Rates of non-alcoholic fatty liver disease are surging and, within the next decade, the condition is expected to be the leading cause of liver transplants in the United States. Tragically, rates among children are surging just as quickly as rates among adults. In today’s episode of New Frontiers, Dr. Fitzgerald talks with one of the founding fathers of functional medicine, Robert Rountree, MD, about this increasingly common condition, how to test for it, and, critically, how to use lifestyle changes and supplements to reduce the amount of fat in the liver and restore health.
In this podcast, you’ll hear:
- The origin of functional medicine
- Why rates of non-alcoholic fatty liver disease (NAFLD) are surging worldwide
- How NAFLD is often overlooked as something innocuous
- How NAFLD is diagnosed
- The limits of ultrasound in tracking the progression/regression of NAFLD
- How NAFLD is a precursor to NASH, which can lead to cirrhosis
- The high incidence of NAFLD in children
- How high rates of NAFLD and NASH are driving up the need for liver transplants
- How experts expect the need for liver transplants to rise dramatically by 2025
- How labeling NAFLD a comorbidity might be a misrepresentation
- The role of high fructose corn syrup in the development of NAFLD
- The hypothesis that fatty liver is the true genesis of metabolic syndrome
- The number one risk factor for NAFLD
- About of hepatic methylome disorders
- The importance of choline for hepatic health
- How to use phosphatidylcholine and phytosomes with patients
- Looking at ALT and GGT as markers for NAFLD
- How to take a detailed history to identify the etiology of NAFLD in patients
- The gut health + NAFLD connection
- How bariatric surgery increases the risk of NAFLD
- Key supplements for NAFLD patients, including curcumine phytosome, guar gum, NAC, and berberine
Dr. Rountree received his MD in 1980 from UNC-Chapel Hill, followed by a residency in family medicine at the Hershey Medical Center. He began his professional career at Wellspring, Partners in Health, in Boulder, CO, a multidisciplinary clinic that was one of the first integrative medicine healthcare centers in the U.S. In 2002, he opened Boulder Wellcare, a private practice specializing in personalized healthcare consulting. Dr. Rountree has coauthored numerous books and written numerous book chapters on integrative and nutritional medicine. He is the long-time Clinical Editor and a regular columnist for Alternative and Complementary Therapies (Mary Ann Liebert, Inc).
In addition to his clinical practice, he is a long-standing member of the core faculty for the Institute for Functional Medicine. In June, 2015, he was given the Linus Pauling Functional Medicine Award by IFM, in recognition of his years of mentoring and training health care providers. Bob also serves as the Chief Medical Advisor for Thorne, a world leader in the development and manufacturing of pure, high-quality nutritional and botanical supplements. Over the past twenty years he has had the opportunity to lecture all over the world to professional and public audiences. Bob is especially passionate about the great outdoors, wild nature and the preservation of biodiversity.
Dr. Kara Fitzgerald: Hi everybody, welcome to New Frontiers in Functional Medicine, where we are interviewing the best minds in functional medicine. Of course, today is no exception. In fact, I am extremely excited to be talking to my good friend and long-time colleague, Dr. Bob Rountree. We’re going to be talking about fatty liver disease today. But before we jump into our content, let me just tell you a little bit about Bob. He received his MD in 1980 from UNC Chapel Hill, followed by a residency in family medicine at the Hershey Medical Center. He began his professional career at Well Spring Partners in Health in Boulder, Colorado, a multi-disciplinary clinic that was one of the first integrative medicine healthcare centers in the US.
So, you’ve been in this for a long time. We’re going to talk about that in a second. In 2002, you opened Boulder Wellcare, a private practice specializing in personalized healthcare consulting. Dr. Rountree has co-authored numerous books, and numerous book chapters in and on functional medicine. He’s a longtime clinical educator and regular columnist for Alternative and Complementary Therapies. In addition to clinical practice, he’s a longstanding member of the core faculty for IFM. He was awarded the Linus Pauling Functional Medicine Award in 2015. You also probably know he is the chief medical advisor for Thorne. He’s lectured all over the world. Most of our audience has likely heard your amazing lectures, and I had the honor of presenting with you at the Immune Module at the Institute for Functional Medicine. Really, every time I have the opportunity to hear you, Bob, or talk to you, I learn from you, and do so in a way that’s always really fun. So, welcome to New Frontiers.
Dr. Robert Rountree: Thank you. It’s a pleasure to be on. A thrill, actually.
Dr. Kara Fitzgerald: Yay.
Dr. Robert Rountree: Yay.
Dr. Kara Fitzgerald: Listen, in your bio, I can hear your story. You jumped in integrative medicine basically out of med school, it sounds like, but I just want to understand a little bit of background around it. As I was mentioning earlier in my questions to you, it’s like you were born with a functional medicine spoon in your mouth. You’ve been in our space for a long time, and you started immediately. Just tell me, how did that happen?
Dr. Robert Rountree: I actually was studying alternative medicine before I went to medical school. When I was 19, somebody gave me this book called Herbs: The Magic Healers by Paul Twitchell. It was about using botanical medicine to treat disease. To be honest, I never thought about anything remotely like that. I wasn’t interested in health and wanted to further my understanding. Somebody just said, “Hey, this is a cool book. You should read it. It’ll help you get healthier.” I read it, and I thought, “Oh my god, all this stuff that I never considered,” because I grew up in the South eating crap. This amazing crap. The area I came from in North Carolina, and then before that, Alabama. They call it the stroke belt, right? I grew up eating black-eyed peas with red-eye gravy on it. Green beans that had been boiled with fat back for hours on end. That was all I knew about diet, and then suddenly I read that there are these herbs that can heal you. I didn’t even know what chronic disease was. I didn’t know anything.
I read that, and I thought, “This is what I want to do. I want to be an herbalist.” I looked around, and it seemed like there weren’t many career tracks being an herbalist. I couldn’t see any future. I thought, “I should just go to medical school.” I mean, really. I wasn’t that interested in mainstream medicine. I just wanted to get the degree. But then I got to medical school and I thought, “There’s something here. There’s good science. I like the scientific method. I like the idea of having a hypothesis and then confirming the hypothesis.” I was surprised at how useful a lot of the thinking was. At the same time, I was shocked at how bullheaded the good old boy network was. I went to med school in Chapel Hill. If you said anything about nutrition, they basically dismissed it as, “Well, that’s the purview of the Home Ec people.” ‘Member home economics? Home economics, that’s what … Nutritionists went to home economics school. Home Ec, we called it.
