Episode 72 - Andrew Kutnik PhD - Pioneering Personalized Nutrition for Improved Type 1 Diabetes Management

What if personalized nutrition could revolutionize the way we manage type 1 diabetes? Join us as we feature Dr. Andrew Kutnick from the Samson Diabetes Research Institute, who brings a wealth of knowledge and personal experience to our discussion. Diagnosed with type 1 diabetes at 16 and overcoming obesity, Dr. Kutnick's journey under the mentorship of Dr. Dominic D'Agostino has fueled his passion for unveiling the intricate relationship between lifestyle factors and diabetes management.  Don't miss this thorough and insightful conversation that seeks to make diabetes management more accessible and effective for everyone.

About our special guest: 

Andrew Koutnik PhD is a Research Scientist at the Samsun Diabetes Research Institute. Santa Barbara, CA.

About the Show

We cover all things related to sports science, nutrition, and performance. The Sports Science Dudes represent the opinions of the hosts and guests and are not the official opinions of the International Society of Sports Nutrition (ISSN), the Society for Sports Neuroscience, or Nova Southeastern University. The advice provided on this show should not be construed as medical advice and is purely an educational forum.

Hosted by Jose Antonio PhD

Dr. Antonio is the co-founder and CEO of the International Society of Sports Nutrition and the co-founder of the Society for Sports Neuroscience, www.issn.net. Dr. Antonio has over 120 peer-reviewed publications and 16 books. He is a Professor at Nova Southeastern University, Davie, Florida in the Department of Health and Human Performance.

X: @JoseAntonioPhD

Instagram: the_issn and supphd

Co-host Anthony Ricci EdD

Dr Ricci is an expert on Fight Sports and is currently an Assistant Professor at Nova Southeastern University in Davie Florida in the Department of Health and Human Performance.

Instagram: sportpsy_sci_doc and fightshape_ricci

Transcript

Speaker 1: 0:04

Welcome to the Sports Science News. I am your host, dr Jose Antonio, with my co-host, dr Tony Ricci. You can find our podcast on Spotify, youtube, apple Podcasts and Rumble. Our special guest today is Dr Andrew Kutnick. He earned his PhD at the University of South Florida. I want to say it's more Santa College of Medicine. Many of you know his mentor, dr Dominic D'Agostino. We had him on the show a few weeks back. We had some really great conversations. In fact, Dominic was telling us how he would paddle out in his lake and there were alligators there. We had that common bond there. Right now, your current position? You're currently a research scientist. It's the Samson Diabetes Research Institute in Santa Barbara, california. So you were thriving over there in California. You left Florida. You went literally you know what's that 2,000, 3,000 miles west.

Speaker 3: 1:00

Yeah, I calculated that a long time ago. I don't even know the exact numbers. A very long way, that's for sure.

Speaker 1: 1:07

Well, tell us a little bit about. Okay, you started at USF with Dominic, so I'm always interested in when individuals pursue a research sort of a research program like you are actually following, somewhat similar to what you did for your doctorate, which isn't always the case. A lot of people will go sort of a different route, like, for instance, for my PhD, I did a lot of skeletal muscle plasticity stuff and then I basically left that entire field to pursue, because when you do a PhD, everyone's like, well, it's really your mentor, it's not really you. I mean, you're sort of the co-pilot, they're the pilot, but you know the co-pilot gets the credit for the dissertation. So what was your thought process for your doctoral dissertation?

Speaker 3: 1:59

and then moving forward from that, so to answer that question, I had to turn back the time even further. So, um, when I was 16, going on 17, I got well. Even before that, let's go a year before that 15, 16, I had struggled with obesity for five, six years in adolescence, so I was, by definition, clinically obese. Uh, and struggle with that, the self-esteem issues, everything that comes along with that ride how tall and how much did you weigh at?

Speaker 1: 2:22

the time with that ride. How tall and how much did you weigh at the?

Speaker 3: 2:24

time. Wow, that's a good question.

Speaker 1: 2:33

I think it was around six, three, almost six, four.

Speaker 3: 2:34

I was in the two 50 to 60 range. Oh, but you're really tall though. Yeah, I am very tall, but I definitely pushed Pat. I hit the criteria and I can tell you, physically I was definitely in the criteria. It was not muscle mass, it wasn't. Physically I was definitely in the criteria. It was not muscle mass, it wasn't. Uh, you know I was used to sit down, I was, I was sitting.

Speaker 3: 2:48

In theory was uh, uh, a common thing for me at that stage of my life played video games and all that good stuff. So, um, but no, I when having that. You know, the biggest focus at that time was to lose weight and you know, exercise, nutrition was the forefront of my mind, and so I became very passionate about that. You know I'd failed multiple times but eventually lost weight. Um, nothing, no special techniques, nothing caloric deficit, uh, engaging exercise, pretty simple, right.

Speaker 3: 3:10

A year later, completely unrelated it, uh, because it was a year apart, separated, um, I get diagnosed with type one diabetes blood sugar. You know, normal blood sugar for your audience is normal Gmic defined 70 to 120 milligrams per deciliter. I was 596 milligrams per deciliter and so, um, I found that out about after throwing up for about 12 to 14 hours straight. Not an uncommon story. For someone with type one diabetes or those of your audience who aren't familiar, that just means that my beta cells pancreatic cells that produce insulin that sends glucose high, low, variable levels, that either turns on or send signals to stop the release of insulin, they stop working. So my thermostat for glucose regulation no longer there right.

