Transcription
Uh, as we get into our topic today, uh, Dr. Bickman, many of you know his book, uh, "Why We Get Sick." And I'm gonna have our team pull up a little PDF, a couple of slides, because our topic today is, is a really interesting one, uh, in Dr. Bickman's book. And you can learn more about his book at insuliniq.com. There's a little tab there where you can learn more about about Ben and about his book. Inside of his book, um, on page, I think it's 74, uh, he taught, yeah, I don't know, I wish I could remember every page. I'm going to have, uh, our teams, yeah, it's page 74. There's a neat thing that we talked about among the coaches this week, and it kind of became part of the discussion that we did in some of our coaching sessions with our clients this week. We talked about fructose and fatty liver disease. And if I have, I'll have our team scroll down. So, at the bottom of this little, this page in Ben's book, he says, in referring to fructose, "Other than sugar, which is half fructose, the culprit is largely our love of fruit juice. Many of us consider it a healthy drink, but all fruit juice is is a potent source of pure fructose. Hopefully, this prompts you to think twice before drinking that cup of apple juice, let alone giving it to your kids." And finally, at the bottom, Ben goes on to say, "This is not, however, a call to avoid fruit because of its fiber content and relatively lower fructose. Whole fruit is very different from fruit juice. In fact, eating whole fruit is better for improving diabetes risk than drinking juice from the same fruit." So, if Ben has said many times, "If you're going to have fruit, eat your fruit and don't drink it." So that's true. With that, is a little bit of a setup. You know, we've had this discussion this week, and, and, uh, Ben said, "Hey, why don't I talk about that on the Metabolic Classroom this week?" I'm going to turn the time over to Ben. He'll kind of frame up this discussion in his laboratory and the metabolic classroom. So, Ben, go right ahead.
Yeah, yeah, thanks, guys. Really, this is such a fun opportunity for me to, to sort of play the role of professor, which is something I genuinely enjoy. So, guys, really, thanks for humoring me. And anyone listening, thanks for tuning in. And be a good student and ask some questions if anything comes to mind during this bit of the, the discussion that we have now. So, to put things in context, Jack, you cued it up well. And just to add to that, people may be listening to this and thinking, uh, well, I don't have fatty liver disease, so it's no problem. Um, more people have it than, than, than they, than they realize. It is the single most common liver problem in the world. In the world. If, if we're worried about liver problems, fatty liver disease is number one. And it's kind of a gateway problem. Just to put things in perspective, someone may think, well, that's fine. If I, I have a little more fat on my body, I have a little more fat in my liver, it's okay. It's just fat. That's not true. It's, it's what the concern is, what it progresses into. And what starts as fatty liver disease can progress into what's called non-alcoholic steatohepatitis, which is when the liver, at first, it's just fat. Then it gets fat and inflamed. And then it can progress all the way to cirrhosis, which is kind of fat, inflamed, and scarred. And now, once you've included that scarring, now you're doing some irreparable damage to the liver. So, uh, fatty liver disease is really a gateway problem. And again, more people have it than realize. And it's, it's, it's sobering what it turns into. In fact, it's such a common problem that when people are trying to find liver transplants, they're, they're running out of liver donors because so many people have fatty liver problems and they just don't know it. And so our actual pool of, of people who can donate a portion of their liver is shrinking as the livers are getting fatter.
Yeah, let me interrupt you one second just to chime in. I read an article, uh, just the other day. In fact, I think I saw the link to this article from one of your followers on Instagram who linked to an article that talked about the epidemic among young people with fatty liver disease.