You do Home Ec, and you learn how to cook for your man, or for a prison, or for a hospital. That’s what dieticians did. Then somewhere along the line, so I was really frustrated, because I had read this book and then I had gotten into herbal medicine in more detail. You start learning what you eat affects your health, all that kind of obvious stuff, but it wasn’t so obvious to my professors who were just into mainstream pathology. Then I heard about this guy named Jeffrey Bland. That was decades ago. One of my friends in medical school went to a conference and Jeff Bland spoke. He said, “You have got to hear this guy, because he is speaking to the science behind nutrition.” Up until that point, we’d heard, “There is no science behind nutrition. It’s just as beneficial to eat a bag of potato chips as it is an apple. It’s got the same nutrients.” I heard that.
Dr. Kara Fitzgerald: That’s amazing. Yeah.
Dr. Robert Rountree: It was amazing how bad … You just can’t even imagine what kind of terrain there was when Jeff first emerged from the darkness. Here’s Jeff with this amazing command of the literature saying, “Well, osteoporosis is a nutritional disorder.” I heard about him, I made plans to go to a conference in nutritional medicine where he spoke. I was blown away by it, but wasn’t quite sure what to do with that information. Then what happened is I went to a residency in Hershey, Pennsylvania, Family of Medicine residency, and one of the professors there knew Leo Galland.
Dr. Kara Fitzgerald: Huh.
Dr. Robert Rountree: Said, “You’ve got to check out this guy’s research. He’s a conventional internist, but he’s looking at the role of essential fatty acids and health as an anti-inflammatory.” This was decades ago. I ended up meeting Leo and really having a good meeting of the minds. We were also getting very interested in all the research on gamma-linolenic acid. You remember all that, right?
Dr. Kara Fitzgerald: Mm-hmm.
Dr. Robert Rountree: The whole evening primrose thing. It was kind of following that track and decided, “This is what I want to do is this high-level nutritional medicine.” Well, when I finished residency, there was a training at the Omega Institute in Rhinebeck. I said, “I want to do that.” It was a week-long training. It had Jeff Bland, Sidney Baker, Leo Galland, and Neil Orenstein. I spent a week with those guys and that was basically, as far as I’m concerned, that was the genesis of functional medicine right there.
Dr. Kara Fitzgerald: Wow.
Dr. Robert Rountree: It basically followed from that point on. I’ve always practiced something you could call functional medicine from day one. Then when the institute, which basically started within the Institute of Functional Medicine kind of started within Metagenics as a training program for how to use Metagenics’s products. Then it eventually broke off and became this independent non-profit. From the very first training, I was involved in the course. We had a very short course at one of the IFM symposia that is what became an applied functional medicine in clinical practice. I spoke at that first short course on inflammation. Then all of this kind of evolved from there. That’s been decades.
Dr. Kara Fitzgerald: Yeah, amazing. Geez. It’s really great to hear.
Dr. Robert Rountree: Amazing. I had no idea that it would become as successful. We just thought we were a small group of nutritionally-oriented, biochemically-oriented people. We have some interesting ideas, and we hope that they’ll get implemented in mainstream medicine. We had no idea it would become phenomenally successful and known around the world.
Dr. Kara Fitzgerald: Right, and really, in rather incredible high demand.
Dr. Robert Rountree: In incredible high demand.
Dr. Kara Fitzgerald: It’s pretty extraordinary. Well, thanks for that background. What’s really lovely is that we still have, well, access to those original guys today. I mean, we still get to hear them speak. I mean, it’s just, it’s a pond that’s growing rapidly, but it’s still intimate.
Dr. Robert Rountree: Yeah, the roads are still intact.
Dr. Kara Fitzgerald: They really are. You’re deep in there. You’re part of the root structure, Dr. Rountree.
Dr. Robert Rountree: Well, it’s a thrill to have known Sid Baker for well over three decades, three and a half decades, and to watch his thinking evolve, and to hear him over and over again.
Dr. Kara Fitzgerald: Yes, yes. He’s always inspirational. I have a clinical development program at my practice where doctors transitioning in are shadowing and seeing what we do. Well, I’d love to have you talk to our people at some point, so we’ll talk about that later, but Sid has inspired the group on multiple occasions, as has Jeff. It’s just really lovely, it’s just lovely that we have access to these human beings.
Dr. Robert Rountree: This is amazing—inspirational, visionary people.
Dr. Kara Fitzgerald: Yeah, that’s right. Okay. Let’s jump into our topic at hand, nonalcoholic fatty liver disease. You’ve been doing some really interesting, and as usual, progressive, comprehensive thinking around it. Background as well as what we want to be thinking about and doing with our patients with regard to identifying it and treating it. Just talk to me about nonalcoholic fatty liver disease. What’s the deal? Give me the details, the epidemiology. Go.
Dr. Robert Rountree: We had talked earlier about how I got into this, which is that I’d heard a presentation by Dr. Lyn Patrick a number of years ago. She’s a well-known naturopath who’s been studying chronic liver disease of all stripes for many years. She gave a talk on the overlap between hepatitis C and fatty liver. This is a number of years ago when nobody was talking about fatty liver as a standalone entity. It just struck me when she said, “We’ve got a tsunami coming our way. The tsunami is going to be this tsunami of people needing liver transplants.” I said, “What are you talking about?” This was before we had the drugs for hepatitis C. I guess everybody thought, “Well, once those drugs come out, you can cure hepatitis C. You’re not going to see so much cirrhosis. We’ve mostly got treatments for chronic hep B. So cirrhosis is going to be in alcoholics, right?” Well, no, it turns out there’s this other condition, nonalcoholic fatty liver disease, that is creeping into our health without announcing itself.
Now what the experts are saying is that fatty liver, especially nonalcoholic fatty liver, is really the pandemic of the 21st century. It’s the number one cause of chronic liver disease in the Western world, and it’s headed towards being the number one cause of liver disease in the entire world. Wow. This is much more common than we ever would have imagined. How is it diagnosed? Typically, it’s diagnosed on a routine lab. A person comes to see a doc and says, “I want a wellness eval. I feel fine, maybe I’m a little overweight, but otherwise, I don’t really have any problems.” They do a chem screen, and their ALT is up. Sometimes it’s up just a little bit. Depending on the lab you use, an upper range is, what? 40 units, something like that?
Dr. Kara Fitzgerald: Mm-hmm.
Dr. Robert Rountree: These are sometimes people that are just a few units above normal. You would tend to think if you see that, “Oh, it’s probably nothing. Maybe they had a little too much to drink the night before.” Or, “Maybe they took one too many Tylenol. Maybe they had some kind of transient viral infection.” That’s what we used to say in the past, but when I see that now, it’s a big red flag. It’s a big red flag. I am much more prone to, well, I always want to repeat it to make sure it’s real. I still do serologies to make sure it’s not B or C. Do the basic kind of workup, and if all that’s negative and the ALT is still up, then I have a low threshold for ordering an ultrasound.
