the major pathways that are entirely omitted in this diagram. So we're gonna take a look here at a figure from a study titled Metabolic Effects of Fructose and the Worldwide Increase in Obesity. And in this figure, we can see clearly the different places that fructose is going.

We can see that after the fructose gets digested, 50% of it is getting converted to glucose from the liver and then being sent back out for the rest of the tissues to use. 25% of it is getting converted to lactate at the liver, and then being sent out for other tissues to use muscles. Love taking up lactate and using that as a fuel.

And then 15% or more, it says at least 15% is getting converted to glycogen in the liver. And if you count all that up, we're at 90% at least, of [00:25:00] the fructose that's come in. And so after that point, we can then see the fructose going to CO2, the carbon dioxide. That's the amount of fructose that's getting metabolized to produce energy.

And then we also have triglycerides media, the amount that's getting used to produce fat. And we can see that as well in the VLDL triglycerides. So we have that, the fact that at least 90% of fructose from, this study. Is going to pathways that are not shown at all on the diagram. And this idea that you know of a full glucose load, only 20% goes to the liver.

That sounds like it's not that much. And so Robert Lustig's suggesting that's not going to overwhelm the liver. But if you consider that of the fructose, even if you consider, even if we're assuming that a full a hundred percent of it is going to the liver, over 90% of that is going through other pathways that he's not describing here.

Only 10% of it or less is going to be available to be oxidized and converted to energy and could potentially overwhelm the mitochondria if there are other problems there. But again, 10% is not that much when we consider [00:26:00] the amount of fructose that most people are consuming the rate of its absorption.

Considering as well the amount of glycogen we can store at the liver and how metabolically hungry our livers are for a TP for energy. So we'll come back to that as well. So that's what we have here As far as that first study goes. We have some other studies that we're going to look at here because.

There's some small discrepancies in terms of the percentages of fructose going to these different places. So we'll just look at a couple others just to give it a fair shake here. So in this study that we're looking at, this is one titled Fructose Metabolism in Humans. What Isotopic tracer Studies Tell Us.

So this is just based on studies looking at fructose that's consumed or infused using an actual tracer so we can see exactly where it's going. And in this case, what they're seeing is 29 to 54% of that fructose gets converted to glucose. Around 28% gets converted to lactate. Based on these studies, because we don't actually have exact iso tracer studies that tell us the amount going to glycogen and glycerol, but we do know that on average less than 1% of the fructose is [00:27:00] actually going to be going to lipids, meaning that the, this pathway that Robert Lustig is pointing to, that the fructose is just going to be converted into fat, is going to happen to less than 1% of the fructose that's coming in instead is going to all these other pathways that he didn't even show.

On that diagram. Now, if you count this up, if we're assuming you know about that, you know about 30% coming from lactate, and if we're assuming, 30 to 50% coming from glucose, then we have between 20 to 40% of the fructose left unaccounted for going to either glycogen or glycerol orders being converted directly into energy.

Now again, from this study, which is just looking at these tracer studies, we don't know the exact amounts going to those areas, but we do have studies that don't involve tracers, but do suggest that over 30% of the fructose is actually going to glycogen. So we can take a look at that here in this study titled Liver and muscle Glycogen in Man After Glucose and Fructose Infusion.

[00:28:00] And in this study they were doing a massive high dose fructose infusion after a, an overnight fast. And then they looked at what happened in the in liver and muscle using biopsies, and this was in humans. So we can take a look here at table two at what happened after the fructose infusion especially.

That's b there, that's really what we're interested in. So you can see that they did a fructose infusion over four hours of 1,508 millimoles. This is a massive amount of fructose. This is around 270 grams of fructose. If you were to get this even from straight table sugar, this would require that you're consuming around 550 grams of table sugar, which is an absolutely insane amount, especially over just four hours.

So we're talking about absolutely massive levels of fructose here that are totally irrelevant to what we would actually consume, but they can still tell us about how well our bodies utilize the fructose in these ridiculous amounts. And so we can see that. Of that fifteen [00:29:00] hundred and eight three hundred fifty six was oxidized, meaning it was converted to energy.

494 went to liver glycogen and 493 give or take went to muscle glycogen, and then the rest went elsewhere. But if we just look at those amounts and we convert these to grams, so we had around 270, actually 272 grams of fructose, 64 of those grams were oxidized. That's 24%. That's a very large amount. If we were thinking before of that earlier study suggesting that 90% of it was going to other places, and then we have 10% left to be oxidized.

In this study, 24% was oxidized, although that's not just the pure fructose. That also involves the the fructose converted to glucose and lactate. But those are details that are not worth going through right now. Aside from that, we can see that around 89 grams went to liver glycogen, which is 33% of the total fructose load.

So in a load of 270 grams of fructose, again, way more than anybody would be consuming on a daily basis on average. Again very small portion of people consuming this amount. And again, I know I said this is about 550 grams of sugar. It would basically take about 12 [00:30:00] cans of soda if you're just using soda as your carb source to get this amount of fructose.