That's right. Yeah. Even in kids. So it's the most common liver problem in the world. That's not just adults, it's kids. And I am, based on what we'll discuss today, I think everyone will be able to agree it is, it is totally what we're feeding the children. And it is this, uh, heavy, heavy focus on fructose and just sugar in general, which I'll attempt to keep as a part of the conversation because that's, that's relevant, uh, when we talk about fructose. So there are three studies that I thought would be helpful to just touch on lightly to really set the stage, because I know this is debated. There are people who, in especially in the low-carb community, who will say fructose isn't that bad. And the only evidence suggesting that fructose causes fatty livers is in rodents, and in humans, the evidence just isn't there. And so I made sure to just strictly focus this discussion on human studies. And the first one was an article published a few years ago. It was in 2009, in a very good journal, the Journal of Clinical Investigation. It's one of the better biomedical journals out there. And there, there are several outcomes in each of these studies. There are other outcomes that I won't touch on, including lipids, really looking at the changes in blood lipids, which is interesting, but a topic for another time. But it is relevant because the liver makes the blood lipids for the most part, triglycerides, LDL, VLDL. It regulates HDL levels. So the liver is, is very much at the crux of, of those processes. So, uh, that, having been said, this first study took people and over a course of, of 10 weeks, changed their diet to keep it isocaloric. So they didn't want the people to be eating more calories than they were before. But what they had them do was start consuming 25% of their calories from either just pure glucose, so a pure glucose solution, or a pure fructose solution. And Jack, you mentioned it well, and we were talking a little bit beforehand where Rich asked about the relevance of this. Uh, the pure fructose consumption is very relevant. This is fruit juice that, that we're drinking all the time. And, and I, I felt very compelled to point that out in the book because as a parent, and, and seeing what is, what we're told, uh, in through marketing, uh, what we should be feeding our kids. A very well-intentioned parent would be thinking, my kid wants soda pop. Of course, the kid does. Every kid does. I'm not going to give them soda. I'm going to give them fruit juice. And I'm a good parent. I'm doing my children a favor by doing this. Little realizing that that you are giving them pure fructose, that is exactly what we're talking about in these studies. Now, what would be more unique is someone drinking pure glucose. That would be uncommon. But when someone is drinking something with sugar in it, like a soda, that is a mix of glucose and fructose. So throughout these two studies, I'll highlight where we're causing fatty liver in people. Um, they're doing it in a glucose group versus a fructose group. You could imagine that when someone's drinking soda, they're getting the both of these. I would say the best of both worlds, but it's really, uh, the worst of both of these outcomes. They're combining, you could, you could really consider that you're combining the negative effects of the glucose and fructose in so far as you're, you are getting it together in sugar, which you get a lot of in soda. So this is relevant, uh, I believe it's something that is very, very common. The liver problems common. And I think it's because of the consumption of fructose and sugar, which is a rich source of fructose. So back to the study, they took these people for 10 weeks and they were getting 25% of their calories from glucose or 25% of their calories from, from fructose. And we're going to attach links to these studies. So any listeners that go in and find the links, just remember this is the study that was published in the Journal of Clinical Investigation. So the, the first, um, or really the main outcome that I want to focus on is, is expressed in table three and in figure one. But basically, they measured the actual, in, in the first, in the table, they measured the cubic centimeters of fat. So the actual, like volume of the fat, um, around the central part of the, the, the abdomen. They measured the extra-abdominal fat, which is the subcutaneous fat, the fat that would be around your waist that you can pinch and jiggle. And then they measured also the intra-abdominal fat. That would be visceral fat. That is the fat that is beneath the layer of muscle on the stomach. And so this could be the guy who, you know, imagine two men who have fat bellies. One of them has the fat belly that hangs down and it's wiggly and jiggly. That's the subcutaneous or what they're calling extra-abdominal fat. Then the other guy has a big round belly, but it's hard. It sticks out rather than hangs down. That's more reflective of visceral or, as they cite in this study, intra-abdominal. And what was so interesting is that in both of these studies, in both of these groups, drinking the glucose or the fructose, both of them got about the same degree fatter, although the fructose drinking group had a little more total fat, um, than the glucose-containing drink, uh, group. And then the different, although it tended to go up in both of them, um, and then what we, what was interesting was noting the differences in those two fat depots, the intra-abdominal or visceral, or extra-abdominal or subcutaneous. And what they found was that the glucose drinking group, uh, selectively had more of their fat accumulating in the subcutaneous space. So it's that pinchable, jiggable, jiggy-jiggy, jiggly, jiggly. That's what I was trying to say. But I'll just show you mine.
No, Rich, don't break up any happy marriages. We don't want to, we don't want to make the other men upset. Jack and our fragile egos can't handle you showing off your shirtless body.