Dr. Kara Fitzgerald: Yeah, I think those…
Dr. Robert Rountree: Typically, what you get on the ultrasound is you don’t get a quantitative report, unfortunately. All you get is a report that says, “If this is true,” a report that says, “You’ve got fatty liver.” I say unfortunate because we really do need to be able to quantify this, because the number one question I get asked is, “If you’re going to intervene, how do you know that your intervention is making a difference over, say, a three-month period of time or a one-year period of time?” In patients where I’ve done serial ultrasounds and I’ve done quite a few of them, all they really are going to tell you is that the liver has gotten bigger or not. The report will say, “Yeah, there’s still fatty liver, and the liver’s the same size.” But what we need to know is what’s the fat content? The definition of fatty liver is when the fat content exceeds 5% of the liver volume. If you think about it, that’s extraordinary. 5% of parenchyma tissue is replaced with fat. What’s extraordinary is that the person can have that going on and have no symptoms. They don’t have pain. They don’t have jaundice.
They don’t have spiders. They don’t have anything that indicates that there’s a problem. So here’s this silent disease, right? The issue with it is not, at least we used to not think that fatty liver in and of itself increased mortality. The issue has always been that fatty liver is the precursor to fatty hepatitis. Nonalcoholic steatohepatitis or NASH, because once you get to NASH, that means there’s inflammation, right? Inflammation is something that you can detect with a C-reactive protein elevation, et cetera. But you would also see inflammation on a biopsy. Technically, the ideal thing would be to have liver biopsies from the get-to. Nobody’s going to do that, but in studies where they have done that, that’s how NAFLD is distinguished from NASH is on a biopsy, you see scar tissue. Scar tissue means you’ve got activation of stellate cells that are laying down collagen. If you lay down enough collagen, the liver will shrink and it will lose function.
The problem in the past was always thought to be one of progression of fatty liver to NASH. That if you get NASH, now you’re in trouble, right? Because NASH can lead to cirrhosis, and cirrhosis leads to loss of function, or hepatocellular carcinoma, right? Once you’ve gone down that path, then you’re talking about new liver. Well, okay, is that a rare thing? Apparently not. I mean, the epidemiologic studies, like the NHANES study, I think, was one of the first studies to really look at this. NHANES, what was it? NHANES III. What are we at now? Are we still at III or are we at NHANES IV? Do you know? I was just trying to look that up, and it’s not … NHANES is a CDC sponsored nutrition survey, right?
Dr. Kara Fitzgerald: Yeah, right. Mm-hmm. I…
Dr. Robert Rountree: We’re either at III or IV, but I know the NHANES III was one of the more recent ones. In that one, they surveyed more than 10,000 people and in that survey, they determined that 22% had fatty liver. But there’s been other studies that have said it’s even higher than that. The current guess is that about a third of the population has fatty liver at some degree of fatty liver. A third of the population has more than 5% of their liver tissue replaced with fat. Do you think that’s scary? I think it’s scary.
Dr. Kara Fitzgerald: It’s extraordinary. Yeah. It’s extraordinary. It’s mind-boggling.
Dr. Robert Rountree: It’s extraordinary, especially with newer studies suggesting that fatty liver itself confers problems. We can go into that in some, in a little bit more detail. The other issue that’s really scary here is that it seems to be even more prevalent in kids. Some studies are suggesting that even in healthy-appearing kids, that some, at least up to 10% have some degree of fatty liver.
Dr. Kara Fitzgerald: Yeah, I know.
Dr. Robert Rountree: If the kid is fat or has type 2 diabetes, then that percentage goes way, way up. Way over 10%. Some studies are saying 30 to 40%. Some studies are showing even more. The big worry is that if you’ve got a five-year-old kid with fatty liver, and you don’t do something about that, that kid’s going to need a liver transplant. The surgeons are talking about this. The liver surgeons are saying, “My god. By the year 2025, some 25 million Americans are going to develop NASH, and 20% of those are going to go onto either cirrhosis or liver cancer, and they’re going to need to have a liver transplant. Where are these livers going to come from?” When we talk about the tsunami, that’s what the tsunami’s about. Suddenly we’re going to have a shortage of extra livers, unless we do something about it. That’s why drug companies are spending millions, tens of millions of dollars doing research on the drug. They’re looking for the drug, right? Because if you can find a drug that reverses this, especially once it’s got to NASH. If you can find the drug, obviously it’s going to be a billion-dollar drug.
But right now, there are not drugs approved. There’s nothing. I mean, there’s maybe some benefit from lipid-lowering drugs or glucose regulating drugs. There might be some benefit, but none have really been shown to reverse NASH, which is, we’ll get into this later, but there are supplements. There are supplements that can reverse it. Here’s the deal is that in the past, we said, “Well, it’s only, this is only a problem if you go on to develop NASH.” But newer studies are showing that, actually, just having fatty liver increases your mortality dramatically. Right?
Dr. Kara Fitzgerald: Right.
Dr. Robert Rountree: Fatty liver by itself means something. I think, this is analogous to the old days when we would say, “Oh, if your hemoglobin A1c is over, what? 6.2, then you’ve got diabetes. If it’s below 6.2, then you’re fine.” Obviously not the case. It’s a continuum. The risk never goes away, but your risk starts at, what? 5.5 or 5.6%? Then goes up. I think the same thing is true with fatty liver.
Dr. Kara Fitzgerald: Let’s just, I mean…
Dr. Robert Rountree: That’s scary. It’s scary, right?
Dr. Kara Fitzgerald: Well, it’s profound. I mean, some of the data that you sent me is just, yeah. It’s outrageous. Those with nonalcoholic fatty liver disease, what’s supposed to be not a big deal, had 70% higher overall mortality. That was specifically due to cardiovascular events. I mean, it’s 70%. These data are outrageous.
Dr. Robert Rountree: They’re outrageous, and I tell you, if you look in the mainstream literature, although this is, it’s really changed in the last year or two because the awareness has dramatically grown. But in the past, fatty liver has always been called a comorbidity, right?
Dr. Kara Fitzgerald: That’s right.
Dr. Robert Rountree: When you talk about comorbidities with type 2 diabetes, you would say, “Oh, gallstones, cardiovascular disease, gallstones, PCOS, and fatty liver.” It’s always been, “And fatty liver.” What has really come up for me in diving into this literature is that it should be, “Fatty liver, and type 2 diabetes, and cardiovascular disease, and all these other things,” right? Maybe fatty liver is much more central to the pathophysiology instead of, “Oh, it’s one of those consequences.” If you think about it, if you’ve got fatty liver, you’ve got fatty muscle. Why are we just, we’re only focusing on the liver here, but if you’re replacing liver tissue with fat, you’re also replacing muscle tissue with fat. We have a name for that which is sarcopenia.
