The Hidden Metabolic Cause of Fatty Liver Disease

Karen: 
We just need to keep pressing forward that it is the insulin resistance and hyperinsulinemia that need to be treated and reversed. 

Amy: 
We saw just across the board great improvements in response to that carbohydrate-restricted diet.

Bret: 
Welcome to the Metabolic Mind Podcast. I’m your host, Dr. Bret Scher. Metabolic Mind is a non-profit initiative of Baszucki Group, where we’re providing information about the intersection of metabolic health and mental health and metabolic therapies, such as nutritional ketosis as therapies for mental illness.

Thank you for joining us. Although our podcast is for informational purposes only and we aren’t giving medical advice, we hope you will learn from our content and it will help facilitate discussions with your healthcare providers to see if you could benefit from exploring the connection between metabolic and mental health.

Do you know what’s unfortunately the fastest-growing cause of liver disease in this country? It’s Metabolic Dysfunction-Associated Steatotic Liver Dysfunction, which is a mouthful, but basically it’s liver dysfunction, liver failure from metabolic disease. And we talk so much about metabolic disease here at Metabolic Mind and all the manifestations of it, whether it’s affecting mental health or whether it’s affecting cardiovascular health and triggering cardiovascular disease or reproductive health and endocrine dysfunction.

But now, we’re going to talk about the liver dysfunction that is so rampant because of metabolic dysfunction. But fortunately, as with other forms of metabolic dysfunction, low-carb and ketogenic interventions have been shown to be incredibly effective at treating and reversing this dysfunction. But it’s not promoted as widely as maybe it should be for those who are really looking for a treatment or possibly even a cure or reversal of their dysfunction.

And today, I’m joined by Dr. Amy Goss, who has a PhD in Nutrition Sciences and is an Assistant Professor of Nutrition Sciences at University of Alabama – Birmingham, who’s done a lot of the research on ketogenic interventions for treating metabolic-associated fatty liver disease.

And I’m also joined by Dr. Karen Jerome-Zapadka, who’s a Medical Doctor and Gastroenterologist who’s the Founder and Medical Director of Trajectory Health, and she has been using carbohydrate reduction and ketogenic interventions to treat fatty liver disease as well for years and seen dramatic results. So, as we talk about it, ketosis and carbohydrate reduction may not be the only approach for improving metabolic health and treating fatty liver, but it’s emerging as looking like the most effective nutritional approach, and that’s an important concept that people need to walk away with.

So, Dr. Zapadka and Dr. Goss share lots of tips about ways to approach this and ways to think about this. So, I hope this interview is very helpful for you or maybe someone you know who has fatty liver disease. Many of the interventions we discuss can have potentially dangerous effects if done without proper supervision.

Consult your healthcare provider before changing your lifestyle or medications. In addition, it’s important to note that people may respond differently to ketosis, and there isn’t one recognized universal response.

Dr. Amy Goss and Dr. Karen Jerome-Zapadka, welcome to Metabolic Mind. It’s wonderful to have you both here. 

Karen: 
Thank you. 

Amy: 
Thank you. Great to be here. 

Karen: 
Happy to be here. 

Bret: 
Yeah, so we are here today to talk about this disease of fatty liver, and it is a diagnosis that really has grown dramatically, unfortunately, and is really connected to metabolic health.

And so at Metabolic Mind, we talk a lot about metabolic and mental health, but there are certainly other systemic repercussions of poor metabolic health with the liver being one of them. And help us understand, Karen, what actually is fatty liver, and why is it such a problem?

Karen: 
As the name suggests, fatty liver, we now call it steatotic liver disease, and we can talk about the name change and I think what that really brings to the table.

I think we really should discuss that. But it is just a situation of abnormal fat in the liver over 5%. If you get above that threshold, you have steatotic liver disease. There are a number of different reasons to have steatotic liver disease, but the largest by far is related to metabolic dysfunction. Hence, the name change that we can discuss.