But we compare that with the fructose drinking group, who had relatively more of their fat, indeed a significant increase in their visceral fat. Now, that's as far as that study went. I'm just highlighting that to set the stage that the glucose drinkers and the fructose drinkers both had more fat over the 10 weeks, actual physical volume of fat in their central abdominal area. The glucose drinkers had more of it in their subcutaneous, and the fructose drinkers had more of it in their visceral. Now, visceral itself can, can really encompass a lot. It can encompass both fat within the tissues, like the liver, or fat literally around, surrounding the tissues, like omental fat. So they didn't, they didn't tease that apart. Now, let's go to the next study then. And this is a study, uh, where the title is "The Effect of High Fructose Weight-Maintaining Diet." And that's how it starts. This was published in another very good clinical journal, the Journal of Clinical Endocrinology and Metabolism, in 2015. Same intervention, 25% of the, of the calories were now in this study coming from fructose. That's just, that was the only arm. And then there was just a control group, which was getting a comparable amount of carbohydrates, but it was coming from complex carbohydrates, so fruits and vegetables. So, uh, but once again, isocaloric, attempting to maintain weight. They, so they weren't trying to make them lose or gain any weight. Um, the results of this were once again pretty, pretty telling where, and we can see this very easily in the abstract. They looked at two measurements of liver, uh, fat regulation. One was the degree to which the liver actually started making fat from, from scratch. And when we're making fat from scratch, that's generally coming from carbohydrate. That's really the backbone of what the liver will use to make new fat. And then in addition to measuring liver fat production, which is called de novo lipogenesis, or the, the creation of fat from, from nothing, or from scratch, or, you know, new. And then, then they, they also measured actual fat, um, within the liver, as measured by an MRI-like scan. So they measure the, the degree to which the liver is making fat, and the degree to which the liver is actually getting fatter. And this was just a few weeks, and over the, in fact, just about a week and a half, um, they did this fructose intervention group. They found that after this period of time, the group that was containing 20, drinking 25% of their calories from fructose, their liver was making about almost 80% more fat. So the de novo lipogenesis had been activated by about 80% higher than in the control carbohydrate group. And the actual amount of liver fat went up by 137%. So they more than doubled, they more than doubled the amount of fat within those livers during this period of time, just by shifting the, a portion of their calories away from even normal carbohydrates into just fructose. And this really would be something like someone just drinking a lot more soda or a lot more fruit juice. And, and they do that with the best of intentions, of course, including making their own. And there's so many times I've had people ask me, well, I don't buy juice at the store, I juice it at home. Your liver doesn't care. And, and to, to the book's point before I get into this last study, uh, it's, I, I, I, I say when I defend fruit, because I think fruit can be part of a healthy diet. When someone's drinking a cup of apple juice, it's like someone would have to go in and eat four apples or five apples. And, and you would never do that. You would just get sick of the apples long before you got through apple number five because of all the substance and even just the labor of chewing it, you would just get tired of the apple. But when you drink the juice from five apples, or you could do that in a few gulps and you'd be asking for more. We have, we change the nature of that fructose. So I don't intend for anyone to hear me to think that I'm just waging outright war on fructose. No, as a species, we've been eating fructose for millennia, albeit very, very infrequently, especially compared to how we eat it now. Now, all of this, so these two studies emphasize that you can take someone and have them eat fructose and make them get fatter in their visceral space, and specifically in their liver, by over double within just about a week and a half. So there's no question this is relevant. It happens. Here are the studies to show it. Now, the follow-up study is kind of the good news. And this was a study, it's called the "Fruitless" study, which is really clever, isn't it? It's published by the American Society for Nutrition. And this was just published at the end of last year. So this is the most recent of all. And this was published in the American Journal of Clinical Nutrition, which is the journal for the American Society of Nutrition. It's their official journal. This was a bigger study. They took, it was almost 50 individuals that had confirmed fatty liver disease. They used something called the fatty liver index, but they also were measuring actual liver fat through magnetic resonance, like an MRI-type strategy. And they split the people up into drinking glucose as a portion of their calories, once again, or drinking fructose as a portion of their calories. And over the, let me scroll down to it. They found in figure two, if someone goes to that, they confirmed that the fructose consumption had dropped precipitously in the low fructose group. So they were sort of shifting between these two interventions. What's so interesting is that BMI itself didn't change, um, although it came a little close, um, but also caloric intake did not change. So this was not a low-calorie. They were just shifting the fructose and glucose consumption. And then in figure three, they measured intrahepatic lipid, or the actual amount of fat within the liver. And they found that the group that was shifted onto the low fructose diet had a significant reduction. And this was a P value, for those that care, of less than .001. That's pretty impressive in a human study, especially of one that was that contained less than 50 study subjects. The fact that it was that significant suggests that it was a pretty real phenomenon. And the reduction was about 25% to 30%. So after just this, the short intervention of cutting back the fructose, um, they were able to reduce the, but not all carbohydrates, but they were able to reduce the fat within the liver by about 30%. And again, just by cutting out the fructose, putting them on a very low fructose diet. So the takeaway from all of this is, if someone knows they have fatty liver disease, or they suspect they have insulin resistance, which then very likely suggests that their liver is getting fat, you don't need to make it very complicated. Uh, it's, it's just this, this first rule that I think is, is necessary for improving the health, which is controlling carbohydrates. Part of that is, as I outlined in my book, "Don't Be So Sweet." Just avoid those sweet things. And that means avoiding fructose, because if it's sweet, it's fructose in nature. And, and that's going to be you avoiding the culprit, the main driver of, of your fatty liver problem.