Dr. Kara Fitzgerald: Well, okay, so you’ve elegantly and perhaps a bit scarily outlined the extent of the problem that we’re looking at. Again, the research on kids is particularly startling…
Dr. Robert Rountree: Disturbing.
Dr. Kara Fitzgerald: 10% of lean kids, ugh. Yeah, it is. It is. All right, so folks, I just want to assure you that we will get into how to work it up…
Dr. Robert Rountree: Something to do.
Dr. Kara Fitzgerald: How to work it out, and what to do. Yeah, we will, but before we jump into it, I want to talk about the risk factors. Move through those. Move through the most relevant risk factors.
Dr. Robert Rountree: How do people develop this? The early papers all said, “Well, it’s because we overeat and under-exercise.” Okay, but that’s our whole society, and everybody doesn’t get fatty liver, so is there something that we’re overeating that’s different? Why do we have an epidemic now, right? You ask the question, “Well, do we know how to produce fatty liver in a laboratory setting or in an animal setting?” Of course we do, and it’s called foie gras, right? Which is duck liver. When you take ducks and geese and you turn their liver into fat, how do you do it? You do it by feeding them grain, right? Specifically corn. You force feed them grain, and people have been doing this as a delicacy for a thousand years, right? It’s not like, “Oh, wow, I never thought of that.” This has been around for a long time. How are we being force fed grain and corn, et cetera?
Well, mostly the number one source is high fructose corn syrup, right? This is what the epidemiologists, the nutritional epidemiologists just step back and look and say, “What’s really different about our society now is that high fructose corn syrup is in everything, every kind of processed food.” Especially sweetened beverages. It was promoted as a beneficial alternative to sugar. “Oh, it’s corn syrup.” But high fructose corn syrup has nothing to do with corn, right? It’s so processed. There’s nothing left. When you track consumption of high fructose corn syrup with fatty liver, they go straight up in parallel. It also goes up in parallel with obesity, right? Again, the idea was, “Well, it’s fructose. How could fructose be a problem? Because fructose doesn’t raise blood sugar.” But fructose causes insulin resistance, even worse than glucose. Free fructose and the fructose that’s in high fructose corn syrup, those are both really problematic. There’s a couple things that would happen. How can eating fructose lead to fat, because fructose is a sugar, and fat is a fat, right?
On the surface, it doesn’t make any sense.
Dr. Kara Fitzgerald: Yeah, run through that a little, just…
Dr. Robert Rountree: Yeah, my understanding of what it does is that fructose actually induces insulin resistance. When you induce insulin resistance, you actually turn on genes in the liver that are … The word is de novo lipogenesis, so you turn on the DNL genes in the liver. You also turn on the inflammatory genes, but you turn on DNL. You might think, “Oh, the person’s got fat in their liver. It’s because they ate too much fat in their diet.” It turns out if you radiolabel dietary fat, that it’s only a relatively small percentage that actually ends up in the liver. Most of the fat that ends up in the liver comes from free fatty acids that are released by adipose tissue. A huge chunk of it is from de novo lipogenesis. If you want to activate DNL, fructose is the best way to do that. It basically turns on the genes that do that. That’s why people are saying, “Gee, if you put all, if you connect all the dots, then what really jumps out is this is the biggest difference in our society.”
The number one risk factor is consumption of high fructose corn syrup. That’s why it’s, if a person is diagnosed with fatty liver, it’s a must that they stop all processed foods, which they should do anyway. I mean, we should all eat less processed food, but we got to stop kidding ourselves that because it says, “Corn syrup,” that it’s somehow okay. The guy that’s done a lot of this work is Robert Lustig, who I suspect you know or heard him lecture. Here’s what Lustig says that’s very interesting. He thinks that fatty liver is the genesis of metabolic syndrome, not the other way around.
Dr. Kara Fitzgerald: Well, that makes sense, doesn’t it? I mean, you start shutting down liver functionality and turning on…
Dr. Robert Rountree: Well, here’s one where it’s Jeff scooped me, Jeff Bland scooped me. I was at an IFM conference in Singapore a number of years ago. I gave a lecture of glucotoxicity and why glucose is bad, and why hemoglobin A1c was such a terrible risk factor for many diseases. Then Jeff got up and said, “Well, that’s all true, and now I want to talk about lipotoxicity.” What he was saying is that when you get lipid accumulation inside of liver and muscle cells, that interferes with insulin signaling. Jeff was onto this many years ago. It was a little bit more hypothetical back then, but now Lustig has been doing research on it. Again, he’s trying to make a case that this is central to the pathophysiology. Again, back to your basic question, “What’s the risk?” The number one risk factor is consumption of refined carbs, especially high fructose corn syrup. Now, if a person is really over-consuming these things and they get fat, if their BMI goes over about 30.
Their insulin levels start to go up. Obviously that increases their risk, but it doesn’t just happen in fat people, and that was the point I was trying to make about kids. There seem to be a whole other secondary set of risk factors that people haven’t thought about. One of them seems to be disorders in the methylome. I know you would love this one.
Dr. Kara Fitzgerald: Right, right. Yeah, I was looking at it.
Dr. Robert Rountree: But this is…
Dr. Kara Fitzgerald: Go ahead.
Dr. Robert Rountree: Oh, this is exploding. The liver, the hepatic methylome. The research is just exploding on that. Part of it came out of this realization that if you put somebody on total parenteral nutrition where you control their entire diet, and you leave out choline, then virtually 100% of those people will get fatty liver. Why is that? Well, you need choline to make phosphatidylcholine. Choline is converted into PC in the liver, and PC is used in VLDL to pack its lipids and ship it out of the liver. If you don’t have enough PC in your liver, then those fats are going to accumulate. That makes sense, right?
Dr. Kara Fitzgerald: Yeah, it makes sense.
Dr. Robert Rountree: Well, a huge percentage of our population is choline deficient.
Dr. Kara Fitzgerald: Right. That’s right.
Dr. Robert Rountree: Right?
Dr. Kara Fitzgerald: Yep.
Dr. Robert Rountree: There’s this flip-flop between, “Well, how do you supply enough methyl groups in your liver to keep the methylome intact?” You can either get it from choline, or you can get it from folate. If a person’s got choline deficiency, then maybe they can make up for it with folic acid, right? But what if they got MTHFR or MT, is it MTD? I always stumble on that one a little bit. It’s the…
Dr. Kara Fitzgerald: MTHFD1
Dr. Robert Rountree: MTHFD1. Zeisel, who’s the choline expert at Chapel Hill, he thinks that’s a more important step to MTHFD1 than the MTHFRs. But people haven’t really talked about it so much. It’s interesting, in reports that I’m seeing in SNP testing in people, if they’ve got the MTHFD1 coming back, showing that they’ve got the slow enzyme, then the number one recommendation is to increase choline. There’s also an enzyme called a Phosphatidylethanolamine N-methyltransferase, the PEMT. If you’ve got a choline deficiency, you can somewhat make up for it if you’ve got this enzyme. You can actually produce PC by another pathway, but if that enzyme is slow, then you need more choline.
