Transcription
Hello, been a while, and you've, you've done a lot since in Academia. Just to do stuff that's not like a manuscript, it's just like a different skill and communication that is worth practicing and and putting out for the public. It's almost as if academicians, scientists, you know, professors, or whatever, and it's not getting out to a general, larger population. It's people that are less rigorous, people that are looking to capitalize on people's naivety or or desperation.
All right, this is, uh, Feed Physiology. Uh, I'm with a very special guest today, a former student of myself and our undergraduate program, um, Amanda Finn. She has gone off and done some pretty, uh, interesting and exciting things and continued her academic and scientific career. So I'm very happy to, uh, speak with her after not having seen her for a couple of years, but excited to get caught up with what she's doing and talk about some of the, the areas that she has been, uh, studying. So Amanda, nice to see you. Um, how, how are you doing today? You mentioned earlier it was a snow day. It's a little bit different climate, but, uh, how are things going where you're at?
Hi, thank you so much for having me. I'm really excited to talk about science and also catch up. Um, I had a great experience in the Kinesiology program in undergrad, so just, um, really good to connect again.
Right now, yeah, like I mentioned, or like you mentioned, we're having a snow day, which is really crazy 'cause I'm from Southern California originally and I've visited snow before, like at Big Bear, but I haven't actually woken up and like heard snow falling. And so today I'm working on one of my manuscripts, and I can give some details a little bit about what that project is about. Um, but then I was also doing some reading for preparing for this podcast episode.
All right. Yeah, I remember the first time. I'm from Central California, so a little different, you know, climate in in Southern. It gets super hot, uh, but it definitely does not snow. Uh, the first time I saw snow when I was doing my PhD at in Albuquerque, New Mexico, I was, I was confused. Normally, you go out and play in the snow, you know, for like, at a couple hours, then you go back inside and get warm. But when you're living in it, it's, it's different. So that's, uh, that is our California bias. For people that are loving California.
Um, yeah, so, you know, you did our, uh, undergrad program, Exercise Science, at at Long Beach. Uh, was probably my first, first couple years there, definitely. Um, but, you know, I don't think we've talked really much about your specific interests or or how you got interested in exercise science or nutrition and health. Um, and then also your, your decision to go pursue, you know, uh, a higher education, a graduate degree. Um, so why don't you tell us, you know, your, your, your background, what led you to the area of exercise science, your interest, and then what ultimately led to you, uh, continuing on that, that education and that development?
Yeah, so I guess my story really begins in community college. So I started off college doing community college because it was affordable and I wasn't really in a place at the end of high school to make a big decision like moving across the country or, you know, getting in debt over my education. And during those years, I majored in Kinesiology because it didn't require a calculus, honestly. And so I want wanted to do a major that taught me anatomy and physiology initially 'cause I wanted to be Pre-Med. But biology would like had these requirements and I was just like, yeah, I don't know, I don't know about all this math. So I did Kinesiology and I transferred to Cal State Long Beach and I was like, okay, this is really great and I'm still Pre-Med minded. And during this process, I ended up becoming friends with some of your students and some were Master's students and undergrad students that were in research at the PEX lab. And, you know, I'm, I'm like, at first, just there 'cause I'm like, oh, it's fun to do these tests with my friends, VO2 maxes and stuff. And like Alec Wallace's Master's thesis. And I was like, you know, this could be good for med school applications. Like, I'll just dive a bit into research. So I talked with Dr. Evan Shik, who's at, um, Cal State Long Beach in your department too, and he became my research mentor. And all the while, I'm thinking, yeah, this is for med school, allegedly. And, um, I wrote an IRB application for a study and it was going to look at glucose-dependent insulinotropic polypeptide, um, otherwise known as GIP. And keep that, put a pin in that hormone for later. But then the COVID pandemic happened. And so I didn't get to do this study related to GIP. But at this point, around like April of 2020, Dr. Shik is like, come on, girl, like, you're a researcher, like, don't lie. And so I was like, oh, okay, I guess I am. And so I did an undergrad research program called BUILD, which I believe they still have at Cal State Long Beach. Um, so that program really helps you do the professional development required to apply for graduate school. And so I applied to some Master's and I applied to some PhD programs during that COVID year. And one of the ones that I found out about was where I currently am, at the University of