So massive amounts here. And as we were saying, 89 grams went to liver glycogen. That's 33% of the total fructose. So a massive amount is going to liver glycogen, which Robert Lustig is specifically saying doesn't happen, doesn't go to glycogen, goes straight to the mitochondria. Now on top of that, we see that 89 grams also went to muscle glycogen.

So again, about 33% went to muscle glycogen, which is also not at all accounted for in Robert Lustig's description here. And that's because a huge portion of that fructose is getting converted to glucose, which is then being sent out and the muscles and other tissues are using that for energy, or they're storing it as glycogen.

In this case, 33% went to muscle glycogen. And then again, a large portion being converted to lactate, being oxidized between. So just in this study, looking at again, the amount of fructose in about 12 cans of, so of soda, 90% of it is accounted for in muscle glycogen, liver, glycogen, and in terms of being converted into [00:31:00] energy.

So these are really not at all accounted for. Of course, Robert Leslie did mention some portion will be converted to energy, but the suggestion being that really that's going to be. A small portion, 'cause the rest is all gonna be stored as fat. But the reality here is we're seeing that even with insane doses of fructose, a lot of it is going to other places.

And when we consider that this is certainly an amount that would overwhelm even healthy livers when we're just consuming normal amounts with meals, much larger portions are going to be converted to glycogen, glucose and lactate and oxidized converted to energy and sent out. Since those are the primary pathways that are used, those are the pathways that our bodies want to favor.

They don't wanna be storing fat here. And they, we wouldn't see the buildup of all those metabolites that drives the signals that causes fat storage, which are the things that Robert Lut is pointing to in that diagram. But they really wouldn't happen because those metabolites wouldn't be building up because the liver would be effectively using that fructose and converting it elsewhere.

So that's what the research is actually telling us is [00:32:00] going on with fructose. And then it's also worth mentioning that in this pathway that he's saying is. Relatively unique to fructose, or at least that he's saying is the main driver of fructose is issues where it's then being converted to the GLYCERALDEHYDE three phosphate, the fructose one, six bi phosphate, and it's then going to the mitochondria.

All of that is the exact same as what happens with glucose. Glucose converts to those exact same metabolites and then goes to the mitochondria to produce energy. So there's nothing unique about that pathway when it comes to fructose. Once you get to those steps, the earlier steps are a little different.

The fructose conversion of fructose one phosphate is unique to fructose. Glucose doesn't have that and some, there's some unique aspects of that conversion that we've talked about in prior episodes, discussing why the conversion of fructose or the production of uric acid from fructose is really not a concern.

So I'll link to those in the in the show notes. We're not gonna dig into that here, but the important point being that pretty much all of this, [00:33:00] that all of that pathway. Is the same as what happens with glucose. And we know that fructose also gets converted to glycogen, just like glucose. So it's really not so different.

And if in that point the question just comes down to the amount that's going to be utilized by the liver, but we already know that 90 plus percent of that fructose is going elsewhere. It's getting converted to glucose, to glycogen, to lactate and the glucose and lactate are sent out from the liver.

So the liver isn't utilizing a hundred percent of the fructose coming to it. Now, it's also worth noting here, as I mentioned, the liver has really high energy needs. They're one of the most metabolically active organs that we have. And it's pretty well known that the brain is the most metabolically active organ.

It's only two-ish percent of our total body weight, but utilizes 20% of our total fuel. It's responsible for 20% of our total metabolic rate. The liver only uses 13% less than the brain. So we're talking about an organ that is using a massive amount of energy and has a huge need for fuel in the [00:34:00] mitochondria to produce energy anyway.

So it's really well equipped to handle fructose, and that's the whole point. The whole reason why, especially as humans, we have livers that are able to utilize fructose effectively, is because this provides a number of things. It provides a store of glycogen that then our brains can use since our brains are far larger and use more energy than other animals.

So we need to have a really good store of glycogen, and our brains can't store glycogen. So the fructose provides that store in the liver for our brains, which are very metabolically active, and we have really active livers that help us regulate our blood sugar. They help us with detoxification. The, there's tons of different effects that are really important in the liver.

We convert thyroid hormones there. It's a really central organ that helps us with digestion and tons of different things. And so we need to have a lot of fuel there and we need to be able to produce a lot of energy there. And so fructose is great for that. And that's why, if we look at our APE cousins that eat tons of fruit and don't get fat and utilize it really effectively, and we look at what happens with humans consuming [00:35:00] lots of fructose, this is why we use it as well as we do.

And the idea that's being suggested here is so far from reality. Now, as I mentioned earlier, when it came to glucose and ethanol or alcohol, if there are impairments in the liver, that's when we can start to see problems with any substrate, whether it's glucose, whether it's fructose, whether it's alcohol, whether it's fatty acids, whether it's amino acids, if the mitochondria are not effectively converting that substrate into energy.

And that's a very sensitive process. If there's oxidative stress, if there are nutrient deficiencies, if. If there are other factors that we'll talk through here in a moment, it will mean that the amount of substrate that can be utilized in the mitochondria decreases and there will be more fat production there.

But that doesn't mean the substrate caused it, the glucose didn't cause it, but the alcohol definitely can cause it due to the acetaldehyde production, due, the endotoxin production and the digestive tract and some other unique aspects of ethanol. So the ethanol itself can actually cause that, whereas the glucose and fructose don't have inherent pathways [00:36:00] that drive that.