Dr. Kara Fitzgerald: Well, not only that, but it’s actually really … That’s a pretty challenging pathway. I mean, there’s three SAM-dependent steps to actually produce phosphatidylcholine as an end result, so. Right. I mean…
Dr. Robert Rountree: Right.
Dr. Kara Fitzgerald: … I think we’ve always considered it, choline, to be conditionally essentially, even though we can make it.
Dr. Robert Rountree: Yeah, I got to say here that there’s…
Dr. Kara Fitzgerald: Phosphatidylcholine.
Dr. Robert Rountree: Well, yeah. I mean, you can make PC. I think both dietary sources are good. I’ve been doing a lot of work with a company called Balchem that makes choline, and so I’ve had a chance to talk to some of the top choline researchers around. It’s really, it’s kind of blown my mind at how much research has been there, because I always thought, “Well, choline is something you give to pregnant women,” right? Because you want it for the kid’s, developing kid’s brain, et cetera. It should be in a prenatal formula, but other than that, who needs it? Now I’ve come to realize from reading work by Marie Caudill, who’s really somebody worth talking to. She’s at Cornell and has done a ton of research on this. She’s made it really clear, again, that we have this massive deficiency of choline in the population. That’s impacting the methylome, and if you basically have a defective methylome, then it’s a setup for fatty liver.
What if you’re consuming sugar-sweetened vegetables, I mean, sugar-sweetened drinks, and then you’re not getting enough vegetables, you’re not getting enough eggs and dairy products, et cetera for your choline? Then you’re in trouble. I’ve got to make a little side comment here, which is that Stanley Hazen at Cleveland Clinic is trying to make an argument that choline is bad for you, because it increases TMAO, right? But I’ve spent a lot of time diving into that literature, and I just don’t buy the hypothesis. I think the high TMAO is a marker for choline deficiency.
Dr. Kara Fitzgerald: Yeah. All right. We’ll just walk that through briefly, but I want to, I do want us to stay on task here…
Dr. Robert Rountree: Yeah. Well, it’s part of the issue. People are saying, “Gee, don’t eat choline,” because they’re worried about TMAO. Well, I think that’s going to worsen our epidemic of fatty liver if people avoid choline and phosphatidylcholine. In fact, the other way around, I give phosphatidylcholine and I specifically like to give phytosomes. As a consultant for Thorne, I’ve had a chance to really dive deep into the whole phytosome technology, and all the stuff from Indena. The silybin phytosome, the curcumin phytosome. The data on that stuff is pretty impressive, and I think is part of solving this problem.
Dr. Kara Fitzgerald: That is the heightened by availability, so you’re…
Dr. Robert Rountree: Yeah, well, it’s not, it’s … The phytosomes do two things. They enhance the bioavailability of the nutrients that can help reverse this problem, but they also are providing phosphatidylcholine, right? You’re solving two different things. I hate to use that word about killing birds, two birds with one stone, but you are.
Dr. Kara Fitzgerald: Let’s touch on a couple, just a couple of other risk factors you point out. You mentioned some earlier that are pretty compelling. Let’s talk about TASH, and then let’s just talk about gut involvement.
Dr. Robert Rountree: If you talk about the big umbrella of fatty liver in general. If you discover somebody who’s got an increased ALT, and that does seem to be the best marker, although I’ve had a few people who had an increased GGTP or GGT, depending on which, how your lab’s reporting it. GGT can be the only indicator of it, right? Or a slightly increased ALT can be the only indicator, right? What is it about ALT? Well, it’s mostly in the cytosol of the liver, so it’s a pretty specific indicator of liver damage, right? Then the GGT, my understanding is that enzyme, it’s involved in glutathione metabolism. If you’re eating up your glutathione, then any process that involves a lot of transfer of glutathione is going to raise GGT. It indicates that your liver’s working. I have to say this, because a lot of the papers don’t really talk about GGT, but I think we should be considering it as a marker.
I’m bringing this up now because I’m saying, “Okay, here’s a typical patient who’s got an elevated GGT and/or elevated ALT, but not necessarily AST.” You could say, “Okay, they’ve got fatty liver. What’s it from?” The first thing you ask them, well, it’s, “How much do you drink?” If they say, “Well, I drink a glass of wine a day,” okay, well, “If you drink it every single day, maybe your liver’s just not recovering. That could be a problem for you, especially if the GGT is up. Alcohol’s a toxin, right? You have to go, “Okay,” you’ve got to make sure that alcohol isn’t a problem. But okay, let’s say you’ve got a patient that says, “I never drink.” Yet, their ALT is up and/or GGT is up.
What if they’re not overweight? Then the next thing is, you go, “Okay, let’s look at your methylome. Let’s consider your choline intake, your folate intake. Let’s look at some of these SNPs that we talked about to see if you’re at risk. Let’s measure your homocysteine.” Well, let’s say you go through all of that and all that’s fine. Their homocysteine is six, right? They already take a Methyl B, and they get choline in their diet. Okay, so now I’ve ruled out, ruled out, ruled out. Well, what are you left with? Well, then you start asking, “Are you on any kind of pharmaceuticals?” Because certain pharmaceuticals we know can cause fatty liver and NASH. Methotrexate is probably the best known. Why? Because it’s depleting the methylome, right? Other drugs that can do it, Tamoxifen. The anti-AIDS drugs. Corticosteroids. Think of those as being toxins.
If you’ve gone through all that list and you say, “Still haven’t found anything,” well, then you start wondering about solvents. What’s the person’s profession? I wouldn’t say I’d worry about the profession as the very last thing. I certainly give people a toxic exposure questionnaire whenever they come in for an initial visit, but that’s a point where I might really go back with a fine-tooth comb and say, “Hey, are you doing anything that’s involving solvents?” Or, “Could you be getting exposed to heavy metals or any other chemicals that are hepatotoxic?” All that amounts to what’s called toxicant-associated steatohepatitis, which Matthew Cave at University of Kentucky has been writing articles on, but now is pretty much accepted. All I can say is it’s out there, and we probably need to study it more.
Dr. Kara Fitzgerald: Don’t you think, though … Okay, so, maybe frank TASH, as caused by clear exposure, but don’t you think the accumulation … I mean, all of these, obviously, if you’re looking from a functional medicine lens, you could have a sprinkling of this, a hint of that. I mean, pesticides on your foods, a mild deficiency of your various methyl donors, and choline insufficiency. I mean, you could have a number of these modestly poor diet. Pieces of all of this would fit into the end result as fatty liver. I would imagine that’s actually probably more the norm with what we’re going to see in our practice.