Alabama at Birmingham. And it's a nutrition program. And initially, I was looking at Kinesiology programs 'cause I'm like, this is pretty good for my bachelor's, I'll just do that in grad school. But I talked to the program director for my nutrition program and she was like, we just really connected. The research interests were super good. I had never heard of UAB before, like from Cali, you know, I know UCLA, whatever. And I was like, damn, like UAB is actually a really good school. Like, you know, us CIE, like we don't think about the South really. But I was like, dang, like I was like, oh, and I remember I emailed Dr. Shik and I said, am I really going to go to Alabama? Like, haha, LOL. Um, yeah, I did. I am in Alabama and I'm pretty happy here. But so I go to, uh, UAB after my bachelor's and I am in a dual enrolled Master's and PhD program. So you would just do your Master's on the way of the PhD. And so my Master's degree was related to kind of like the personalized nutrition umbrella of trying to figure out if there's some biomarkers that could be used to predict diets that could help somebody with fat loss or with weight loss. And so mine was about insulin as a biomarker, which it overlaps into like carb-insulin model theories. But then there's also other aspects such as like, how does someone's insulin sensitivity affect their adherence or their responses to calorie restriction? So I completed that Master's thesis a year ago and it's not published. Um, but I can talk about it in the context of the general literature in that area as well later. And what I've been doing now is I got some funding to look at GIP. So that hormone that I was interested in in undergrad, I didn't get to study it, but now I got to study it. And I'm looking at the associations between GIP and glucagon and metabolic outcomes following three types of weight loss: Roux-en-Y gastric bypass, sleeve gastrectomy, and a very low energy diet. And so that is what I'm working on. And I submitted an abstract for the American Society for Nutrition conference in 2025. So that's in a few months. Um, where I'll share those findings. If anyone's going, say hi. So that's kind of like a, a big picture from community college to my PhD.
That's awesome. It's, uh, when you go from, when you change sort of fields or areas of of focus or or subject matter, you know, that kind of indicates you're actually pursuing this thing because you're actually interested in rather than staying on a track or something that you're familiar with or something that you know. And, you know, for example, going into an exercise science PhD program, exercise science PhD program. Um, but following your your interest is, is, uh, pretty cool, pretty cool. So, um, before we get into some of the specific, uh, research aspects and talking about, you know, some of those hormones that, that you mentioned and are getting into and, uh, and studying, uh, how was the transition from Southern California to Alabama? What, what part of Southern California are you from, first of all?
So I'm from the Santa Clarita Valley area, which is about an hour, I mean, I think traffic has gotten worse since I lived there, so about an hour to an hour and a half north of Long Beach and kind of like the LA City area. So, one of the things that I noticed, and it took me some time to really notice this and how it affected me, was like, I'm Hispanic, like on my mom's side, they're Honduran. And in Southern California, you just take for granted all the Latinos that are around and the businesses, the fact that at a grocery store, you're going to have Tortillas and you're going to have all these, like, you know, Masa brands. And I come here and it took me some time. When I, I was like, at Target and there was a Hispanic couple and I went, oh my God, like I was like, I haven't seen like, like those, you know, people in in a while. And it started to kind of weigh on me where I was like, I miss being able to have have certain foods or just, you know, feel that same type of like culture, but have it be like low-key, just like, this is how it is, right? And I didn't really think about it because people in Alabama when I was interviewing and stuff, like people weren't bringing that up as a concern necessarily. And so the low, I guess, percentage of Latinos here was one thing that kind of affected me. However, as I've been here longer now, I know where to look for this culture. So I got into, uh, Latin dancing and I go salsa and bachata dancing, for example, or I know where the grocery stores and the, like, where to get pan dulce from. And it really is like, it's like such a small thing of like going to buy like conchas. It, it makes my whole like week. And now it's more normal 'cause I can go do it like whenever I want. But the first time was, I was emotional. I'm like, oh my God, like I can have the conchas, yay. Um, but otherwise, I really love rain and the outdoors. And so this place in Birmingham, it offers you a lot of great, like trails and mountains and like, just the casual rivers and streams that we have here is, is just so awesome to me. So there's definitely some pros and then there's some cons. Um, but I think I'm pretty happy here and like, I'm not desperate to move back to California 'cause it's just so, oh, it's so much cheaper here as well to live.