Now, there is a bit of a caveat here that I'll get to, which has to do with how a lot of research is done looking at the effects of fructose at the liver. And there's two issues here there's a few issues, but this first one, in the vast majority of studies that are done on rodents, which is most of them, most of the studies are done on rodents.

They're given pure fructose as a very large portion of their total calories. Now our digestive tracts and rat digestive tracts don't absorb pure fructose very well. And that makes sense because in nature we never get pure fructose. Anytime we get a food that has fructose in it, it's balanced out with glucose, and the glucose helps with the absorption of fructose in the intestines.

I've discussed this in a previous podcast episode, so I'll link back to that. But when we don't digest and absorb that fructose, whether it's us or rats, given pure fructose, the fructose then doesn't get absorbed. It doesn't actually go to the liver. Of course a portion will, but a large portion doesn't.

It goes down, it feeds bacteria. Those bacteria produce various toxic things including lipo [00:37:00] polysaccharide or endotoxin, which then gets absorbed, goes to the liver. I mean it causes intestinal permeability. It gets absorbed, goes to the liver and is massively toxic. There actually something that's toxic there actually causes massive inflammatory effects, directly interferes with mitochondrial production and causes a number of other problematic effects.

And so when you have a study where you intentionally or unintentionally create massive endotoxin issues and then provide a substrate like fructose, you're going to see. A large amount of it go to fat. Same with fatty acid, same with glucose. If you have a large amount of endotoxin and then you provide substrate, you're going to see liver fat accumulation.

And that's what happens in these studies. Looking at rats, looking at apes, looking at humans where they provide pure fructose. There are studies where they provide antibiotics to clear out bacteria so there's no endotoxin production, and it prevents the inflammatory effects of the fructose. It prevents the fatty accumulation from the fructose.

So we know that one of the main issues, one of the main reasons why you might see increased inflammatory processes [00:38:00] and increased fatty accumulation in the case of pure fructose dosing in poorly designed studies on rodents and on humans and on apes, is due to this bacterial endotoxin issue, which is of course not at all accounted for here.

And if you were to just look at the bottom line, the conclusion of those studies that say fructose causes fat production in the liver and it causes inflammation at the liver, you might come away with a diagram like the one that Robert Lusty showed here, but it is not accounting for this massive issue of endotoxin.

Another example here, and I'm just gonna touch on these briefly. I'll be studying the studies in the notes as we have talked about these before. But polyunsaturated fats are another major driver of liver inflammation, of fatty liver disease. And rodent diets are very high in polyunsaturated fats.

Human diets are very high in polyunsaturated fats. That's what all the seed oil talk is about. They're basically one of the highest sources of polyunsaturated fats. And there are studies showing that if certain compounds are used to block the metabolites of pufa to block the [00:39:00] downstream products of polyunsaturated fats that cause inflammation and cause oxidative stress, that also prevents the inflammatory effects of fructose and the fat production from fructose even when the same fructose is provided.

But we block the effects of the polyunsaturated fats. We don't see those issues with the fructose. So again, two primary drivers here of fatty liver disease that are totally independent of the fructose, but are often blamed on the fructose. We also have the fact that rats are an extremely poor model for studying liver de novo lipogenesis from fructose.

There are studies looking at the enzyme levels in human livers versus rat livers and what compartments they're contained in and how each type of liver utilizes fructose or any substrate. And they basically show that rats don't utilize the fructose as well, and they're much more likely to produce fat in the liver.

So when we look at these rodent studies showing that fructose is causing fat production, even if we account for the endotoxin and pufa, we're still going to see greater rates of de novo lipogenesis greater rates of fat [00:40:00] production, which is just because of the fact that our human livers are far more efficient at utilizing fructose than the rats, and that these rats have generally poor metabolic states or generally in a poor place metabolically to be able to use the fructose.

So it's just a feature of that, and it's not actually something that we can translate to humans and human livers. So these are a few of the primary reasons why we might actually see some of the problems that could happen with fructose in research, but they're not actually due to the fructose itself.

Now, I also have to make another caveat here, which is that if you provide incredibly high doses of fructose, like you know that study we were talking about earlier, 270 grams, there are many other studies that use massive amounts of fructose. 25%, 30%, 50% of total calories. Sometimes they'll take the total amount of calories and add an extra, they'll do an overfeeding study where they add another 30% of total calories just from fructose.

Typically, they do this in metabolically unhealthy [00:41:00] people. When you do those kinds of things, you can see overload at the liver. You can see that production of the liver. You can see inflammation at the liver. You can see uric acid production at the liver. And we talked about this in that uric acid episode, which was episodes 84 and 85.

But this is totally irrelevant to metabolically healthy people eating lots of fructose or even metabolically unhealthy people eating typical amounts of fructose because the amounts that they're providing are in massive quantities. Typically, they're overfeeding and have all sorts of other aspects of this study.