Okay, Ben, what are the long-term effects of having a fatty liver?
Yeah, yeah. So it's really what I outlined earlier. The progression of NAFLD, or non-alcoholic fatty liver disease, then it progresses toward, progresses towards, uh, steatohepatitis, where it's fatty and inflamed. Then it's cirrhosis, which is inflamed and scarred. And then it's cancer, potentially. That's really the progression. And I meant what I said, fatty liver disease in and of itself, you would make the case, and I would agree, it's, it's benign. Itself isn't going to kill you. It's a gateway problem. At the liver, though, not only in the liver, but as the liver is getting fatter, it's very likely becoming increasingly insulin resistant. And that, when the liver becomes insulin resistant, that's one of the key tissues, if within the body, that flips the switch, as I say, flipping it from just insulin resistance or pre-diabetes up to actual type 2 diabetes. When the liver is becoming insulin resistant, it starts pumping, releasing glucose like gangbusters, you know, thereby driving up the blood glucose and then getting diagnosed with type 2.
Yeah, you want to take a few questions? We've got some questions related to this topic from, from Michelle. How long does it take to reverse fatty liver? I've been keto and carnivore for three and a half years. I had an ultrasound that showed mild fatty liver disease and mild to moderate fibrosis. The question is, how long does it take to reverse fatty liver?
Yeah, well, this study found significant reductions, about 30%, in liver fat after just, I think it was two weeks. Six weeks, sorry. It was six weeks. More, more than I thought. So after six weeks of just low fructose, it went down by almost 30%. So I, I guess we, I don't know whether I'm sure there's a diminishing returns or the rate of reduction starts to slow down. But I would think within six months or so, that's a problem that you would could have resolved. I know Robert Cyrs, the gastric bypass surgeon, who, he has a big voice on the internet. He talks about when you go in for a gastric bypass, fatty liver is a big problem. They need to get your liver, uh, your fatty liver under control so that they can see everything and do the surgery properly. And he talks about how he just puts people on like a broth for two days, and it, it controls their fatty liver pretty quickly. So I've always thought it was something like insulin resistance or insulin, at least levels, you can reverse very quickly. But, you know, you might have to over time play around with what you're doing and maybe incorporate some fasting to kind of see the benefits of it long term.
Yeah, in fact, I love that you mentioned fasting. One worry I would have is that most of the fat that is stored in the liver comes from fat flowing in the blood. Whether it is fat being released from fat cells as free fatty acids, or whether it's triglycerides coming from liver, uh, coming from the diet, like from chylomicrons, from what we're eating. So I, I could imagine a situation where someone goes really very, very low carb, but is still very high fat, or even higher calorie in general. I am, I'm a bit, I think focusing on calories first is not the prudent strategy. But when it comes to clearing the liver out of fat, I could imagine a problem if you are eating too much fat. You might want to, you know, actually go through that period of fasting. So I could see why Robert would kind of go on a, you know, extremely low-calorie diet for a couple days. I think when it comes to the liver, it's so good at pulling in fat to store, although that is accelerated with insulin, that it might nevertheless be prudent to focus on fasting for at least a period of time.