Yeah, so like I can afford a one-bedroom off of my, uh, T32 like NIH stipend. But that's the same stipend they give you if you're in San Francisco. And it's, it sucks. Like, you know, same. Yeah, like, how, how are you going to give somebody $30,000 and just be like, yeah, do that in California, do that in DC? And it's like, no. So that was definitely part of my decision in coming here is I knew it would be more like financially feasible to just have a better quality of life, even if some of the cultural aspects are a little different.
Yeah, yeah, yeah. We, uh, we did a, um, a modified oral glucose test in, uh, on my one of my classes labs recently. Brought in some bundles. I saw that. We took blood sugar, blood glucose over. That was for extra credit. Yeah, I want to see that. Haven't had it before. What's that? I want to see that in a paper. You know what, that might be an idea. Yeah, that's a BUILD project right there. Yeah. Um, yeah, okay. Very cool, very cool. Uh, I have not, not had to have the experience of not living in a place where there wasn't taco shops and taco stands and banda around. Um, you know, in in Albuquerque, there's, uh, a Hispanic population there, so it was always, always accessible. But that would be rough. That would be rough.
Um, okay, well, um, let me ask you then. You know, you had mentioned a specific hormone that you were interested in, in, uh, looking at. Remind me what it was.
GIP.
GIP. And just spell that out.
Glucose-dependent insulinotropic polypeptide.
Okay. I myself am not familiar with that, with that peptide, but with, with that hormone in mind, and maybe some of the others that you are, um, getting into, what sort of perspective or what role or what question are you looking to answer in relation to that? So maybe with that, you can give us a little bit of a description of what its function is, what its effects are, what its relevance is in health, obesity, disease, uh, things like that.
Yeah, so GIP. And I, I'm so, like, I'm always sorry to say the full, you know, its full government name 'cause it's, it's just like, people hear insulinotropic polypeptide and I'm like, yeah, they, if they're not in physiology, they're lost. Like my behavioral science friends, I'm like, I'm so sorry. But anyways, GIP is a hormone that belongs to the class of hormones called incretins. So have you heard about incretins? Incretin effect? Yeah. So that is one hormone that belongs to the incretin hormones. The other one is GLP-1, or glucagon-like peptide-1. So GIP, I heard of that one. Yeah, yeah. So GIP, GLP-1 belong to this incretin family. And what they do, one of the things that they do is they help with your insulin response. So in GIP's name, it's insulinotropic, so it helps with your insulin secretion. So that's one of its functions. And GLP-1 does that too. So they're both gut hormones. They're secreted from the small intestine after you ingest a meal. GIP tends to be a little bit more sensitive to fat. So if you're eating a mixed meal, it's got fat in it, you're going to have some GIP secretion. And GIP, GLP-1 both help your pancreas and it kind of like fine-tunes the type of insulin response you'll get. And so they're pretty good in, like, I consider them good in that way. I mean, it's kind of like black or white terminology, but that tends to be good if we're concerned about someone's, you know, ability to respond to a meal in the postprandial state. And besides their commonality, GLP-1, GIP, they have that commonality with insulin responses, then they deviate a lot in their actions. And so GLP-1, we hear about a lot with weight loss drugs because it acts in the brain, it helps with satiety. GIP has been rather controversial. And so controversial as in whether it would help or hurt in weight loss. So GIP, it has some effects on promoting lipid storage or fat storage. And so it's a lipogenic hormone. And in the fed state, that kind of makes sense. Like you've had a meal, so okay, it's time to store up that meal in fat. And so for that reason, people have been kind of like, yo, maybe it's not like, maybe it wouldn't be a good thing to put this into a weight loss drug. However, what we find is when we do this in like pharmacological doses, the GLP-1 and GIP combined actually helps with weight loss and helps with type 2 diabetes. And so that's one area that maybe people who aren't interested in the endocrinology, but are interested in like, you know, the weight loss drugs and they're hearing about Ozempic and stuff, so you might hear about GIP there. But I'm sorry, is it an additive effect where the GIP and GLP-1 are additive in terms of it outperforming as a regular GIP by itself?