And it is a multifactorial, very complex disease that is affected by genetics and sedentary behavior. The gut microbiome is playing a role. But above all else, it is related to nutrition, over-calories, and the types of calories, particularly the starches and sugars that are ubiquitous in our diet now. And driving insulin resistance and hyperinsulinemia, which as we’ll discuss further on, plays a key role in the propagation of fatty- of steatotic liver disease.

It’s becoming a worldwide epidemic. Probably 30% of the adult population has it. I think if you’re a child, at least 10% of children. If you’re an obese child, the statistics are anywhere from, 40 to 50% of obese children, and I’m sure Amy will get into that further, which really is a national tragedy that it’s become such an epidemic.

Bret: 
Yeah, and if, it progresses enough, it leads to the liver failure and the need for liver transplantation, which is quite dramatic, obviously. 

Karen: 
Oh, absolutely. It is now the number one cause of liver transplantation in women. And you know I’m a gastroenterologist by trade, and I cannot go one week on call, barely, that I don’t see a woman in her 50s, 60s, early 70s that presents with decompensated cirrhosis from steatotic liver disease, metabolic induced.

It’s just so sad. 

Bret: 
And in your clinical practice, you have seen the incidents rise. We’ve heard the stories and I’m sure you experienced this. It was called non-alcoholic fatty liver disease because you see someone come in with fatty liver 30 years ago, and they were an alcoholic, no question.

No question. And then all of a sudden, people were coming in not being alcoholics, not over-consuming alcohol, and it was like, what’s happening? What’s happening? And then the connection was made to this metabolic dysfunction. So, eventually, the name changed from non-alcoholic fatty liver disease to be more representative of being metabolic in nature.

So, tell us about the new name and why that is. 

Karen: 
Yes, So, just as you say, non-alcoholic fatty liver disease told us what it wasn’t, but really didn’t get at the core of what it is. And there was a lot in my space, a lot of discussion about this name change, and many people liked it, many people didn’t.

I personally thought that it was the most wonderful opportunity to really bring to light to people what is this metabolic dysfunction that underlies steatotic liver disease. I just gave a talk at the National Liver Gathering in Pittsburgh, and I was tasked with, the name of my talk was What is the Dysfunction in MASLD?

And I think it’s our opportunity to get people to understand that it is insulin resistance and hyperinsulinemia that really are at the core of what is happening with this. So, I personally have embraced the name change. 

Bret: 
Yeah, so metabolic associated steatotic liver disease. 

Karen: 
Metabolic dysfunction-associated steatotic liver disease.

Bret: 
It’s a mouthful. 

Karen: 
And that’s the joke. It’s a mouthful, and then you just say to the patient, “You have fatty liver disease.” 

Bret: 
Yes. So it is a mouthful. Now, originally, we saw the rise in adults, but then as time went on and the metabolic health of the country and the world got worse and worse, we started to see it in younger patients, in adolescents, in pediatrics.

So Amy, tell us, how you got interested in this, especially with your research looking at the pediatric population for fatty liver. 

Amy: 
Yeah, certainly. In doing some research about fatty liver disease and different ectopic lipid depots and how they might be affected by diet and how those depots are influencing other metabolic diseases like Type 2 diabetes, I became very interested in fatty liver disease in particular, and the techniques around imaging the liver.

And turns out that in doing all this research, we had a pediatrician over at, an endocrinologist pediatric endocrinologist, over at Children’s Hospital of Alabama who we’d done some work with. And we knew that fatty liver was prevalent in adults, but understanding how many patients we might have access to that had fatty liver in a younger population.

And it turns out just doing like a search of the medical record, there were thousands and thousands of kids that had been diagnosed with fatty liver, or likely had it because we saw persistently elevated liver enzymes that probably had it, but hadn’t been diagnosed yet because it’s not something that’s always diagnosed and sent for ultrasound to figure out if it’s steatotic or not.