Dr. Robert Rountree: Yeah, I totally agree. You have to look at all these factors together, but then we’ve got, there’s another wrench to throw in the works, which is dysbiosis.
Dr. Kara Fitzgerald: Yes. Yeah, let’s talk a little bit about this.
Dr. Robert Rountree: That’s when you would go, “Wait a minute. What does that have to do with the liver?” Well, if you think about core pathophysiology of leaky gut, which is that you get leakage of endotoxin, right? If that endotoxin is going into the lymphatics and that’s draining into the liver, that’s causing inflammation. Maybe that doesn’t initiate the process of fatty liver, although it could. It could throw things off just enough that you’re going to get an increase in de novo lipogenesis, but it certainly can play a role in the progression of fatty liver towards steatohepatitis. That’s otherwise known as metabolic endotoxemia. That’s a concern when a person complains of chronic bloating. Not just that they’re uncomfortable for the bloating, but what does that indicate about life in their small intestinal microbiome? What’s going on there? There’s an actually fairly surprisingly large body of data that links dysbiosis with both fatty liver and NASH. What that says is that you’ve got to address what’s going on in the gut as part of your overall approach.
Now, when I said, “Okay, I’m going down my algorithm. I ask about alcohol, I ask about drugs, I ask about diet, I ask about profession.” It’s not either/or, right? In functional medicine, we have our nice little matrix where we’re just saying, “Okay, all of these things are influences,” right? Then the final thing on that list would be, “What’s going on with your gut?” Now, unfortunately, if somebody doesn’t have bloating, and maybe they don’t have lower GI symptoms, that doesn’t necessarily mean they don’t have dysbiosis.
Dr. Kara Fitzgerald: Well, absolutely. I mean, arguably, we’re all walking…
Dr. Robert Rountree: I mean, most of us have dysbiosis. What it says to me is that you probably should consider doing something for the person’s gut to help this condition. That something, at minimum, would include a probiotic and probably some kind of prebiotic at very, at minimum.
Dr. Kara Fitzgerald: Yes, at minimum. You’re casting a really pretty wide net, and gut is a piece of it, and choline consumption, of course.
Dr. Robert Rountree: Choline consumption and/or phosphatidylcholine. I want to emphasize this, because I’ve had people ask me lately, “Well, isn’t phosphatidylcholine bad because Stanley Hazen said it increases TMAO? Isn’t that toxic?” I really think it’s the other way around. I think that TMAO indicates choline depletion.
Dr. Kara Fitzgerald: Right, right, right, and because the bugs are consuming it.
Dr. Robert Rountree: The bugs are consuming it …
Dr. Kara Fitzgerald: The dysbiotic bugs.
Dr. Robert Rountree: … so it’s not available for the methylome. This is a lot, isn’t it?
Dr. Kara Fitzgerald: It is a lot. It is a lot.
Dr. Robert Rountree: It’s a lot. It’s like, “Oh my god. This is a…”
Dr. Kara Fitzgerald: But you know what…
Dr. Robert Rountree: … whole new thing I’ve got to think about in my practice. Oh my god.”
Dr. Kara Fitzgerald: Except that I would argue, everything that you’ve brought up thus far, diet, high fructose corn syrup. Anybody practicing functional medicine and the world beyond, we’re becoming more and more savvy. Even Archer Daniels Midland arguably is probably thinking about it to some extent.
Dr. Robert Rountree: Everybody’s thinking about it.
Dr. Kara Fitzgerald: Yeah, exactly. I mean, if you practice functional medicine, if you lean on the matrix, if you take a good history, if you transition somebody onto a whole foods diet, you get them to eat as much organic, at least the clean, looking at the dirty dozen and that kind of thing. You’re going a long, long, long way to turning it around, even without the level of understanding that you’re outlining here.
Dr. Robert Rountree: Here’s an interesting case in where all these things dovetailed, is I just saw a patient yesterday who I diagnosed about a year ago with fatty liver. ALT was up, ultrasound showed fat. All the usual stuff. She wasn’t a big woman, but she had a lot of visceral fat. It was just her body type, but she also had SIBO. I put her on a low-FODMAP diet, and she lost all this weight. I was trying to get her to do a bunch of supplements, and she couldn’t … Interestingly enough, she couldn’t really tolerate them, but the low-FODMAP diet made her lose weight, and her liver’s fine now.
Dr. Kara Fitzgerald: That’s pretty impressive. Yeah, that’s not the first thing that we would think to turn around fatty liver. That’s…
Dr. Robert Rountree: It’s not what, go low-FODMAP, because the concern there is now with low-FODMAPs, you’re taking out prebiotics. Isn’t it going to lead to dysbiosis? But she had so much weight loss, she lost like 15 pounds.
Dr. Kara Fitzgerald: Right, right. Well, and you…
Dr. Robert Rountree: It’s such a restrictive diet.
Dr. Kara Fitzgerald: Well, I mean, arguably, you turned around the ratio of her microbiome, even as you were fasting it. Less choline consumption, more available for liver. Less choline consumption by the micro, by the dysbiotic organisms. I mean, I think it was, it’s just really multifactorial, what you did.
Dr. Robert Rountree: It brings up the point of like, “What’s the mainstream approach to this?” Everybody agrees that if you lose weight, that fat will come out of your liver, right? If you can get people early enough, and that’s really the key, is the sooner you can diagnose this, the sooner you can do something. Just assume that if you’ve got a patient with type 2 diabetes, assume they’ve got fatty liver, right? If their BMI’s over 30, they’ve got fatty liver. Just assume it regardless of what the biomarkers show. Then there’s going to be other people where you’re not quite sure. Again, those people may not be overweight, may not be diabetic, but they’ve got this elevated liver enzyme. If you confirm it in them, then even those people could stand to lose body fat. But you need to lose at least 5% of your body weight, so we’re not just talking about a pound or two. If you’re moving towards NASH, which you would probably not be diagnosing based on a biopsy, but because their CRP is up or their transaminases are way high.
Those people need to lose at least 10% of their weight, which is really hard to do, right? Without some kind of more aggressive intervention. Here’s a little rub, is when people get bariatric surgery and go through that rapid weight loss, then fatty liver is a fairly common consequence of that. Because you suddenly, you release all these free fatty acids. You stopped eating all the bad foods, but then, all that adipose tissue’s going to release free fatty acids. It gets recycled and ends up in the liver. The bariatric surgeons know all about this, so that’s a subset of people where you go, “Okay, what interventions would you do for them?” Because you’re already having them eat less. Obviously, you have to tell people to stop the high fructose corn syrup. Try to get people to exercise at least 150 minutes a week. All those things are critical. Work on their…assume that they’ve got some dysbiosis. Work on their gut. Should you give them drugs, if they don’t have high blood sugar or high lipids, how are you going to justify giving them a prescription drug?