Speaker 3: 3:56

So then I lived the rest of my life managing type 1 diabetes, but went on to study exercise physiology. I was passionate about bigger, stronger, faster, but realized that I really wanted to follow a different path, which was to understand a personal journey of mine, which was the interaction between lifestyle and a disease I was managing, which was type one diabetes. And so I joined Dominic D'Agostino's group at Metabolic Medicine Lab at University of South Florida Morsani College of Medicine and studied all things nutrition and the interaction to disease. And all this was mostly focused on preclinical models, although we did do some collaborative work with some collaborative human work. We also did some studies with NASA at the time, looking at underwater physiology.

Speaker 3: 4:38

So after that, your question is you know why you know you usually steer away from this path? Your question is you know why you know you usually steer away from this path? Frankly, the reason I'm in this path is because I'm so interested about how to move the needle in my disease and type 1 diabetes patients living with my disease, most patients with type it's an average blood sugar around an estimated average blood sugar around 180 milligrams per deciliter, with a standard deviation around that around 60 milligrams per deciliter above and below, so a range that's slightly higher than 120 milligrams per deciliter. So for those in your audience who haven't experienced that, it accompanies a whole list of symptoms of hyperglycemia, hypoglycemia. It's really, you know, fatigue, irritability, loss of concentration and on the severe end, if you get high enough, you could end up in the hospital, like I did when I was first diagnosed. And on the low end you can also have life-threatening, basically neuroglucopenia, or better stated as low blood glucose in the brain, which causes a ton of symptoms of stress, anxiety, but also it could be fatal. Right, you can get a coma seizure if you get low enough.

Speaker 3: 5:52

And I was just so interested about my journey with nutrition and so many other people's journey with nutrition because I walked into exercise physiology class at Florida State University, an introduction to exercise phys, and I remember the very first seminar. The very first seminar was, you know, the focus of that seminar was largely focused on hey, we have all this understanding of how pharmaceuticals and other things relate to health, but look, here's exercise, here's nutrition, which has some of the most potent potential implications in health and disease performance. But yet the science isn't as appreciated and, frankly, isn't as robust as because we don't have the funding has been less, the investigation has been less. I mean it. There's a lot of reasons for that, but we're at a different stage and age nowadays, but nonetheless, I was very passionate about that.

Speaker 3: 6:44

How do we apply things that we should be doing?

Speaker 3: 6:48

I mean, frankly, almost everyone should be doing healthy nutrition and exercise and how do we apply that to a disease state and maybe move the needle, but not just a little bit, a lot. Can we really move the needle a lot in the context of type one? So that was something that drove me from finishing my PhD at University of South Florida, and I actually joined an institute called the Florida Institute for Human and Machine Cognition where they were very interested in exploring the impact of metabolites that come from low-carbohydrate diets in all these ketone bodies. Can they apply to unique military warfighter circumstances? When completing that work, I wanted to transition to studying my disease and type one diabetes. So it was a is a unique path of you know my personal journey with obesity, then type one diabetes, exercise, phys and then university of South Florida, preclinical model disease to military applications of performance and resilience, to then actually studying very directly what we do now at the St Sam's Diabetes Research Institute, which is the application of interventions like nutrition to ultimately move the needle in diseases such as diabetes.

Speaker 1: 7:55

Let me ask you a question about when you interact with clinicians, and it's interesting. You mentioned the value of exercise and nutrition, and as exercise scientists, we're always screaming from the rooftop about nothing moves the needle like exercise and then, secondarily, good nutrition. Yet it seems to be at least from my experience being on this earth a bit longer than you, a little, maybe a teeny bit longer than Tony clinicians don't seem to, I guess, put as much importance as we do, and maybe we're biased because we study it, but it's not just we're biased, but we're actually right. So what is your experience and how do you deal with clinicians who would tend to view type one, diabetes or really any other kind of serious illness, really more from a I hate to say it, but a pharmaceutical point of view versus exercise and eating?

Speaker 3: 8:46

Yeah, that's a wonderful question that will cry as a good bit of nuance in how I describe that and some careful tiptoeing Tiptoe away yeah, I will do some dancing. No, to be very blunt and direct, when you speak to clinicians who are actually managing patients on a day in and day out basis, one thing that comes to mind is and even back to a personal example, I'll give you a personal example. I remember walking in my endocrinologist who treats diabetes, a clinical physiologist who treats diabetes. I walked in and I was going in to see my quarterly checkup and get blood work. Look at everything. Do height, weight, give blood work. Look at everything. Do height, weight. And about 15 minutes at that point I mean we're like barely getting past you know an update. No discussion about like where we should go, what medications should we try, interesting things that I wanted to talk about alarm goes off and I was like what is that? She's like oh, I have to go. That's my, my timer. I have to go see the next patient. I was like, okay, yeah, and it wasn't like they were happy about that. They were in like I don't think they wanted to run out of the room.

Speaker 3: 9:48

After talking to me. He'll say it is possible, um, but uh, you know I. So that that's one example, albeit a bit extreme, illustrating the barriers. You know, when you talk about exercise and nutrition, you can say, hey, go walk some more. Or hey, remove sugar laden beverages, you know, easy, like low hanging fruits.

Speaker 3: 10:06

But actual implementation of unique dietary strategies or advanced nutrition, exercise-based approaches, uh, isn't so simple, right? Um, it can be complicated and it can be hard because a lot of times it requires some effort and some handholding and some support, which doesn't necessarily come out of 15 minutes, you know, sometimes it takes a lot more time to really do that. So you often see people preaching. Frankly, I might be one of those of the importance of this, but I've also lived the journey of looking for it for myself. No clinician told me how to exercise and eat a certain way. I did that on my own, I looked at it on my own, I looked for resources and then tried things out and saw what worked and what didn't work. It doesn't mean they didn't try to help me. They gave me general recommendations which I largely did not follow, to be frank, and so there's barriers in the way. I mean, I don't think-.