So, anyway, all that to say, we identified just a huge population at Children’s Hospital of Alabama in Birmingham, where we’re like this is a perfect opportunity to do a pilot study, randomize them to either carbohydrate-restriction versus a sort of standard of care, low-fat diet to see if we see a signal, right?

If we can get these kids to adhere to a carbohydrate-restricted diet plan. And, it was an eight-week study that we did initially that was funded by the Thrasher Pediatric Research Fund, and then also our NIDDK-funded diabetes research center here at UAB.

We randomized families to either carbohydrate-restriction or fat-restriction, measured their liver fat using MRI, and over that eight weeks, we saw pretty dramatic improvements in the kids’ liver fat. We saw improvements in insulin sensitivity. We saw just across the board, great improvements in response to that carbohydrate-restricted diet.

Bret: 
So, from a research standpoint, I think it’s so interesting how you did this, that you tried to match the calories. And so, hopefully, not to have weight loss as a contribution because there is the feeling that whatever, however people lose weight, it’s going to help. But then the question is, are there more effective ways of losing weight or more effective dietary interventions irrespective of weight loss that can have this impact?

So, do you think from your research, although small studies but still well-designed, do you think you really showed that signal towards carbohydrate reduction having more of an effect than other dietary interventions? 

Amy: 
Yeah. I think so. It’s going back a little bit, that there’s data out there to suggest that carbohydrate-restriction does have a metabolic advantage, particularly in the case of fatty liver.

I believe it’s Jeff Browning’s work who’s published sort of short-term studies suggesting that’s true in adults. We wanted to test that in kids. And I think from our pilot study what we did find, unfortunately, we didn’t have the budget to control it as much as we would like and feed the families every single thing they ate, but just with count, we provided groceries for part of the study to have them adhere to the diet. We provided counseling for the remainder of the study.

The kids did lose some weight in that particular, we intended it to be weight maintaining. They did lose a little bit of weight. Despite that, like, when we adjust for weight loss, we did see there is that benefit of carbohydrate-restriction above and beyond what we would see with the low-fat diet.

Now, right now, we’re doing a, the NIH has funded an R01 study, right? So, a much larger study that we are actually feeding families all of their food for 12 weeks to try to really tightly control their intake so we can keep them in weight maintenance. Our goal is to keep them in weight maintenance to see truly if that carbohydrate-restriction affects hepatic metabolism to a greater extent than a lower fat diet.

And we, our hypothesis is that it does, and it has pretty profound effects on hepatic metabolism such that it depletes liver fat to a greater extent. 

Bret: 
Are you currently enrolling for this study? 

Amy: 
We are, yes. So, this study’s been going on for the past four years. We’re in year five of the intervention.

We are currently still enrolling. We’re trying to wrap up the last cohort of the study so we can start analyzing the data and get some publications out there from it, which we’re really excited about getting close to the end. But, yeah, so it’s, the R01 is for six months.

The families are enrolled in the study for six months. They come to us. The first 12 weeks, we have dieticians that sort of design the menus specific to the energy needs of the adolescent that has fatty liver. They design the menu. We give them specific instructions on how much food the adolescent is to eat to keep them in weight maintenance, and then hit their macronutrient targets, whether they’re on a carbohydrate-restricted or low-fat diet.

We provide, so they get weekly grocery deliveries for everything. The whole family is expected to adhere to it. We’re doing measurements of MRI at baseline at 12 weeks, at 6 months. We’re doing a euglycemic hyperinsulemic clamp at baseline at 12 weeks to measure changes in the hepatic insulin sensitivity.

Our hypothesis is that the low-carb diet will deplete that hepatic lipid. And then, in turn, we’ll see improvements specifically in the hepatic insulin sensitivity. 

Bret: 
Wow. Sounds like a great study. Now, do people have to be local in Alabama to get this done?

Amy: 
Yes and no, as long as they’re willing.