Yes, that that seems to be the case. And I'd have to brush up on those studies, but I do believe GIP, GLP-1 co-agonists do outperform the GLP-1 receptor agonist when it's just GLP-1. GIP by itself, that, nah, like it's, it's not going to be the best one. Um, which is why we don't see those types of drugs. But within a regular physiological context, here's the reason that GIP doesn't do the same thing when it's just made in the body versus when you give it to someone in a drug, is because of the degradation. So our bodies have these enzymes that will degrade GIP and GLP-1 very quickly. And they're called DPP-4, so dipeptidyl peptidase-4. So when you have GIP, it's going to get, um, it's going to get degraded quicker. So that's why it's not really useful to try to like endogenously raise your GIP or your GLP-1 because you're just going to be breaking it down. These drugs, they make them in a way where they don't get broken down. And so I think overall, because GIP has those different effects, it can be good for your insulin secretion, which might be of interest for people with diabetes or impaired glucose tolerance. But then it also has those like potentially lipogenic effects, which maybe is bad if you're just considering obesity. It's why I was interested in studying GIP and understanding better in like physiological, like an endogenous context, is it good or is it bad to have an increase or a decrease in GIP? And so I can say, well, I just don't want to talk too much about my results until they're peer-reviewed. Um, but it does appear, because it's my results are so far, uh, in agreement with other studies, it does seem that having increases in your GIP can be associated with increased insulin resistance. So while I do love GIP, I won't lie, I don't want to talk bad about it, but, but yeah, it may be associated with poor metabolic outcomes. And so that's kind of where I'm at, sending back my draft of my manuscript to the co-authors, hopefully this today or this weekend. Um, but that's kind of the story with GIP. And I don't know if you have any follow-ups.
Yeah, okay. So why don't you describe, um, how you studied that and how you came to those conclusions or how that results were were generated in terms of correlating the insulin resistance and the, the, the GIP? How was that assessed, established, and and studied?
Yeah, so what I was doing is I used, it's a secondary data analysis in a clinical trial. And they compared three weight loss treatments where people lost the same weight, the same, had the same body composition changes. So it was controlled, um, but it was not randomized because two of these weight loss interventions were bariatric surgeries. So it was trying to see differences between Roux-en-Y gastric bypass, sleeve gastrectomy, and then very low energy diet, which is like 700 calories per day. And so these three groups, sample sizes are small, um, but in these three groups, they got blood samples, they got indirect calorimetry, insulin sensitivity at baseline, and then at follow-up. And so what I was looking at was how from baseline to follow-up was the association between changes in GIP levels and changes in like HOMA-IR as an insulin resistance index, or changes in respiratory quotient, for example.
Mhm. I looked for interactions as well, which I did not find interactions. Um, so the associations were consistent in all the three groups that we looked at.
Okay, okay. And these would have been baseline measures? Yeah. So baseline, we got fasting and postprandial GIP. Okay. And then so the, the correlation with the insulin resistance is going to be correlated to the HOMA-IR scores? Yeah, so like a HOMA-IR. Yeah, which is your fasting insulin and fasting glucose.
Were there any differences going from the pre-intervention to the post-intervention that would presumably have produced, uh, weight loss differences? In like, what do you mean? Like, was it, was a correlation present pre-intervention and post-intervention?
Oh, I see, I see. I don't, I didn't look at that, but that would be interesting to see, like cross-sectionally. Yeah.
Mhm. Yeah. The previous research has been cross-sectional. And so mine was looking at like change during weight loss. But yeah, the previous research that's been cross-sectional, they have seen the associations between GIP and insulin resistance.
And was, was there any influence of amount of weight lost? Was there any difference, any effects on that correlation when looking at the amount of weight lost?