Speaker 1: 10:54

Wait, wait, wait. Did you say, you did not. They gave you general recommendations that you did not follow.

Speaker 3: 10:59

Correct Yep. Yeah, correct Yep.

Speaker 1: 11:01

Yeah, what were those general recommendations?

Speaker 3: 11:04

Yeah, if you want to go, this gets into a very unique space and I'm willing to go as deep as you guys want to go into this. The general recommendations at the time for exercise was, you know, just be more physically active. You know, do some aerobic exercise, resistance exercise, like I was so jazzed about being bigger, stronger, faster, especially having dealt with obesity. I was all about trying to understand how to optimize this. You know, I wasn't satisfied with just going in for a walk 30 minutes a day and then maybe trying to do some body weight resistance, like I was very interested, um, and they're not giving ACSM recommendations, by the way, they're like, just, hey, move more, that's what we know helps. But I wanted to be as big, as strong, as fast as I possibly could be. So you know periodization, you know specificity to the application I want to do, which was weightlifting, powerlifting at the time, and so that's from an exercise perspective. But nutrition gets a lot more interesting because at the time I was diagnosed 2006. Um, the recommendations were largely to eat just a healthy diet. So, like you know, jose, tony, hey, you guys want to eat a healthy diet. What do you eat? Okay, you know generally like whole foods, you know, high carbohydrate based approach. Um, don't, don't do these kinds of fringe approaches over here, over here. You know they're not really evidence-based. Well, I did that for a while. Um, the problem is that my blood sugar wasn't where I wanted to be, my performance wasn't where I wanted to be, and so I went off the rails a little bit. I actually because of the hype a long time ago, which I think was largely unfounded. Um, there was all this hype about you could do a ketogenic diet or a low carbohydrate based diet and retain muscle mass, you know, and lose all this fat, like you just burn the fat away and muscle just stays there. Well, obviously, that was wasn't totally evidence-based by any means, but it led me, in my ignorance, to try it right, like, okay, let me, let me give this a shot, this might be interesting. I walked into my doctor's office about three months later, you know, and get my blood work, and my doctor goes what are you doing? And at the time, this is my doctor's ADA president, and so I, you know, probably one of the best doctors I've ever had my entire life I'm being completely frank, an incredible human being and he goes what are you doing? And I said, well, you know, I'm all jazz now, like I did something special. And I said, well, I've been doing this like a low carbohydrate based diet and dah, dah, dah, dah, dah. And um, he goes, okay, well, your HbA1c is, uh, 5.6. You know, we don't see that in type one diabetes, I haven't seen this in this office. And I go, oh okay, you know, like now I'm doing something, I must be doing something really special. He, this guy's telling me I'm doing something special, I must be doing something special.

Speaker 3: 13:44

And that led a journey from that point forward to really be extremely interested in this interaction between how food interacts with a disease. You know, I, you know you walk into exercise physiology class, um, and you hear this message that you should study exercise nutrition for, for, for application, beyond just being healthy, like for diseases. And here I am a lived example of someone who kind of went off the into the you know some people call this fringe um of trying this, all the alternative nutritional approaches, and have this unbelievable success, at least based on the biomarkers that we know matter in long-term outcomes and acute and chronic complications and type one diabetes. And so I, I that was going against the grain and, frankly, it's still pretty much against the grain, um, to do such a thing.

Speaker 3: 14:26

But I was very passionate about that because now we're at a state of affairs where you know there are no randomized controlled trials using an approach like that for their audience's awareness over seven days, of a very low carbohydrate diet, at least if you define that less than or equal to 50 grams per day of carbohydrates. Um, however, there's observational analysis, a ton of case report and case series, uncontrolled interventions that have shown the ability to achieve normal glycemia in patients with type one diabetes, which occurs in less than 1% of patients. So suffice it to say it led me to be very curious and interested. And it led me to be very curious about diet in general. How do we leverage nutrition, diet and the ability to modulate the key biomarkers of health in unique diseases, metabolic diseases such as type 1 diabetes?

Speaker 1: 15:15

You know what's interesting? Oh, I'm sorry, Tony.

Speaker 2: 15:17

No, just a quick question, andrew. Could you elaborate just so our audience would know too? So we're in the keto type or approach. We're under about 50 grams of carbs per day Now, and I guess the purest form of keto would be somewhere around 80% fat, actually, or 15% protein. But what was the remaining macronutrient distribution of your proteins and fats that brought so much success to lowering the A1C? As an example?

Speaker 3: 15:43

Well, I'm actually. So I'm actually gonna skirt around that question to be obvious, because the truth was never was about. It was never about chasing ketone bodies. It was about getting normal glucose control. Okay, um, and so for me it wasn't. It was never about how much protein or or fat it was.

Speaker 3: 15:58

We know that in the diet in type 1 diabetes, there's no surprise to anyone that the most glycemically impactful macronutrient in the diet is carbohydrates. That's a given. Okay, plenty of data going back centuries well, not centuries, well, decades showing this, looking at glycemic and insulin response, postprandial acute studies. So it makes sense that you know, quite obviously, if you reduce that most potent impact, you may lower some of the difficulties of managing type 1 diabetes, where you have insulin that you inject from outside the body. So people may not be seeing this, as they're listening to this, uh, via just their headphones and not visually. But you know, in this little pouch right here and on the back of my arm, uh, you can see it a little bit right here is an actual pump that's constantly administering insulin. But unlike you, jose, and you, tony although I'm assuming you guys don't have type one diabetes or type two diabetes it's so far progressed you're taking exogenous insulin.