We talked about this in the uric acid series where in a couple of studies, in, in one set of studies, in order to see increased uric acid, they had to feed pure fructose at 35% excess calories, and they had to restrict movement and exercise to the point that the participants were only allowed to do one hour of leisurely exercise a week.

That was the type of protocol they had to use to actually see increased uric acid. They had to see you eat your full day of calories, then you [00:42:00] add an extra 35% of pure fructose, fructose sweetened beverages or some other form, I think it was fructose sweetened beverages in order to see any amount of increased uric acid.

And you're not allowed to exercise or even just, do leisurely activity more than an hour a week because that would prevent this effect. And then in other studies, they would feed pure fructose sweetened beverages at 25% of the total calories. Someone's consuming in overweight people and obese people who have some level of metabolic dysfunction.

And then you can see some increase in uric acid. So the types of studies that are suggesting that fructose increases uric acid or de novo lipogenesis to any significant amount or inflammatory states are based on really faulty protocols that are not at all accounting for the nuances of fructose, digestion, absorption, and metabolism.

It's worth touching on all those things very briefly, and we're going to go through a study here looking at an example of how much fat is actually produced from fructose. And in this idea that Robert Lustig is putting forth that fructose is inherently toxic. It's inherently a [00:43:00] poison in contrast to glucose, which is totally fine.

It's the energy of life. Fructose is a poison, glucose is fine. We're gonna look at a study here comparing the consumption of glucose and fructose and if it actually increases liver fat production. Now we could use this as an example or as a marker of whether everything else is happening in this diagram that Robert Lusty has because all of it is dependent on that excess fructose going in the mitochondria producing liver fat, that driving inflammation.

If we're not seeing the liver fat, we know this is not happening. So we will take a look at this study. Titled De novo lipogenesis during controlled overfeeding with sucrose or glucose in lean and obese women. So again, we have an overfeeding study. This is the type of thing you have to do if you wanna actually see de novo lipogenesis in an appreciable amount.

And if we were expecting to see, if we were assuming that Robert Luci was correct, and that fructose is a poison and it's uniquely fattening, uniquely inflammatory in the liver, it's very different from glucose. We would expect that, especially in an over overfeeding study like [00:44:00] this, that with the sucrose group, which is table sugar, half fructose, half glucose, we would see far more de novo lipogenesis than in the glucose group.

Just pure glucose, no no extra fructose there. And so we can take a look at what they did here. They state and their conclusion where they state, firstly that de Novo lipogenesis was measured during 96 hours of overfeeding by 50%. 50% of total calories. So if someone is eating a 3000 calorie diet, they bumped 'em up to 4,500 calories.

So a massive amount of extra calories being consumed that they added via sucrose or glucose. And they did add some fat as well. And then they compare that to an energy balance treatment that controls in eight lean and five obese women. So this is the the general protocol, 96 hours, which is four days of massive overfeeding using primarily sucrose or glucose.

Of course, again, sucrose has the fructose in there. And, they compared that to a control group that didn't have any increase in overfeeding, any increase in calories. There was some fat [00:45:00] provided in the overfeeding, and the way they did this was using sugar sweetened beverages. So they basically used an equivalent of a Soda Cola that either was made with pure glucose or sucrose.

Now this is if we were ever going to see excess de novo lipogenesis in a group. It would be the group consuming the sugar sweetened beverages, which is the exact villain that Lustig is often discussing. It's, at the end of his sugar, the Bitter Truth talk, and many of his others, he is advocating for attacks on sugar sweetened beverages.

This is D culprit here that he's pointing to. We're not discussing whole food forms. We're not discussing eating fruit or something like that. This is what we would expect to be the worst of the worst, 50% overfeeding using sugar sweetened beverages. Now again, as I mentioned earlier, we can't really effectively look at pure fructose studies.

It's still worth looking at them and saying that they're even then not even showing much in the way of de novo lipogenesis and uric acid and all of that. But we have to remember that pure fructose does not get well absorbed. So it then feeds [00:46:00] bacteria, causes endotoxin production, which we know will cause issues at the liver.

But in this case, we're looking at sucrose, which is far more relevant. And again, you're not getting pure fructose in your diet. So this is the one that's actually relevant to what people can eat. Now, what they found was that de novo lipogenesis was two to threefold higher after overfeeding by 50% than after the controlled treatment in all subjects.

The type of carbohydrate, overfeeding, sucrose, or glucose had no significant effect on de novo lipogenesis in either group. So there was an increase in fat production at the liver by two to threefold, which sounds like a lot, but we're actually only talking about a few grams here. So I'll get to that in a second.

But there was an increase, but it was no different between sucrose and glucose in massive overfeeding of either of them. So we have a nail in the coffin right here. Now, again, just to touch on this, the de novo lipogenesis amount in the control group, the group that wasn't overfed was estimated at about one to two grams, a couple of grams of fat being produced at the liver.

Again, this isn't concerning. There's always fat going [00:47:00] in and out of the fat stores. You're gonna have fat release from the fat stores that the liver and from the body fat stores. So there's always a little bit that's going to be going into storage or a little bit leaving. But when they talk about, a two to three fold increase, the increase was really only up to about three to five grams.