So we’ve had some folks that are not In Birmingham. So, a lot of our families do live in Birmingham. But if they are at a place where we can get groceries delivered to them through an app, like Instacart or Shipt, and they’re willing to come to UAB for testing, we can put them up at a hotel room for the testing, which takes a couple of days.

And then as long as we can get the intervention to them, we can do it remotely. So, yeah. 

Bret: 
I look forward to having you back to hear about the results of the study, or when it’s published, for sure. 

Amy: 
Yeah. we’re planning on it. We’re getting close to the end of it. 

Bret: 
Okay. Okay. 

Amy: 
That’s awesome. 

Bret: 
And now, so Karen, you’ve been a practicing gastroenterologist as this epidemic was progressing, as we were seeing more of the fatty liver, as it was becoming recognized to be associated with poor metabolic health.

How did you first learn or experience that low-carb could be an effective intervention, and what was your first response to that? 

Karen: 
Well, in the community, I gave talks for a number of years, probably over 20 years. I was first interested in all of the cancers that were associated with obesity that probably now are more likely associated with insulin resistance.

But at the time, we called them obesity-related cancers because so many of them were gastrointestinal. pancreatic, liver, colon, gastric, esophageal. But it wasn’t until probably about 15 years ago, I had an encounter with a patient that had, we were consulted as an inpatient, she had full-fledged metabolic syndrome, every aspect of it.

We were consulted because of an unresectable hepatoma, a liver cancer that just could not be resected, and also had evidence of cirrhosis. So, for her cirrhosis management. And after speaking with her, she literally looked up at me from her hospital bed and said, “Doctor, did I eat myself to death?” And it was so demoralizing because now we were seeing all of these fatty liver patients. And wow, I think that she did, but I didn’t understand any of the mechanisms and, at that time, was clueless about insulin resistance, hyperinsulinemia, the metabolic drivers. Didn’t really know that much about metabolic syndrome.

So, I went on to get my board certification obesity medicine and began to think about treating obesity. We developed an obesity medicine practice that in the beginning was more low calorie based. We were doing low calorie meal replacements. And no surprise to anyone, it was not very successful. But it was after beginning to get into the low-carb space, attend some of the meetings, begin to really truly dig into insulin resistance. What it is, how it is impacting the fatty liver. We came home from some of those meetings and totally transformed our obesity medicine practice into a low-carb practice, using low-carb and very low-carb into the ketogenic range.

And from there, the light bulbs were just going off. We just were seeing so much success. So, dozens of patients with steatotic liver disease, reversing it by imaging. We were using FibroScan technology at the time. Now, we’re using Velocir Scan. So, we’re documenting by scan and by insulin levels, HOMA-IR scores, lipid levels, triglycerides, all the markers that we want to see normalized.

We’re seeing them normalize by focusing our treatment on treating the metabolic syndrome. And so, we’ve had wonderful success. We’ve had family medicine residents rotate with us. And to see their expressions as they go through a day In our clinic and to see the results of these patients and just put their hands up in the air and say, “What is happening here?”

And to see these results that they had never seen before and to see that patients can truly heal themselves by really the lifestyle changes, but primarily the nutrition. We don’t want to forget about physical activity, which in these patients is so important. And if we have time, we can talk about that.

But that was my metamorphosis. And I now feel that I have a very firm grasp on the drivers of insulin resistance and how to get it reversed and turned around.

Bret: 
Clearly, by your clinical experience, and Amy, by your research, that carbohydrate reduction, ketogenic interventions are an incredibly effective treatment for treating fatty liver and the underlying metabolic consequences.

But, they’re not the only treatment, right? There could be, there are other potentially effective treatments, whether it’s low calorie diets for those who can maintain them or any diet that’s going to improve metabolic dysfunction, could improve it, and certainly GLP-1s.

But it sounds like Amy, from your research, would you say that yes, there are other means to do it? But I guess you were revisiting that even though there are other means to do it, carbohydrate reduction appears to have the most efficacy that we’ve seen. 