Speaker 3: 16:54

I had to take an exogenous insulin which, through the route of administration, is hypersaturating the peripheral tissues and causing what was well-established in type one, at least in every study conducted so far in systematic meta-analysis iatropic hyperinsulinemia, so an elevated level of insulin in the periphery, similar to type 2 diabetes, even though most people with type 1 diabetes don't have the same level of body weight adiposity lipid problems, although it's expediting and becoming much more of a prevalent issue.

Speaker 3: 17:18

Those issues are also confounded on top of the dysglycemia that occurs in type 1 diabetes. And so I could go on and on about this, but suffice to say, in the context of type one diabetes, a very unique disease where you essentially get to be a human knockout model of type one or of insulin. Right, you know, people in science often look at models where you knock out a specific pathway to see what happens on type one. You know you're a human knockout model of insulin. You get to play around with the lifestyle factors that affect glycemia and how it interacts with actually administering insulin. So could go on and on about that, but I'll pause there.

Speaker 2: 17:53

No, but there's some great info in that. Thank you.

Speaker 1: 17:57

I have a question about like, for instance, in the exercise world. When I was going through graduate school, the primary organization conference I went to is ACSM, american College of Sports Medicine. I actually transitioned out of that into the NSCA, the National Strength and Conditioning Association, and mainly because and then I'll get to my point mainly because back in the 80s and 90s the American College of Sports Medicine, I mean it was the largest sports medicine organization, at least for those of us who had an interest in exercise. But I felt that they were getting very ideologic and the example I give is back in the 80s.

Speaker 1: 18:35

I remember going to talks where they made fun of people who lifted weights and it wasn't like I was a weightlifter. I just thought, well, this is really strange. All I heard was aerobic, this, aerobic, this aerobic, this, and I'm like, and I actually like cardio. So it wasn't like I was this weight training guy who was like why are they making fun of people who lift weights? And making they especially made fun of bodybuilders. They would put pictures of bodybuilders. They would say, look, no one's ever died of small muscles. I mean, you know, notwithstanding sarcopenia, et cetera, et cetera. So I'm always interested how these large organizations and I'm going to transition that to the American Diabetes Association how they view a problem like this, which I think is. I think it's unique in a sense, particularly when you start looking at their nutritional recommendations.

Speaker 1: 19:21

And my specific question is this On the American Diabetes Association website, they have a list of what they call superfoods. Okay, I'm just going to name them and then you're just going to tell me what you think. So these are their superfoods uh, beans, which include kidney beans, pinto beans. Uh, dark green leafy vegetables, citrus fruits, berries, tomatoes, fish I love fish nuts. Uh, whole grains. Uh, milk and yogurt. Uh, and those are the big ones.

Speaker 3: 19:50

Okay, so I could have gone one by one, so you get just the ones that come off the top of my head.

Speaker 3: 19:55

So the first thing that goes in my head is not like, okay, how much protein, fat and carbs does have. The focus is what's the impact on my glycemia Cause that's going to affect how I feel right now, for the next three hours and maybe for the potentially rest of the day if I mismanage this. Um, so beans, okay, let's say I ate a regular serving of a cup or two. Um, I don't know. We're talking 30, 60, you know grams of carbohydrate, just give or take the type of bean. Okay, do I do? I want to do that, because if I do that, then I have to give insulin. I have to give insulin. That we know is about three to four times slower than carbohydrates are based on ingestion. Uh, kinetics, um, and so it's not. It's not going to match. So should I even give that a shot? I'm a little hesitant, so I might not do that, okay, uh, the next one nuts okay, that's pretty reasonable. Probably won't have much of an impact.

Speaker 3: 20:39

I'm more concerned about caloric intake. No big deal, uh, yogurt, okay, well, what's in that yogurt? Okay, because a lot of yogurts are not all the same. Uh, you can even look in the back of a yogurt that says keto yogurt and it has sugar in it or some form of sugar that isn't labeled s-u-g-a-r but, like maple syrup, honey, blah, blah, blah, blah. And so you're. You quickly become an expert on label reading hidden sugars. You can't hide from sugar as a person with type 1 diabetes, either direct or something that will convert to it.

Speaker 3: 21:09

So when I look at that list of foods, I mean that's, that's everything you would see on a picture that says healthy food. But when you think, as a patient with type one diabetes who no longer has endogenous insulin production and the insulins we currently give are so much slower than what happens in, let's say, jose or Tony, I have to start contemplating the the negotiate whether that's worth it for me. Or should I try to focus on foods that will have less of an impact? Because it's not. If you go online, someone your listeners can go google right now type 1 diabetes, continuous glucose monitoring trace and just look at what the common trace looks like.

Speaker 3: 21:48

As I mentioned, the average is about 180, the standard deviation is 60 above and below. That is a very different quality of life and feeling than, let's say, I'm assuming you guys are both athletic, eat probably very healthy. These are assumptions, but I assume they're true. Jose told me before we got on the podcast he's a world champion paddleboarder. He could be anyone who's listening. So you know you have all those things considered, then you know.

Speaker 3: 22:16

I see no issue with foods like that. But if you're contemplating in type one diabetes, you have a whole different list of considerations around kinetics of insulin, the type of insulin how's that going to affect you? And I think is largely kind of pushed to the side. Okay, like, okay, we're not going to focus on that as much as you know. Focus on you can eat whatever you want and you know, generally these are the targets of reasonable ranges that you might be able to achieve. But the truth is that there's no free pass. Okay, uh, we know that.