It wasn't a large increase in absolute values. It's only a couple grams, but. Of course that is a lot in terms of a percentage, but again, not particularly concerning where we're talking about fat stores. And we have studies talking about how even in these massive overfeeding studies, the amount of de novo lipogenesis from the carbohydrate is only a fraction, normally about 1% of the amount of fat that's being consumed, which is much more likely to be stored as fat anyway.

And we'll come back to that in a little bit. It's also worth mentioning that the amount of de Novo Lipogenesis increase was a little greater in the obese group. I don't believe it was statistically significant, but it was a little bit bigger there, which we would expect when there's metabolic issues.

That's when we're going to see a bit more de novo lipogenesis. As we discussed, we wanna work on fixing those metabolic issues. They then conclude with this last quote stating the results of the [00:48:00] present study show that overfeeding with mainly glucose or sucrose for 96 hours increased de novo lipogenesis to the same extent, which suggests that in the long term, the fructose component of sucrose ceases to have a strong lipo effect.

And the reason why they're talking about the long term here is because there are other studies looking at, a few hours after consuming fructose, what happens. But this is looking at it over a longer term, which gives us a much better idea over four days straight, with large amounts of fructose coming in, showing that it's not uniquely converting to fat or causing an inflammatory state at the liver, even in this case of massive overfeeding.

Now, as I was saying, we do know that if there's dysfunction at the liver, let's say there is fatty liver disease present and you're consuming a large amount of fructose, you will see more de novo lipogenesis than glucose. 'cause more of it does go to the liver. It's important to be clear here that's not because the fructose is causing this issue.

It's not because it caused the inflammatory state of the liver. It's not because it's interfering with mitochondrial respiration and preventing it from producing energy using the fructose. It's because the liver's [00:49:00] already inflamed and damaged, which is reversible by the way. And even in this case where you're having this liver dysfunction, it's not the fructose that is primarily responsible for the fat production.

Even in these cases, free fatty acids are far more responsible. These are the primary substrate that are used to produce fat in the liver. And we'll go over a study on this in a little bit, showing that in the case of fatty liver disease, it's the fat that's actually being utilized to convert to fat, not the fructose or other carbohydrates.

So again, to conclude, in terms of Robert Lustig's pointing out all of the reasons why fructose is a poison, they're entirely dependent on a, the idea that a hundred percent of fructose, it's just gonna be used to to go to the mitochondria, which is. Completely and blatantly untrue. I don't know how he can put something like that in his presentation that in multiple presentations that millions of people will see.

And I've never seen him acknowledge it elsewhere. So [00:50:00] that's the first thing. And then the second thing being that all of these negative effects are dependent on the buildup of these intermediates, like the fructose one, phosphate, lyce, aldehyde, three phosphate, the fructose one, six bi phosphate. And those are all dependent on the fact that the fructose doesn't have anywhere to go.

Essentially, it's building up, it's not being used efficiently in the mitochondria. It and it's not being converted to these other places. So you have this backup that causes a buildup of these products that trigger fat production and inflammation, which, by the way, fat production in a case like that is the point.

It's a, it's an adaptation to say if we're consuming such a massive amount of substrate far beyond what we can use, we're going to start putting it in the last place we can, which is storage. But. Again, this is not unique to fructose. The Glyceraldehyde three phosphate, the fructose one six bi phosphate are also produced from glucose.

And as we've noted, even though a lot of fructose goes to the liver, the vast majority of it is being sent out or stored as glycogen. Some combination of those things. And the liver is very metabolically [00:51:00] hungry, so it's going to be converting very large amounts of that fructose into energy far before any amount of it is being converted into fat.

And again, we know that based on the various studies that we've been looking at here. Alright, so that brings us to a separate but related topic here. When it comes to the suggestion that fructose is toxic, it's a poison because this is one of the primary narratives in the low carb sphere. Low carb keto diets carnivore diets.

And people who are advocating for these will use these mechanisms. They'll just say, Dr. Robert Lustig says that, pointed out he showed everybody, he's proven that fructose is toxic and you can, look at his work to see all of that. Of course, we've gone through that already. And then they'll go ahead and promote a low carb, high fat diet.

And it's worth noting that certain aspects of the low carb high, the low carb, high fat diet, actually drive the exact same mechanisms that Robert Lustig is saying are the problem. Shows a little bit of hypocrisy here, especially considering that Robert Lustig [00:52:00] himself has actually advocated for this.

We're gonna take a look at a clip here. This is from a recent interview about a year ago on the Primal Podcast, where Robert Lustig discusses how a high fat, low carb diet is actually the right approach. And we're going to talk in a minute about how this actually activates and drives the exact pathways that he's saying are problematic due to fructose.

Robert Lustig: So if it's a. High fat, low carb approach, okay? So it doesn't have to be straight keto, high fat, low carb, okay? What you're doing is you're suppressing the insulin, and if you're keeping the insulin down, that's the goal. And so I'm for that, but here's the problem with that approach, okay? Not that there's anything wrong with that approach, that actually is the right approach.

Jay Feldman: Okay, so the important point here, I know you started talking about insulin and things that are not particularly relevant here. I will link back to some of the previous podcast episodes we did describing why insulin [00:53:00] is not the bad guy here, but he is very clearly saying low carb, high fat diet is the right approach.