Dr. Kara Fitzgerald: Right. Well, look…
Dr. Robert Rountree: Go ahead.
Dr. Kara Fitzgerald: Well, you know what? We don’t have a ton of time left, and I want to talk … The fact of the matter is, as you pointed out at the beginning of our talk, we can turn NASH around using functional medicine and using supplements. Very old school liver protocols included choline. I mean, we’ve known about this in our space…
Dr. Robert Rountree: Lipotropics. They called them liptropics.
Dr. Kara Fitzgerald: Exactly.
Dr. Robert Rountree: This old naturopathic remedy.
Dr. Kara Fitzgerald: Super old school stuff. We’ve been doing this forever. Across the board, regardless of the underlying cause or causes of fatty liver, we’re going to be looking at a handful of all-important supplements. I want you to walk through those. What are your top considerations? Anybody walking through your door, what are you doing?
Dr. Robert Rountree: A prebiotic I think is really helpful. The question is, so if a…
Dr. Kara Fitzgerald: Which one?
Dr. Robert Rountree: … person’s got SIBO, if they bloat, with prebiotics that, prebiotic foods … I tell people to eat garlic and onions, bananas, asparagus, things like that that are good prebiotics. Some people will bloat with those foods. If they do, there’s one called partially hydrolyzed guar gum that I think is awesome. Now, when years ago, I remember all this research done by Dr. Anderson on guar gum for diabetes. He had some pretty good data showing that guar gum would lower blood sugar, et cetera. It was a great fiber, but that, guar gum is nasty, right? People bloat like crazy on it, and it tastes terrible. They made these guar gum crackers.
Dr. Kara Fitzgerald: I don’t remember this.
Dr. Robert Rountree: Oh, I mean, just … You remember those?
Dr. Kara Fitzgerald: No, I don’t.
Dr. Robert Rountree: Just disgusting. Oh my god, just disgusting. We, a number of years ago, I was helping Thorne design some fiber products. Part of that came out of problems finding a clean source of psyllium, right? It turns out most of the psyllium that’s sold in the market is terribly contaminated, right? You’d be amazed at the kind of contaminants you find in there. Thorne was selling a psyllium product and said, “We just can’t sell it anymore. We can’t justify it. It’s not clean, and we need another fiber.” We stumbled on this stuff called Sunfiber, which is partially hydrolyzed guar gum. I was very skeptical because of my previous experience with guar, but then I started looking at the data, and it’s quite impressive. It’s like, “What is the only prebiotic that’s not a FODMAP?” There’s really good animal data on it showing that you increase butyrate levels with it, that it increases beneficial bacterial, especially lactobacilli, and it also decreases liver fat.
I love that stuff. I love that stuff, and recommend it a lot. How much do you need? Somewhere around five to eight grams a day of the Sunfiber. That’s the first thing that I do is try to get the gut in line. Then I have some go-to supplements that I think are really helpful. Probably the one that I like the most is curcumin phytosome, which is … We sell, Thorne sells as Meriva. The reason is, this is interesting, when I first started doing this research on fatty liver, I went at it from a treatment agnostic perspective. I just started doing searches, the National Library of Medicine, just looking for supplements in fatty liver. You read a paper on fatty liver and it says, “Well, there’s no treatment besides weight loss and drugs to lower lipids.” But if you type in, “Dietary supplements and fatty liver,” suddenly you get all these hits. I’m thinking, “Why aren’t these things listed in the mainstream papers on this?” Because the data is pretty impressive. In particular, I started finding all these hits on curcumin phytosome.
Specifically, for fatty liver. It kind of blew my mind and I went, “Wait a minute. Curcumin phytosome, isn’t that Meriva?” I looked it up, and sure enough, that’s what they were using.
Dr. Kara Fitzgerald: Wow.
Dr. Robert Rountree: I had no idea. I wasn’t saying, “Okay, I like Meriva. Where are the papers that support it?” It was the other way around. “Oh, looks like curcumin has been helpful for fatty liver. Is there any research on this?” I type it in, and curcumin phytosome comes up. How much were they using? Not a lot. Two caps a day of the 500s.
Dr. Kara Fitzgerald: Wow. That was it?
Dr. Robert Rountree: I think that was it
Dr. Kara Fitzgerald: That was the only intervention?
Dr. Robert Rountree: That was the only intervention. I’m like, “What?”
Dr. Kara Fitzgerald: Wow.
Dr. Robert Rountree: That’s why the Meriva’s pretty much my go-to product for fatty liver. Everybody should be on it with fatty liver, because it’s so well tolerated and because this data’s pretty compelling. I mean, there was one study, so typically they give a 500 BID for about eight weeks. They’re finding huge reductions in liver fat, but lipids are getting better. People are losing weight. Their liver enzymes, their transferase levels are coming down.
Dr. Kara Fitzgerald: Wow. That’s pretty fascinating.
Dr. Robert Rountree: One study found on 500 BID of Meriva for two months in people that had ultrasonically proven fatty liver, there was a 75% drop in liver fat based on ultrasound.
Dr. Kara Fitzgerald: No dietary changes? No exercise?
Dr. Robert Rountree: My understanding from reading the paper was that both groups got put on a diet where they said, “Okay, cut back on the junk food and the sugar, et cetera.” Both groups got the same intervention, but you got a much bigger improvement in the intervention group. The control group had a little bit of improvement, which is not enough to just say, “Cut back on the sugar.” It’s just not enough, right? Once you’ve got pathology going on. So, again, Meriva does two things. It gives you curcumin. We know that’s highly absorbable, and you also get the phytosome, which is made of sunflower phospholipids and mostly sunflower phosphatidylcholine.
Dr. Kara Fitzgerald: You’re getting a therapeutic amount?
Dr. Robert Rountree: Yeah, if you’re doing a gram a day, a huge chunk of that is phosphatidylcholine.
Dr. Kara Fitzgerald: Huh. Okay. That’s pretty cool. All right. So give me…
Dr. Robert Rountree: It’s a two for one. It’s a two for one.
Dr. Kara Fitzgerald: Now, what about, GGT is often up, and we know there’s a serious redox imbalance in fatty liver. What about your NAC and lipoic acid, et cetera? I mean, at what….
Dr. Robert Rountree: I mean that’s sort of a go to. Something I learned from Leo Galland, who I interviewed last year, was that you really need, that NAC is a great supplement, a great precursor to glutathione, but you really need to give it at least twice a day if not three times a day, because the half-life is pretty short.
Dr. Kara Fitzgerald: Hm. Interesting.