Speaker 3: 22:43

Even a paper that came out, I believe yesterday or this last week, that showed that time and range defined in type one diabetes is 70 to 180, which is not normal glycemia, much, much larger range in type 1 diabetes because of the difficulty in managing these swings with food without exogenous insulin. The kinetics again I'll reinforce this just don't match and so it's extremely difficult. And there was a paper that showed that time and type range, which is something that a lot of people in the type 1 community are very adverse towards, which is 70 to 140, is if you get higher percentage of time and time and tight range versus time and range, you see larger reductions and long-term complications of micro and macro vascular disease is absolutely zero surprise to anyone who knows anything about physiology, glycemic control outcomes, that's no surprise. But it is not necessarily the message that's generally given to patients, not because anyone has nefarious, alternative negative um motives, but just because of the difficulties in managing this disease. So I went on a bit of a tangential diatribe there post-nutrition, but that's what I would go, that's what goes through my head, that's what goes through my head as a patient living with type one diabetes, thinking about should I or should I eat this food? And that's why food in and of itself?

Speaker 3: 24:03

Because it's a controversial topic in type one, because, god forbid, you get diagnosed with a disease it's not your fault, and then you can't necessarily eat certain foods on top of it. We don't want to present that message and that message goes a hundred years back, actually, in the Institute that I'm standing in right now. Uh, and William Sansom, who he himself, who was the first person to synthesize and minister insulin in the United States, um, was here in Santa Barbara, california, um, and world famous for that. He also recommended the shift away from what was prior to that, the standard of care, which is these very low carbohydrate based diets, and so that has kind of persisted ever since, even though we lack randomized control trials to prove first high and low carbohydrate comparisons which one is actually more efficacious. Despite that, there have been guidelines that have been given to patients with type one that have modeled the general population, even though the physiology and lack of beta cell production completely change the lived experience and dynamics around managing the disease, around nutrition.

Speaker 1: 25:02

Could you comment specifically on because I see this a lot on clinical websites consuming whole grains? It's often touted as just it's healthy to consume. Obviously, for you there are issues that go beyond that. So what do you think of whole grains?

Speaker 3: 25:17

outside of type 1 diabetes, it could it could no with it with it.

Speaker 3: 25:22

Oh, with type 1 diabetes, uh, I don't touch them, but I I am. Yeah, to each their own, let me. Let me say that up front. I'm not telling you what to do. Each person has to live their own life and their experience and manage their disease around cultural considerations, religious considerations, uh, but whole grains. What is going to happen? Let's say I ate 50 grams of whole grains, I will see a blood sugar spike that probably peaks within 30 minutes. Um, I will then wait for the insulin I administered to have its full impact, which won't happen to 90 to 120 minutes. So I'm going to go and then I'm going to wait for it to come down over the next two hours. So I'm going to sit in hyperglycemia.

Speaker 3: 25:58

In fact, I did a mixed meal tolerance test the other day, jose Antonio, which is a validated test for looking at beta cell function. 25% of your calories, 55% of those calories, come from carbohydrates. Based on my caloric needs, around 3,000 kcal per day, that's around a hundred grams of carbohydrates. Just for a fourth of my calories in that meal I consume. That I went from a hundred to 370 milligrams per deciliter, utilizing an automated closed loop insulin delivery system, which is the next generation technology to help patients control themselves into better glycemic control. And I came down three and a half hours later, um, with a mean blood glucose over that period of time of 180, with a standard deviation around uh 60 milligrams right to what is normal. So do I. Do I, a patient, would have to consider, beyond what they're told in any environment, is that something they want or not want? And you can manage that by lowering the carbohydrate intake. You don't have to completely remove carbohydrates. I mean, this is all dose dependent and we've done an analysis on this, jose and Tony. We've done.

Speaker 3: 27:04

Because of the interest in this and because of the controversy around it, I was very curious to actually look at the data, right, because, jose, you talk about you know ACSM before, about how they used to have what you described as a dogmatic view towards aerobic exercise and maybe antagonistic views towards resistance exercise. But in the context of type one diabetes, there was this stirring of controversy around how many carbohydrates so much consume and all this concern about what if you don't eat carbs, are you going to have growth deficits as kids? Are you going to? If you don't eat carbs, will you produce ketones and cause increased risk for diabetic ketoacidosis, you know, eating disorders, all these things right.

Speaker 3: 27:45

So we worked with Belinda Leonard's at Boston Children's Harvard Med on a review looking at this and from that was pretty clear that we needed to do a much more systematic approach to this. So we actually took a systematic approach and pulled every study ever conducted where there was a confirmed patient with type 1 diabetes, there was carbohydrate intake was reported and there was a biomarker that was relevant for long-term cardiometabolic health. So, for example, hba1c, you had to be on the diet for at least two months. Health. So, for example, hba1c, you had to be on the diet for at least two months. Insulin seven days, lipids at least three weeks. So that's how we approach this and we pulled other biomarkers as well. We did look at the compliance growth, all sorts of things out of that analysis and what we found preliminarily and I will be presenting this at the American Diabetes Association this year is that if you look at all these studies and actually the inclusion hold over a hundred studies looking at type 1 diabetes nutrition, carbohydrate intake over the spectrum and there's a clear dose response relationship, not between carbohydrates at the average carbohydrate intake in patients with type 1 diabetes at 45% of total calories or higher, because that's the average. But if you go from 45% of total calories or higher, because that's the average, but if you go from 45% of total calories or lower, there's a dose dependent reduction in HbA1c a long-term measure of your overall glucose exposure, incrementally all the way down to hypothetically zero carbohydrates. And that was for every 50 gram reduction in carbohydrates you saw a 1% reduction in HbA1c. There is no technology on the market right now that competes with such a number.