It's a good approach. This is in contrast to, high fructose diet, high sugar diet that's going to be causing the problems that he's describing. One of the primary things that happens in a low carb diet. Also that happens in fasting, which I've never heard Robert Lusty suggest, but is something that's suggested by a lot of the other people talking about fructose being a poison for all these reasons.

One of the main things that happens in a low carb diet and in fasting is an increase in free fatty acid levels. Talked about this a bit in the recent podcast episode, talking about lipolysis and free fatty acids. But essentially when the body shifts from using mostly carbohydrates, relying on glycogen stores and utilizing glucose as a fuel to utilizing mostly fat, it relies more on its fat stores as it's storage.

And so you have a lot more fat going in and out of the fat stores and a lot more fat in the blood because that's the primary fuel that's being used. So you tend to see far higher free fatty acid levels in low [00:54:00] carb diets and in fasting, and as we'll get to the free fatty acids are actually primary drivers of the pathways that rubber lust is saying are the problem in the liver.

But first we'll just take a look at these two studies looking at free fatty acid levels in fasting and in low carb diets. So this first study is titled, effective Short-Term Starvation versus High Fat Diet on Intracellular Triglyceride Accumulation and Insulin Resistance and Physically Fit Men. And in this in this study, they were looking at a pretty long-term fast of 67 hours, and then they were looking at a low carb diet and then a controlled diet, which contained to carbohydrates, no fasting.

And they looked at what happened with free fatty acids. And so we can see here, this is figure two C, where we can look at the control group, which is on the bottom. These are the ones that had carbohydrates. We can then look at the low carb group. This is the one in the middle with the unfilled circles.

And then we have the fasting group on top with the triangles there. What we can see is that very reliably the control group, the diet that has carbohydrates, when people are consuming carbohydrates, their free fatty acids are [00:55:00] far lower. When you look at the low carb group, the free fatty acids are far higher.

Looks like about double, I don't remember the exact values here, but. It looks like about double. And then you see that the fasting group is even higher, maybe about triple of the carbohydrate containing group. So you're seeing massive increases in free fatty acid levels, in low carb diets, and in this case, in a slightly longer term fast.

But you'll see it with intermittent fasting as well. And you'll see that this even happens after consuming a meal. We can look at this in another study titled Glucose and Lipid Homeostasis and Inflammation in Humans Following an Isocaloric Ketogenic Diet. So here we're looking at figure two A and B, and we have a very interesting study here where two groups were on either a regular carbohydrate containing diet or a ketogenic diet for four weeks.

They then had them consume a carbohydrate containing meal and that they would've had on their carbohydrate containing diet versus a ketogenic diet meal. And they had each group try both meals. So on the left here, [00:56:00] this figure a the graph here. We're looking at both groups, the keto diet and the carbohydrate containing diet consuming the regular carbohydrate containing meal.

What we can see, first off, at time zero and before the baseline diet, the diet that had carbohydrates had far lower free fatty acid levels maybe 40% lower, so it looks like maybe 0.5 versus 0.8 which would actually be a difference of 60%. But in any case on the ketogenic diet, free fatty acid levels were far higher before consuming the meal versus the diet containing the carbohydrates, they then consume this meal, and even with the carbohydrate containing meal, the people on the ketogenic diet still maintained far higher levels of free fatty acids.

Whereas the people who had been on the carbohydrate containing diet, they saw their fatty acids decrease with the meal. When we then look at B on the right here, what we're looking at is both groups consuming the ketogenic meal, the low carb, high fat meal. And again, we see before the meal, the carbohydrate, the people on the carbohydrate containing diet had far lower free fatty acids than the people on the keto diet.

And [00:57:00] after the keto meal, you actually see the same thing that the people who were on the carb containing diet maintained far lower free fatty acid levels than the people on the keto diet. You do see one difference between the two, which is that the free fatty acid levels increased on the carb containing diet after eating this meal versus on versus when they ate the carb containing meal.

But in any case, we're seeing very clearly here that both fasting free fatty acids and postprandial free fatty acids, meaning after eating, are far higher on people eating a low carb diet. Now, let's look at what happens with free fatty acids at the liver. First thing, as I alluded to earlier, is that the free fatty acids are actually the primary substrate for fat production for de novo lipogenesis in the liver.

I'm gonna say that again because. Regardless of how many times I say it, I think people will be blaming fructose. But the primary substrate for fat production in fatty liver disease is free fatty acids. So we can see this study here explaining that where the study is titled [00:58:00] Sources of Fatty Acids stored in liver and secreted via lipoproteins in patients with non-alcoholic fatty liver disease.

And they state of the triglycerol, the triglycerides accounted for in the liver around 59%, we'll call it 60%, arose from non esterified fatty acids. That's free fatty acids around 25% from de novo lipogenesis. That's from carbohydrates and around 15% from the diet. And in this case, they're talking about fat from the diet.