Dr. Robert Rountree: If somebody’s got fatty liver, that’s just a little take home message here is that it’s probably better to give lower amounts, five or 600 milligrams a day. Five or 600 milligrams a dose, BID or TID, than it is to give a huge dose all at once.
Dr. Kara Fitzgerald: That’s pretty interesting.
Dr. Robert Rountree: I’ve always done that, and for years, like, “Oh, okay. Do 900, 1,800 milligrams once a day and you’re fine,” but Leo kind of makes a case for spreading it out. You also raise glutathione from milk thistle. There’s another product that, made by Idena, sold by Thorne, called Siliphos. There’s actually several published studies on Siliphos, which is silybin phytosome for fatty liver. I think they combined it with vitamin E and also with alpha-lipoic acid. That’s a really effective combination, silybin phytosome, vitamin E, and either alpha-lipoic acid or NAC. A lot of the people that I’m treating, they don’t just have fatty liver. They’ve got other conditions.
If they only had fatty liver, I might just say, “Give them Meriva or give them Siliphos,” but they’ve got a lot of other things going on with their cardiovascular system, so I’m definitely wanting to increase their glutathione. Which, like you said, if your GGT’s up, that kind of indicates to me that they would benefit from more glutathione, because maybe they’re exposed to toxins.
Dr. Kara Fitzgerald: Well, how are you going to raise that? Are you going to expect that to happen with the silybin and the lipoic acid or the NAC? I mean, are you using glutathione?
Dr. Robert Rountree: I usually start with NAC and/or alpha-lipoic acid, Siliphos, and vitamin E, right? If we’re talking about more liver-specific, metabolic-specific conditions. Now, if somebody’s got other issues like autoimmune disease or brain disorders where I think they really need glutathione, if they’ve got Parkinson’s disease, then I am really pushing the glutathione there, and I would go with a time-released glutathione. A lot of different options on the market. Well, I like the precursors, because the precursors, to me, they’re not expensive, and there’s pretty good data on them. I mean, milk thistle raises glutathione.
Dr. Kara Fitzgerald: Yes, yes. I think there’s really good data. In fact, I don’t know that the jury has concluded as to whether or not precursors are, or actual glutathione, which, as you know, is extremely expensive, is clearly superior to precursors. I mean, have you…
Dr. Robert Rountree: I don’t know why NAC isn’t standard of care, let’s put it that way, for a whole lot of different conditions. I just, I’ve taken it myself for 20 years, because it’s got so many other benefits. The antiviral effects of that glutathione. The brain support of effects, not just the redox impact. I take both.
Dr. Kara Fitzgerald: Oh, you do? You take NAC and Glutathione?
Dr. Robert Rountree: I take NAC and alpha-lipoic acid.
Dr. Kara Fitzgerald: Oh, and lipoic acid
Dr. Robert Rountree: I mean, we’re all exposed to toxins. It’s kind of a, “Why not?”
Dr. Kara Fitzgerald: All right. In our, we…
Dr. Robert Rountree: Can we talk about Berberine a little bit?
Dr. Kara Fitzgerald: Yeah, we can. We can, but we have, we’ve got a minute, so just give me the other main interventions in our toolbox
Dr. Robert Rountree: All right, so Berberine is definitely a go-to for me. I’ve already talked about Meriva, curcumin phytosome. I talked about the Sunfiber. Vitamin E, you need about 800 to 1,000 units. Omega-3 fatty acids, several grams a day. Pantethine, something that not many people know about. About a gram a day of Pantethine. It’s got very good data on it for reversing fatty liver. Melatonin, vitamin E. Lots of different options. Then I would say, last but definitely not least, is the Berberine, which people think of Berberine as an anti-microbial, but it’s one of the best things out there for metabolic syndrome. I think of Berberine as almost an anti-aging pill. Where I, I really see the benefits is in about a gram a day.
Dr. Kara Fitzgerald: Okay.
Dr. Robert Rountree: 500 a day, not so much, but when you hit 1,000 to 1,500, that’s really when you start seeing metabolic changes, and in some people, I see weight loss.
Dr. Kara Fitzgerald: Oh, interesting.
Dr. Robert Rountree: Not everybody, but when you get to 1,500, it’s not that unusual for people to say, “Gee, I started losing weight without making any other changes.” But there’s several studies on it, animal studies and human studies, for fatty liver.
Dr. Kara Fitzgerald: Yes, yeah. One more thing. What about NiaCel? I think it’s a great product.
Dr. Robert Rountree: I love it, but NiaCel, yeah, nicotinamide riboside. It’s a whole other story that’s kind of emerging is that NAD levels tend to drop with aging. Why is that? Because you get damage to your DNA, you activate the repair enzymes, the PARP enzymes. PARP consume NAD, right? There are papers now showing that NAD deficiency leads to fatty liver. They’re animal studies, but they’re pretty compelling. Nicotinamide riboside has been clearly shown to increase NAD in these animal studies, and there are now human studies showing that nicotinamide riboside increases NAD in the body. I definitely think it’s part of the mix there. I always combine it now with resveratrol. I either use NiaCel and PolyResveratrol, or I use a ResveraCel, which is the combination product. For a lot of people that combination product, which is resveratrol, nicotinamide riboside, quercetin, and a little bit of TMG, to me, it’s kind of an ideal product for fatty liver.
Dr. Kara Fitzgerald: Yeah, it’s like a next generation lipotropic.
Dr. Robert Rountree: Next gen lipotropic, yeah, and anti-aging.
Dr. Kara Fitzgerald: Well, listen. You unpacked a lot. Any papers that you would want our listeners to be aware of, or any content you can share? Just to kind of underscore some of these points. If we, it…
Dr. Robert Rountree: Well, I wonder if I could send you, I could send you a PDF of a presentation? Is that…
Dr. Kara Fitzgerald: Oh, that would be perfect.
Dr. Robert Rountree: Yeah, or maybe, yeah. If you do that, turn it into PDF…
Dr. Kara Fitzgerald: Yeah, absolutely.
Dr. Robert Rountree: … and the PDF, got nice graphics…
Dr. Kara Fitzgerald: Perfect.
Dr. Robert Rountree: … and got references in each page.
Dr. Kara Fitzgerald: Yeah, that would be fabulous. We will feature it on the show notes of the page, and everybody will greatly appreciate it, because you did unpack quite a bit of useful information. Listen, Dr. Rountree, It was so great to spend this time with you today. I’m giving you a big hug through cyberspace, and I know I’ll be seeing you soon in Atlanta.
Dr. Robert Rountree: Yes. Absolutely.
Dr. Kara Fitzgerald: All right. Thanks for joining me today.
Dr. Robert Rountree: All right. You bet. Thank you. Take care.
Dr. Kara Fitzgerald: Ciao.
Dr. Robert Rountree: Bye.