Speaker 3: 29:17

Now this is observational in nature. It just pulled every study ever conducted and ran an observational epidemiological analysis of it. So this isn't a randomized controlled trial long-term. But what it's looking at is every single piece of data that we've ever collected from randomized controlled trials, controlled interventions, uncontrolled interventions, observational analysis across the entire spectrum. And that's what the relationship looks like, even when controlling for the type of study and other confounders related to nutrition, type 1 diabetes and HbA1c. The same relationship is present for insulin as well. So the data is very clear that carbohydrates have a direct, potent impact on glycemic control. But that relationship may be infinitely more important in the context of type one diabetes and, while it's controversial or not, this is a conversation we need to be having.

Speaker 1: 30:10

You know it's interesting doing any of these kinds of trials, particularly when you're changing someone's diet. Um, doing an RCT is is incredibly hard, um, particularly when you're dealing with issues of compliance. Heck, when I have, we did some of these high protein. I'll call them diet studies. But we, we really didn't change diet, all we did was supplement them with a lot of protein powder. Even complying Theselying, these were well-trained, resistance-trained individuals, men and women. Even complying with that is hard and all they had to do was just consume more protein powder.

Speaker 1: 30:44

So I don't think people understand the difficulty of running an RCT and having them and looking at being able to titrate carb intake all the way down to, I mean, you said a theoretical zero. I guess even if you're just eating meat, there's still a little bit of carbs in there, right? So I guess my question to you and this is both for type one and type two diabetes I'm much more familiar with type two rather than type one, but if you deal with just diet alone, whether it's ketogenic or low, low carb, high protein or whatever how do you approach those? Or you know type one versus type two, cause I think type two is more prevalent. You can correct me on that. I'm not sure.

Speaker 3: 31:22

A hundred percent correct.

Speaker 1: 31:23

Yeah. What's the dietary approach that is different between those two?

Speaker 3: 31:28

if it is different, so in the context of type two diabetes. So I just want to say for the record, there's been plenty of randomized controlled trials, ton of clinical trials and context of type 2. There's been man I think that number might be close to triple digits now um, not necessarily a ketogenic diets, but maybe low carbohydrate, defined as less than 26 percent of total calories from carbohydrates, um, in various forms. Both you know these hardcore, rigorous, multi-site clinical trials to you know a single site clinical trial, um, in the context of. Let's start with type one okay, you're insulin deficient. You have to give exogenous insulin, um, so you are basically your own pancreas, you're playing your own pancreas. So, in this context of, if you were to try a very low carbohydrate diet, you have to consider the dynamics of the food you're consuming around your insulin management strategy. So it's not as much about how do I optimize my internal metabolism to manage the disease, because it was resistant to managing it. In the context of type two, you are literally manually playing your own pancreas and basically being a biological mathematician, estimated biological mathematician to estimate impact of that food on glycemia, amount of insulin required. And you're really focusing on protein now because, even though it's not commonly looked at or even clinically managed. Protein has an insulinogenic effect and a glycemic effect right, I know you guys appreciate that, but others may not as much and there's been direct studies 1983, collier and Odeo and plenty of other studies around that time showing that protein has a much lower impact around 2.5 fold lower on insulin needs and much lower impact overall on glycemic control in healthy individuals, but it still has an insulin impact, which means it still has a glycemic impact. So it you still have to manage protein in the context of low carbohydrate based diets.

Speaker 3: 33:20

The management strategy, although based on standard of care, is that you just give fast acting insulin, basal bolus strategy. So you take a long acting insulin to manage the chronic release of glucose into the bloodstream from your liver, and then you're also giving a bolus, which is more rapid acting insulin in response to food or post-prandial insulin administration. The difficulty, though, is that traditional fasted, ultra rapid insulins do not match the kinetics of carbohydrates, nor of protein, neither. Okay, and so how do you even attempt to manage that with current management strategies? Well, right now, a lot of patients are using things like regular insulin for protein and fat-based consumption female consumption because the impact of regular insulin, which is viewed as an archaic form of insulin, is very slow over time and last actually somewhere between four to six hours in your system. Well, not that different from protein. It seems to work very well for patients who report on this. In fact, there was a survey of patients who do very low carbohydrate diet, a lot of which are using regular insulin, where the average HPL and C in those patients observationally was less than 5.7, so 5.6 something so normal glycemic control. But a lot of those patients are using regular insulin slower, slower, peak or smaller, peak, longer action. There's also new systems called hybrid closed loop systems or pumps, where you can actually set more prolonged administration with these insulins. So it's a totally different game.

Speaker 3: 34:49

In fact, when I got diagnosed and I was in the hospital in Washington DC thinking about how do I manage my disease, the education that went into that, I was in the ICU for almost a week and then stayed in the hospital for another week, so two weeks and I was getting just like blasts in the face with how do you actually manage this disease with nutrition? How do you manage it with insulin? It was a full educational profile. That same education is not available to people right now for low carbohydrate based dietary strategies in type 1 diabetes. There are no guidelines on how to actually administer very low carbohydrate diets in the context of type 1 diabetes and let me say, for the record, it has been one of the most popular eating strategies in the context of type 1 diabetes and yet we lack guidelines on how to manage it. That is a huge problem. There's been a number of studies that have shown that dieticians at least a colleague of mine at university of British Columbia surveyed this during COVID looked at a number of clinics and actually showed that 66% of dietitians don't feel prepared to implement or administer therapeutic carbohydrate restriction, which is the o-ring of carbohydrates below 26% of total calories.