So again, to reiterate, 60% of the fat in the liver in non-alcoholic fatty liver disease is coming from free fatty acids. 25% is coming from carbohydrates and 15% is coming from fat in the diet. To act as though going on a diet that is a low carb, high fat diet is the right suggestion here. Yet, free fatty acids are actually the ones that are following the pathway that Robert Lustig pointed out in his fructose in his fructose diagram is it's hypocritical.

I I don't know what else to say about it. What you're actually suggesting [00:59:00] is that people should, can, should eat a diet and should live in a way that increases the thing that actually goes through those pathways, which is free fatty acids. Now, I will put the caveat here before we go on to the next point, which is that I'm not saying that a low carb, high fat diet or fasting are the primary drivers of fatty liver disease or the primary drivers of liver inflammation.

We'll circle back to that in a bit. I'm just pointing out the hypocrisy of this advice that you're blaming these particular pathways in the liver or metabolic syndrome and fatty liver disease and saying that fructose is the one that'll be triggering. These pathways are going through these pathways when the reality is that the other substrates in this case, free fatty acids, are far more responsible for those pathways being triggered in the liver in fatty liver disease.

Now, there's also no shortage of studies. I'll cite them in the show notes showing that free fatty acids when they reach the liver, activate the exact same inflammatory pathways, including, the j and K pathway and increasing react oxygen species production and tons of others [01:00:00] that Robert Lustig is pointing to in his diagram that he's suggesting that fructose is activating.

The reality is that free fatty acids activate them to a far greater extent than fructose does. Now, again, this doesn't mean that anything that increases free fatty acids is the problem to begin with, just. An extremely weak argument and poor way of looking at what's going on in the liver. We're just isolating these particular pathways and saying anything that could increase them in any context must be the problem, must be the driver of the state, and that's really not the case.

I don't think that most people are dealing with fatty liver disease due to a low carb diet or due to fasting. It's not impossible. I've definitely seen people with fatty liver disease after doing those things, but I don't think that's the primary driver, especially for the average population. Instead, we actually need to take a better look at the complete physiology of what's going on in the liver.

We need to take a look at what's going on in the mitochondria and all the things that block it that are going to cause substrate coming into the liver, whether it's glucose fructose, or fatty acids, or even [01:01:00] amino acids. We need to look at what's going to cause those substrates to be stored as fat and to activate inflammatory pathways and to see buildup of the intermediates.

That could also increase things like uric acid and those inflammatory pathways. That's what we need to be focusing on. What is causing the problems with utilizing those substrates, not just blaming it on a particular substrate that's not actually causing the initial problem. And then just to touch on one other thing, one other concern when it comes to the free fatty acids, there's a number of them.

We don't, in general, wanna be doing things that increase free fatty acids because things that increase free fatty acids meaning that these are things that trigger the release of fat from the fat stores are generally stressful things. Things that increase stress hormones like glucagon, adrenaline, and cortisol.

Those are the types of things that increase free fatty acid release from the fat stores. So we generally don't want to do those sorts of things. And just like those stress hormones, which interfere with thyroid hormone production and conversion and reproductive hormone production and things like that, you see those same effects from free fatty acids.

You do see them interfering with glucose metabolism. You do see that they decrease [01:02:00] thyroid hormone binding to thyroid thyroid binding globulin. That they actually prevent the thyroid hormones from having direct effects inside the cells. They block. The capacity for T three, the active thyroid hormone, to bind to what's called its receptor and be able to activate, the metabolic state in the cell that we want from T three.

So free fatty acids are a concern for a number of reasons. And I, it's also worth noting as well that this is going to be far more pronounced with the polyunsaturated fats. If you have a lot of polyunsaturated fats stored, and that's what's being released as free fatty acids, you'll see a lot more of these other problems.

Versus if they're saturated fats, in any case, free fatty acids, while they're not ideal, we don't want to be dramatically increasing them to act as though a low carb diet increases free fatty acids. So it's the primary driver of fatty liver disease would just be a massive leap that I think, is obviously inaccurate, even though there are major costs to a low carb diet.

And obviously that's a far smaller leap than the kind of leaps that Robert Lustig has made in his presentation. [01:03:00] So to wrap up here with some concluding thoughts and to talk a little bit about what this actually means for us, dietarily, assuming that these pathways that Dr. Robert Lustig has pointed to are not the full picture, and that we don't need to be so fearful of fructose and it's not so different from glucose and it's not the same as alcohol, it doesn't produce the acetaldehyde and all of that.

Considering that those things are not the case, considering that fructose is not a poison, considering that it's not toxic, and instead recognizing that kind of like Robert Lustig emits is the case with glucose. That it's the energy of life, it's a vital nutrient. The same applies to fructose. With all that in mind, does that mean we just want to be drinking sugar sweetened beverages?

Do we all just wanna be drinking soda throughout the day and eating candy? Is that what I'm advocating for here? Am I saying that, the problem in our current environment is that people aren't drinking enough. I. Soda. The kids are all drinking too little soda and candy, eating too little candy.

Of course, I'm not saying that despite what some people might suggest in the comments, not suggesting that processed foods are healthy or that [01:04:00] those are the, or are inherently healthy and that's the problem. We're not eating enough processed foods. But what we are saying here, what is important to recognize here is that fructose is not inherently a poison.