Amy: 
I think so.

I think there’s still more data coming out regarding the GLP-1 receptor agonists and their effectiveness at depleting liver fat, whether it’s secondary to just energy restriction, right? Because individuals are, they’re restricting what they’re eating, and we know that weight loss does result in a reduction in fatty liver.

The question is, is it, and we ask this question in adolescents in particular and in kids, because sometimes severe energy restriction isn’t a good recommendation for a child who’s still developing, right? And there can be adverse side effects from whether it’s development of bone density or lean mass and the hormonal changes children go through.

Is it a good recommendation to have them severely energy restrict to the extent where they’re going to see, they’ll see loss of fat mass, loss of liver fat, but also they’ll see loss of other tissue, right? 

Bret: 
Yeah. So great. I’m glad you brought that up. That’s so important. It’s not just, can it reduce the liver fat, but what else is the intervention doing to this human being? 

Amy: 
Exactly.

Bret: 
Who has so many other needs, nutritious needs and yeah, so that’s such an important point. 

Amy: 
And I think that’s an important question to ask in lots of different populations, whether it’s older adults who are at risk of losing lean mass. And kids that are developing, and they’re wanting to hit these peaks in bone mineral density and things like that.

I think that’s one of the sort of interesting things is can we, in the absence of caloric restrictions, simply manipulate the content, the composition, of what they’re eating, and will that alone be enough to affect the hepatic metabolism in a way that shifts them away from depositing that lipid and towards fat oxidation in the liver and towards all these metabolic improvements?

And I think our data suggests that it is entirely possible. 

Bret: 
Yeah. So Karen, you’ve got the clinical experience, and you’re seeing the research come from Amy and her colleagues and others. Is this catching on with your GI colleagues or when you go to GI conferences, or is it being drowned out by GLP-1s and by medications as so often happens with lifestyle interventions?

Karen: 
I think Wegovy, as is now approved for what we call at-risk MASH. So, if we’re thinking about steatotic liver disease, we really, the first goal is really to stage it. Do they have simple steatosis or are they advanced enough that they are into the F2, F3 range of fibrosis?

So, that’s a different ballgame. And I think at that point, if they have F2, F3 fibrosis, they are a candidate for one of two medications that are now FDA-approved, Rezdiffra, which works on a thyroid receptor in the liver itself, and then Wegovy. Those would be two FDA-approved drugs for that class of fatty liver F2, F3 fibrosis.

That’s a subsegment of the millions of people that have steatotic liver disease. That’s just a small subsegment of that population. So, for the other millions, that’s where we’re really talking about the lifestyle changes. So, I think the thing that sticks out to me, or at least really raised my attention, over the past couple of years is that we have multiple studies now in the literature looking at reversal of steatotic liver disease with carbohydrate-restricted diets right up to the mechanism.

Luukkonen and Gerald Shulman published a study in PNAS that looked at changes in the redox of mitochondria that with a ketogenic diet steered that fat from building triglycerides to ketogenesis. Right up to looking at NMR of the mitochondria in the liver. I can’t quote all the details.

I’m not a research scientist. But they show the mechanisms of how a ketogenic diet at the mitochondrial level is changing fat to go toward ketogenesis rather than building intrapatic triglycerides. So that, those studies exist. There are multiple studies looking at ketogenic diets, both research studies, narrative reviews.

When I was looking at the major guidelines for all the major societies and all the references that they listed, what stuck out to me was my living room floor was covered with articles about the ketogenic diet, but they were nowhere in any of those guidelines, bibliographies of references. And what is the disconnect here?

So, we have, there’s a lot of work to be done in that area. I think the research is there. It’s lying all over my floor. Why is it not getting out there to the general practitioners to let them understand that this is a very viable way to reverse steatotic liver disease, especially if it’s early disease and we don’t have MASH, the metabolic associated steatohepatitis with fibrosis?

If we can catch it early, early stages, diagnose it early, reverse it very easily. 