Speaker 3: 35:51

So what does a patient who has type one diabetes? What are they supposed to do if they want to do this diet they've heard of and they want to manage it? There's a whole different thing. I can get on a soapbox about and go on and on about, despite this being utilized as a therapeutic strategy for over 100 years. And here we stand with no randomized control trials over seven days. So it's an absolute and no guidelines, a clear-sided disconnect between patients going rogue and not communicating with their healthcare providers. In fact, when I looked at the systematic analysis and actually looked at the route of administration that patients went for doing these interventions in type 1 diabetes, half the studies actually over half the studies reported patients doing this with minimal or no healthcare support. So it's dangerous, right? So, unfortunately, jose, the real answer, if I was being very conservative and just purely data-driven, I'd say well, we don't know. But the truth is we do know how patients are doing it in the real world and accomplishing these goals, but yet we don't have guidelines to inform the clinicians, to help the patient. It's a system situation that needs to be corrected.

Speaker 3: 36:54

But to flip over to type two diabetes, there's often the consideration, the main consideration is other medications, right? So if you just lower carbohydrates in the diet, there's plenty of studies in healthy and unhealthy individuals that you can see almost immediate reductions in insulin, even within starting at the first meal. Immediate reductions in glucose, and a lot of patients are already on glycemic lowering medications. Metformin SGLT2 inhibitors are already on glycemic lowering medications. Metformin SGLT2 inhibitors, glp-1s is extremely commonly utilized nowadays through their efficacy. All of those hypertension medications okay, all of these are affected by very low carbohydrate diets, at least the evidence from systematic reviews and meta-analysis shows. So that's a totally different management strategy because you already have the internal machinery to manage it.

Speaker 3: 37:33

It's just not working as well. It's an old, rusted car, so to speak, and so you want to fine tune that car, fix it up, but it takes time, it doesn't happen instantaneously. But there's some things that when you first implement you had to immediately be actionable on. And that's why you see, in my opinion, some of these trials, such as the verti trial, which is very controversial for some folks, but why it seems to be so effective is there's a very high touch therapy to it. They really, they were basically having interactions nonstop on these trials and you see remarkable outcomes and those are largely mirroring what has been seen in the real. Other other settings outside of like, say, you know, virta, you know, but other companies as well. But yeah, it takes almost instantaneous action.

Speaker 3: 38:17

And you know, often in type two you're considering weight reduction where, in the context of type one, patients were historically lower weight and so you didn't necessarily want to caloric restrict, which can inadvertently happen on these lower carbohydrate based diets. So I could go on and on, but suffice it to say it's a totally different approach. You just don't lower carbs, which is the error you see in these studies. When people attempt to do this, what happens is that patients often increase their carbohydrates even more. They run into issues. They're not changing insulin strategies and that's the problem.

Speaker 3: 38:44

That's rampant in type one because there's no guidelines or evidence-based approaches to doing this. We also lack randomized controlled trials, but in the context of type two there are. Literally you can go to pull up the ADA's website. They have a guideline that's a pamphlet, I think, like 50 pages long on how to do this in the context of type two diabetes. So there's a big disconnect here between the two diseases, and so we really have to speak in type one on the real lived experience and the weight of the evidence. And then over here in type two we can look at randomized control trials over a long period of time and really point to the gold standard of evidence over there um, what are some, um, as exercise scientists?

Speaker 1: 39:23

you know, we know in general if you're training for hypertrophy, this is what you do there. You know many roads lead to rome, but we sort of know. If you're training to increase muscular endurance, we kind of know, uh, training to increase max vo2, although I don't know anyone does that, but let's pretend we sort of know tony doesn't do that, you sure, I thought he was saying that's what he does. Tony's training for the lowest max VO2 possible.

Speaker 3: 39:47

Okay, no, actually, tony does a lot more running.

Speaker 1: 39:51

I don't run anymore. Tony actually does a lot more running than me. So at least running max VO2, tony wins, paddling max VO2, I beat everybody. Yep. So training with type 1 diabetes what are the? You know, when you're thinking of the extremes? You have aerobic exercise, you have resistance training, you have everything in between. What are the issues you have to deal with when you have a type one diabetic who wants to train, whether it's recreationally, so that's one issue, but let's say they're a competitive athlete. Let's take the extremes distance runner versus power lifter.

Speaker 2: 40:24

By the way, just quickly, there are a couple of UFC fighters who are type one.

Speaker 3: 40:27

Yeah, there's actually a number of professional athletes who are type one and largely they just like I explained earlier, kind of doing their own approach on their own path. Right In the context, exercise is actually one of the biggest issues in type one diabetes Because the second you start exercising, a patient with type 1 diabetes quickly realizes just how impactful lifestyle, movement and other factors can immediately switch insulin action. So the biggest, you know, either hyperglycemia or hyperglycemia. The common guidelines are to keep your blood sugar slightly elevated into the hyperglycemic range, free bolus with carbohydrates if you're sitting, even in normal glycemia, to mitigate the risk of going to hypoglycemia during exercise. If you're too high, wait until you come into a normal range, typically above 250 milligrams per deciliter. You know there's all these things to mitigate the risk of exercise, not to optimize exercise so much, but to mitigate the risk of it, even though we know how powerfully important it is to overall health. So a lot of patients with type one are largely deprived of the access to do this or to feel it safely. So a lot of the guidelines are about mitigating risk and even the next generation hybrid closed loop technology called automated insulin delivery system this is one of their biggest deficits and problems is around exercise and there's a lot of funding from philanthropic entities like the Helmsley trust trying to find ways to further improve this Um. So I want to introduce with that first.