Sucrose is not inherently a poison pointing to those things as the problem is totally detracting from what the real problems are. So it is a part of the problem here. It is preventing people from actually getting healthier. It is preventing people from changing the food supply in a way that's actually beneficial.

It is preventing people from making dietary changes that are more important for their liver health than restricting fructose, which as we've found out here, is not uniquely toxic or poisonous. So we do need to make sure that we're actually addressing what the real culprits are, and we do wanna make sure that we're exonerating the things that aren't actually the culprits.

So when it comes to fructose and sucrose, obviously these are found in sugar sources in our diet. This does include table sugar. It does include soda, it does include candy, but it's also the exact same sugars that are found in fruits and honey and maple syrup. Those [01:05:00] natural sources contain the same fructose, they contain the same sucrose, they contain the same glucose.

So the sugar itself is actually not different. Of course, there are other things in fruits and honey that are uniquely beneficial that we aren't going to get in candy. But again, that doesn't mean that it's the sugar itself that's toxic or that those other things are just making up for some sort of toxicity.

But what it does mean is that we don't need to be fearing fructose and sucrose, and we need to look at the foods as a whole and what they're doing physiologically in terms of our digestion, in terms of our liver health, in terms of our nutrient status, in terms of our, in terms of our mitochondria, in order to determine what we should be doing, how much of them we can, should be consuming, which ones we should be consuming.

So again, not saying here we all just need to be drinking more soda and eating more candy, but I'm saying let's look at the full picture. And with that in mind, we don't need to fear sugar or carbohydrates in general. We don't need to take on this obviously dishonest position, that they're poisonous, that they're toxic.

We don't need to take on [01:06:00] this inaccurate position that they're driving fatty liver. And again, I'll link back to the entire fatty liver series. We did an eight part series talking about what actually is driving fatty liver. But we don't need to be concerned about these carbohydrates so we can consume them in forms that are generally beneficial, that have nutrients that we need for, liver function and brain function and reproductive hormones and all of the rest.

And that also contain polyphenols that have benefited our gut and that also contain the carbohydrates that we actually need to produce energy, that our brains need to produce energy, that our liver needs to produce energy. So with that. I generally recommend that we favor sources of carbohydrates like fruits, juices, honey, maple syrup when we're talking about fructose containing carbohydrates.

Those are great sources of carbohydrates that contain fructose and have a ton of benefits and help not only with our fuel needs, but also the nutrients have the polyphenols that provide other benefits. We can also get carbohydrates from other sources [01:07:00] that don't have as much fructose like root vegetables, white rice, and squashes.

And I have known some people who do have issues with fructose. It's not totally outta the question, but it, again, it's not caused by the fructose. If that were the case, if someone was one of the rare people who do seem to have direct issues from it, then consuming more carbs from root vegetables and white rice and squashes would be a good option.

And it's worth noting that I've seen tons of people reverse even severe fatty liver disease consuming all of these things, consuming fruit juices, consuming honey consuming sources of sucrose. So these can be directly compatible with actually fixing our liver health because that they're not actually the driver here.

They're not actually what's causing fatty liver. They're not actually what's causing the metabolic issues that are driving metabolic syndrome and non-alcoholic fat fatty liver disease. As I mentioned, we did discuss what is causing these things in much more detail in the fatty liver series. So I'm gonna link back to that.[01:08:00] 

We talked about things like endotoxin in more detail. We talked about the polyunsaturated fats in more detail. We talked about nutrient deficiencies and which ones in specific are related to fatty liver disease. And we talked about other factors as well, other things that are causing stress in our environment that might be causing excessive free fatty acid release, which could definitely be increasing fatty liver in the case that these metabolic issues are there.

So we went through all that in detail, went into how it's all working in the mitochondria, and I think it's a really great series to check out if you're interested in all that physiology. And wanting to understand the details. Again, the physiology, the biochemistry of what's going on in fatty liver disease and what's actually causing it because it's not fructose.

And aside from that, if you're looking for more direct help with reversing your fatty liver disease or other liver issues, or other metabolic issues, and you're looking for clear action steps and strategies alongside personalized guidance from me, then you can head over to Jay Feldman wellness.com/solution where you can find all of the information for the Energy Balance Solution Program.[01:09:00] 

This program includes customized health coaching. It includes a video library with videos on how to restore gut health, how to regulate your blood sugar, how to lose weight without destroying your metabolism in the process, how to get amazing restorative sleep, how to rebalance your hormones and tons more.

It includes resources like sample meal plans, the calorie and macronutrient calculator supplement guide also includes a private community. So there's a ton of really helpful resources in there, and you can head over to j feldman wellness.com/solution to check out all the details for that program. With that, we're gonna wrap this episode up there.

As always, if you enjoyed it, please leave a like or comment if you're watching on YouTube and if you're watching elsewhere, please leave a review or five star rating of those things. Really do a lot to help support the podcast and are very much appreciated. And as always, you can check out the show notes@jfeldmanwellness.com slash podcast.

I'll link to the studies and articles and everything else that I referenced throughout today's episode. And with that, I'll see you on the next one.