Bret: 
So, what do you think when you hear that, Amy? That here you are doing this work and putting all this time and energy in to do these studies, and you hear it’s not catching on yet. It’s not in the guidelines.

How do you feel about that? 

Amy: 
Yeah, no. It’s something where you talk about pretty often is, I feel like there’s a lot of literature out there to suggest that it has beneficial effects, yet there’s still. We’re fighting that idea or the notion that somehow that it’s harmful for some one reason or another.

And I think more and more people are becoming more familiar with the fact that it has so many metabolic benefits. And maybe there’s not as firm a foundation for those critiques of it where people are saying it’s harmful, for whether it’s heart disease or something like that. Those have been debunked, right?

And I think we’re in our department at least, we’re in the Department of Nutrition Sciences at UAB, we’re working to retrain, or at least to train the next generation of whether it’s dieticians, or how do we get this into more literature and medical schools? And that sort of thing to de-stigmatize the effects of this particular pattern of eating. And I tell people, we have a clinic, too. We recently in our department started our metabolic health clinic where we are seeing patients, teaching them how to follow-carbohydrate-restricted diets. This is a spinoff of our research. We were like, we need to start offering this to the community, right?

We’ve done so many research studies where we’ve seen the profound beneficial effects. Let’s start offering this clinically to our patients. We do have the Metabolic Health Clinic, and what we do in our clinic is we measure insulin. We focus primarily on chronic diseases, Type 2 diabetes, pre-diabetes, fatty liver disease.

So, we’ll take patients. We measure their insulin. We do an oral glucose tolerance test to look at their insulin response to a challenge, to all give the patient information about what’s their beta cell function look like, what’s their insulin sensitivity. And then, we can track over time how the diet’s affecting their insulin because insulin is such an important hormone that’s not, in most primary care or most clinics, they’re not measuring it.

Glucose can only give you so much information about someone’s metabolic health. We have plenty of patients that have normal or low glucose, but that’s because their insulin is sky high, right? So, the glucose is only one piece of that puzzle, and so we think it’s just super important clinically to help a patient understand what their insulin levels are and how their diet is affecting it, and how their, once we put them on a carbohydrate-restricted diet plan, how their insulin’s responding to that. I think is very important information about treating chronic disease and reversing it.

Bret: 
Yeah, I love that you’ve got that clinic there at Alabama to do that. Yeah, so Karen, say someone goes to their doctor, and the doctor says, “Yeah, you have fatty liver, metabolic dysfunction-associated steatotic liver disease,” if they want to give the whole, mouthful.

“So, you need to cut your calories, eat a low-fat diet, and increase your exercise. And if that doesn’t work, we’ll start you on a GLP-1.” So, if that’s the advice they get, which unfortunately, I think is fairly common advice. 

Karen: 
It’s the best .

Bret: 
What would you recommend? What do you think people should, obviously not giving medical advice, but just your general thoughts on what somebody should do at that point?

Karen: 
Yeah. I think first, do your own research. Just go online and research and really look at some of these studies. I think the other issue is, as far as the low-fat diet, and it’s in the literature. I think it was Schwartz from 2003, American Journal of Clinical Nutrition.

He looked at subjects that were obese with normal insulin, obese with hyperinsulinemia. He gave them low-fat, high-carb diets and low-carb, high-fat diets. In the low-fat, high-carb diet, the patients that were insulin resistant with hyperinsulinemia had five to six times higher de novo lipogenesis fat building in the liver, and with that came significantly elevated triglycerides.

And this raised a huge concern for me because of all of the recommendations for low-fat diets. This study convinced me that not only do low-fat diets, they may not work, they may if someone’s significantly insulin resistant with hyperinsulinemia, may make the issue worse. And so, I think that really opened up my eyes, no question.