I didn't see that. And one thing that you bring up with the, um, correl, or with like a cross-sectional, um, question is with some hormones, it's very difficult to disentangle it from like total fat mass or total body weight. 'Cause you know, the amount of insulin that you secrete, maybe be associated with your adiposity, for example. So that is always a thing where it's like, we can't determine causation. Like, it, it might be doing something, or it might just be also associated with their body size, which can also be associated with insulin resistance as well. So yeah, that's, that's always a, always something with the hormones to worry about.
And what is your, uh, speculation or hypothesis in terms of why that trend might exist or why that relationship might exist?
That's a good question. Um, I, I believe that there, so I'll, I'll say that I looked at postprandial and fasting GIP for their correlations with insulin resistance. And postprandial GIP was not associated with insulin resistance, but fasting GIP was. And we don't know very much about GIP in the fasting state, to be honest. So what I think is, based on what GIP, fasting GIP was also associated with, it was other fasting markers of metabolic health, such as RQ, fasting RQ, and HOMA-IR, which is fasting insulin resistance. So this may be painting a picture that GIP could be, it could at least, at least be associated with things related to your fasting metabolic state. And so I think that there just needs to be more research about what GIP can or can't do in different tissues. So that's an issue with the incretins is that sometimes their action is dependent on your glucose state, for example. And so that's something that I think it may be something for preclinical research to tackle, or it could be done clinically, I think too, to like see if it's really possible for GIP to influence your adipose tissue at fasting glucose concentrations, not just at your postprandial ones.
Right. Yeah, no, you mentioned the causality aspect of it. It's, it's hard to establish causality, right? Especially if you don't know all of the specific, uh, mechanisms or all the specific functions of a particular molecule or hormone or something like that. Uh, I've, I've got involved with a group from Iran, actually, and they've, you know, with them worked on some papers that have looked at interval training and things like, uh, what's it called, Aisan thing, like some antioxidant sort of neutral, plant-based antioxidant supplements and adipokines. And in some of the data, you know, say in the case of obesity, an adiponectin, you know, that's a molecule that is secreted from the adipocytes, the fat cells, right? An anti-inflammatory adipokine, like is good, right? It is anti-inflammatory, has good effects, good, um, function, right, on overall health and and whatnot. But you might look at some literature and, you know, getting into this area, I've looked at some literature that this anti-inflammatory adiponectin is elevated in obesity or in diabetes. And one might think, well, why is it upregulated if it's good? Why is it upregulated in this bad condition, this pathological condition? And, you know, it might just be a compensatory mechanism, right? To deal with that pathological condition or the, the pro-inflammatory or the oxidative stress that is present in certain conditions. This good adiponectin might be elevated to help deal with that. So even though it's correlated with a bad thing, it could still be a good thing in terms of, you know, it's trying to offset some of those negative, uh, consequences.
Yeah, that's a really good point. And I remember, uh, I don't remember what paper it was, but recently in journal club, there was something similar where this unhealthy group, they, they had some like anti-inflammatory cytokine that I don't remember the name of. It was an interleukin, and it was elevated in this group that was supposed to be at risk. And we were discussing in journal club why. And it's like, well, it's probably high because their inflammation is high. And so they have high levels of anti-inflammatory, um, you know, molecules, but it doesn't necessarily mean that it's an, like that they're, that it's the same context as in people that are lean and exercised for example, that might have it too.
Yeah, yeah. It, the functions and mechanisms of certain molecules or things are interesting and have to be considered within like the physiological context that they exist in, right? And I think, you know, you probably see this and come across this, you know, on YouTube or social media or what not. But, you know, there's often times a lot of confusion in terms of looking at say, more mechanistic data, cell culture data, and seeing, you know, something happen in a Petri dish and then extrapolate that into the human context. Which, you know, in a Petri dish, there aren't hormones, right? There's not vascularization, there's not blood flow, there's not catecholamines, right? The human body has a billion things going on within it. And so extracting causality, right, and and the actual function in in real life is much more difficult than than looking at it in a Petri dish or some other model that you can have very, very tight, uh, controls.