Speaker 3: 41:55

But when you think about the spectrum of exercise, it's well-established, or at least well believed within the community um, that you know aerobic exercise over time is going to slowly cause you to go down, whether immediately or over time. Now the immediate action is largely probably due to insulin absorption quickly getting into the bloodstream, not necessarily insulin sensitivity, but over time you do have the GLUT4 translocation effect and post-exercise you have insulin sensitivity effect. So the rationale might be different but it's almost an immediate effect, often in the context of type one with aerobic or lower intensity exercise. As you start going to mixed model or mixed level intensity exercise you might have a mixed effect and it really depends on your stress response to that, your heart rate, other intensity factors that may lead to the duration. All these things play into it. It's really the ultimate self-experiment.

Speaker 3: 42:47

And to insulin and glycemic biology and type one diabetes, when you think of lifestyle and exercise, when you start getting to like power lifter or that's not a good example, let's say sprint based exercise like high intensity interval training, where you're actually going to max, you could actually see like a 30 second sprint, so three by 30 seconds.

Speaker 3: 43:06

You get active recovery between you can see a rapid spike in blood glucose levels. In fact, I've I posted a number of things. Um, historically, looking at this and showing this that even if I were to go for like, let's say, hill sprints, like truly max effort Jose's hill sprints, uh, and heat, you know, add some stressors on top of there and I immediately go do that I could see spikes over a hundred milligrams per deciliter Um, from that. If I even gave like a quarter of a unit of rapid insulin five minutes before, I could completely block the effect. Okay, so, um, we know that various forms of exercise have differential effects on glycemia and we also know that the interaction it has with insulin is incredibly important, not only during exercise but following exercise due to change in insulin sensitivity. So it's not so straightforward and simple and often very difficult to manage and most patients are kind of just figuring it out, so to speak, with quotes around it.

Speaker 1: 44:01

Tony, we have just a few minutes.

Speaker 2: 44:02

If you have any final words or questions for Andrew lack any of the guidelines that Andrew was referring to, and it's surprising to me, and I hope you know some substantive changes are made, because you've really elucidated the importance of both diet and physical activity. So the information is incredibly informative and I'll tell you this I'm really surprised at what we don't know based upon the information, what you presented just now and you're fascinating there's a lot to learn for any of us who are going to attempt to help someone manage this condition. It is a lot more nuances, as you just noted. It's not just exercise, it's not just some standardized macro approach to dietary practice. There seems to be a lot of individual variants and a lot of things that we have to be cognizant of to really mitigate the effects of the condition or, as to your point, even optimize lifestyle with it. Fascinating information, though, truly.

Speaker 3: 45:09

Antonio, I'll piggyback off that and just say you know, hey, there are guidelines, just not for some of the most popular approaches that people are actually doing in the real world today. And it's not so much about optimization, it's about mitigation, and I'm a live person with type 1 diabetes. I believe that everyone should have access to having normal glycemic control to have zero complications at the end of their life, which is expected that every patient with type 1 diabetes will have at least one complication at the end of their life and expected to lose at least 10 years off their life. That's the average life expectancy. So for me, if you were to even look at the historical Google searches and citations revolving technology or medicine, um, compared to things like diet in the context of type one, that's about fourfold different and lower for diet, right, even though we know that every patient has to eat food and has to live a certain nutritional strategy and should be exercising, um, it's. It's something that we need to tackle and and and do as much as we can to learn from it, because the rest of the world has learned a lot from type one diabetes Most of the understanding around glycemic control, um, and its implications on long-term adverse outcomes.

Speaker 3: 46:16

A lot of that came from type one, the whole movement and continuous glucose monitors. It started in type one. You know a lot of these, uh, a lot, a lot of these. You know things that we're understanding from biology are learned from understanding. If you just knock out insulin production, reintroduce it, or you can induce hyperglycemia without adverse body weight, like what are the implications directly of that? And type one has taught us a lot. But I also hope that we can move the needle and actually changing patient outcomes, which it has improved over time. Complications have come down. Tools and technologies have certainly made a big difference in helping. I don't want to poo-poo those things, but I am a staunch advocate of trying to make sure that lifestyle is at the forefront of that and synergistically working with these other tools that we have in the context of type one. So I'm honored to speak here today with you guys, jose and Tony, and maybe whenever I'm back in Florida because I was from there, my family's there.

Speaker 1: 47:04

Me and Jose will have to get on a paddleboard and see what's up, absolutely, absolutely, and for people who want to find out more about your work, are you giving a talk at any conference? Let the audience know where you might be.

Speaker 3: 47:16

Yeah, so I spoke at an ADA American Diabetes Association their webinar, looking at this specific topic in the context of type one. I think it's behind a paywall, um and yeah. So if you don't have an ADA membership you might not be able to see it. I've given a number of talks that I actually provide free resources. If you go to my Twitter page, there's a little link at the top that says link tree. You click on that and I try to give a ton of free resources for patients. Uh, I have like a five page document of various links, free content that I put out there and websites and all sorts of stuff to help patients.

Speaker 1: 47:47

What's your Twitter handle? Your ex handle?

Speaker 3: 47:50

A-K-O-U-T-N-I-K so Akutnik.

Speaker 1: 47:53

Awesome. Well, thank you so much for being a guest on Sports Science Dudes. Certainly I've learned a lot and I think the audience will find this very fascinating and certainly quite informative. So thank you so much and again, enjoy the rest of the day. Thanks, Andrew.

Speaker 3: 48:09

Hey, likewise guys.