And so, from that moment forward, clearly that convinced me that it, I’m not going to be recommending low-fat diets. I think low-calorie diets, we tried that for two years in our obesity center, and that did not work as well, not meaningfully. Everybody lost maybe 20 pounds and then stagnated. And then became hungry, and started to eat again. So, not much success with that.

So, I feel like I’ve tried it all, and this is where I’ve settled that I think works the most consistently, if it’s followed. We get consistent results, if it’s followed. So, this is where we are with the state of things. That we just need to keep pressing forward. That it is the insulin resistance and hyperinsulinemia that need to be treated and reversed.

And we know from the literature on metabolic syndrome the best way to do that nutritionally is with a carbohydrate-restricted diet. That is, there’s no question about that in my mind. 

Bret: 
Yeah. So, I think it’s clear if you’re going to do one thing, then following a carbohydrate-restricted diet is likely going to be the most impactful.

But as you alluded to before, there are other lifestyle factors that can improve metabolic health. And therefore, likely improve, MASLD, and that includes getting regular physical activity, right? Getting restorative sleep, managing your chronic stress, all these things. They probably don’t contribute as much as what you eat, but they certainly can contribute.

So, is that something you focus on with your patients as well? 

Karen: 
Oh, yes. Our new practice is a total metabolic practice. We have Nutrition Network low-carb certified health coaches. We have a certified exercise instructor. We screen for sleep apnea, sleep issues, depression, anxiety. We’re into, we do many behavioral types of things with patients.

We screen food addiction. So, it’s really much, much more comprehensive than our previous obesity medicine practice. And we’re looking at all of those lifestyle changes. They’re all related. We’re also screening for all of the other metabolic issues that come along with fatty liver. As the highest mortality in steatotic liver disease is not the liver.

It’s cardiovascular disease and cancers. And so, we are making sure that they’re up to date with all of their cancer screenings. I’ve ordered more CT coronary calcium scores than I ever have in my life, and nearly all of them are positive because of long-standing metabolic syndrome. So, we’re screening for that and trying to align with some cardiologists that will be on board with what we’re trying to do.

Bret:
And that is such a crucial point. You can focus in on the liver and the fat content of the liver and what the scans show, but really for the health of the patient, you also have to consider all the other manifestations of metabolic dysfunction, with cardiovascular disease being a big one, and cancers.

Karen: 
Absolutely. I think the take-home point is MASLD is a systemic disease, and you really need to be looking at everything and addressing every risk factor. And really evaluating for all of the other underlying problems that can come along with it. 

Bret: 
wow, this has been a great discussion.

I really hope people can take away a lot of these clinical nuggets and a lot of the research that’s happening, and have a better understanding of this and how to approach it as this broader systemic metabolic disease. So, Dr. Goss, if people wanted to follow you and your work, where can we direct them to go?

Where can they find you? 

Amy:
Yeah, certainly. We have a website at UAB in our department. We have our clinic website where we’re posting updates about our research. if you search and Google, UAB diet for diabetes, you’ll find our page. I try to post updates occasionally on Instagram and LinkedIn as well under Amy M. Goss. You can find me, Dr. Amy M. Goss. 

Bret: 
And if they want to enroll in your ongoing study, would they go to the UAB? 

Amy: 
Yeah. 

Bret: 
Site on the UAB or? 

Amy: 
Yeah. So, if you go to our page, there’s a dropdown with the different studies that are available, and then there’s an online form you can fill out with your name and email address. And we’ll get in contact with you, and see if you qualify for any of our ongoing research.

Bret: 
Great, great. And Dr. Zapadka, how about you? Where can people follow you? 

Karen: 
Okay. I’m in the Pittsburgh area. The name of our practice is Trajectory Health Partners. Our website is trajectoryhp.com. I’m also on LinkedIn and Instagram, Facebook. They’ll be able to find us through the practice. 

Bret: 
Great. Thank you both for joining me and providing all this very important information. So, I really appreciate it. 

Karen: 
Aw, thank you for having us. Thank you so much. 

Yeah, thanks to you. 

Bret: 
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