And I actually want to bring up a paper that made some waves, I think it was in 2023 or 2022. And it was about erythritol and cardiovascular disease risk, or major adverse cardiac events. Do you remember anything about that?
No.
Okay, 'cause it was a big deal in my field. And I presented on it twice because I was so, like, it was exactly what you were saying. Erythritol is basically like a sweetener. It's not even an artificial sweetener. First of all, and I think the title said artificial sweetener, erythritol. It was published in Nature or something. So first of all, like, it's being conflated with an artificial sweetener, but it's not. It's technically like naturally produced. Whatever they saw in a Petri dish that it was really bad for, you know, cardiovascular events, like blood clots. And the paper was not a bad one, it just the takeaway was like, oh my God, anything with erythritol is going to give you a heart attack. And we had so much fun in our, you know, academic circles discussing the limitations and all this. But I think to most people, they're not going to know, like, oh, this is a preclinical model, here's the limitations, or this was a cross-sectional epidemiological study, study, they didn't control for this factor, that factor. So people could like, years later, be affected by a headline that CNN or ABC or whoever ran related to our stuff. And it's just like, how do you combat that when people also online are making misinformation? It's not just like me, like, you know, traditional media, it's regular influencers that profit from this too. So like, like I'm like, I can't get upset all the time, but sometimes it is upsetting.
You, you got to pick and choose what, what to get bothered by 'cause there is no, there is no end to it. Um, yeah. And then one thing that, you know, I think gets overlooked a lot of times, and especially with maybe social media, podcast, influencer type people that either, uh, are doing it intentionally or unintentionally, they just don't know, or they're doing it intentionally and they do know and they're just trying to push and sell some [ __ ] is, you know, you also have to like balance outcomes or balance effects, right? So is this, uh, erythritol, that's, yeah, erythritol. Is it, is it, is it non-caloric? I think it is. And it is in, it can be a sweetener in like energy drinks. So Monster energy drinks, when I, when I was reading this paper, I looked through my pantry. I saw at the time, Monster energy drinks, don't sue me, but like, they had that, um, so it's, it's in some foods as a sweetener.
Yeah, yeah. So, you know, with, with this, or even other non, uh, caloric sweeteners, artificial sweeteners, non-caloric sweeteners, right? If there are some data showing, let's just say that there is human data that you can tie to some potential negative outcomes, right? Just not saying that this is the case. But even if that were the case, right, you would still have to consider the actual practical implications of it. Because if people are swapping out full-sugared sodas, right, and high-sugared drinks, or consuming things that have a lot of sugar in it, and therefore a lot of calories in it, and that is contributing to obesity, which we're going to talk about, and it's more complex, and, you know, even probably myself, give, give, uh, consideration to. But if it's contributing to obesity, and if people make a swap of artificial sweeteners, and guess what they lose? You know, a significant percentage or significant amount of adipose tissue. Well, that on the whole is positive. And that likely has a much greater impact on their metabolic health, their cardiovascular health, their overall age-related health, than whatever some fraction or small influence of some artificial sweetener that might have some data showing, oh, maybe it has some harmful effects, but it could be minuscule, often times, compared to what the actual practical outcome is of, you know, say, for example, again, artificial sweetener.
Yeah, it's the difference between statistical significance and the effect size. And so, you know, sometimes something can be significant, and that's great for us in academics because then we'll get published. But then, but then it's like, okay, so then when somebody asks you a question like, so, so how much weight is the difference between this diet or this diet or whatever it is? And you're like, two pounds. You're like, uh, two pounds? Yeah, but it's special because of p-values. So yeah, there's a, yeah, exactly. There's a difference between statistically significant differences versus meaningful practical clinical physiological, uh, differences. Definitely.
And then also, you know, again, take into consideration how those things play out in the real world, you know? Yeah. And that, that, that those are things that, you know, obviously can't get captured in a study or a single study, you know? Yeah.
Okay, okay. That was a, that was a nice little, uh, tangent and aside. Um, so what are you, what are you looking at next in terms of, uh, GIP?
So I don't plan to look at GIP next. However, I do plan on trying to look at obesity and when people may be metabolically healthy and have obesity. And what are kind of some of the factors that are associated with metabolic health, whether you have the high BMI or not. And so that was one of the topics that I wanted to do a little deep dive with today. Um, and it helped me also do some literature search while I prepare my research questions from my mentor in a meeting coming up. And, and, you know, so two birds with one stone. Um, so you've, I think, talked about like energy balance and obesity and those sorts of topics before, right?
Mhm. Yeah.
So part of my training is nutrition. My degree is in nutrition, but I feel like I have more expertise in obesity because that's what my, like, predoctoral training grant is in, is in obesity. And I've done classes in obesity, um, physiology, and things like that. That, so obesity is defined by the BMI scale, and that factors in your height and your weight. And that's good at the population level, but on an individual level. And I remember learning about this in undergrad too, at the individual level, it doesn't really give the full picture of your metabolic health. So in Kinesiology, it's pretty common people work out, people have higher muscle mass, probably in that major than all the other majors. And so it's an easy example there, like, hey, the bodybuilder with the high BMI has a lot of muscle, and so they don't necessarily have the metabolic issues we associate with obesity. But on the other hand, there are also going to be people in the population that do have a high waist circumference, but they still are not going to have the metabolic issues related to obesity. And this is kind of a newer is thing in the field that's getting more and more traction and and kind of trying to understand metabolic health for people with obesity. Like, is it something? Is it a real phenotype? First of all, how do we try to understand this? What are some policy implications? These are all sort of the questions that I've been reading about in the literature.
Okay, so let's, let's, let's get right into it. Yeah, I, I have mentioned, um, you know, some of these things, you know, on this YouTube channel, and then, you know, I don't know if, um, I had mentioned this when you had me, you know, back a couple years ago, but I have added a section in terms of looking at the, the differences in, um, say, health risk or difference in metabolic function or dysfunction in, in obesity. And, and there are differences, right? Like, like you're going to allude to. Um, so that is definitely an interesting area and and topic 'cause, you know, you can just think anecdotally or in real life, you know, someone might be higher on the BMI and, you know, it might be relevant for them 'cause it might be excess adipose tissue, excess fat mass, but, you know, their blood panel looks fine, right? Or their insulin sensitivity looks fine, and their, their levels of, you know, uh, inflammation, uh, are fine, blood pressure, right? And, like, you're going to discuss, it is pretty heterogeneous, right, in terms of the, the metabolic, um, phenotype that obesity might, might present. So why don't you, you know, start getting into that in terms of talking about this phenotype, whether it is a phenotype or not, of, uh, metabolically healthy obese?
Yeah, so the way that metabolically healthy obesity is described is when somebody has a BMI greater than or equal to 30, but they don't have the metabolic disturbances or metabolic issues that would be associated with obesity. And then the research starts to do all sorts of different things, and it's not unified at all, which is one of the main issues with this field right now. So how do we classify metabolically healthy obesity versus metabolically unhealthy obesity? They're in agreement, okay, we got the BMI, we got that definition for who's obese, who's not. But then we go into metabolic health. How do you try to capture that? One way they do it is with the metabolic syndrome criteria. So this means that they're going to consider factors such as blood pressure, the HDL cholesterol, triglycerides, fasting glucose to try to see if somebody has a high number of these characteristics. So if they have high blood pressure and they have high triglycerides, they might be scored as having worse metabolic health. But some papers, they do it where it's like a continuous variable. So maybe somebody has four out of four, four out of five of these traits. Other studies will make it dichotomous. So it's like, people that have two or less are healthy, people that have, or if they have less than two, they're healthy, more than two, they're unhealthy. Um, so there's differences in how they do those classifications, but it tends to revolve around.
I'm sorry, just to just to add to that point, the paper that you sent me, the Peterson paper, mhm, uh, mentioned that, right? And so they give an example, example of someone could be considered metabolically healthy and they have type two diabetes.
Yes, yes. So, yeah, that's precisely the point. So sometimes in a study, they're going to have these, they're going to have a score based on many different traits, which are different. They're the reason that someone could have like high cholesterol versus high fasting glucose are fundamentally different, and they would be managed differently, but get put into one category, whether that's healthy or unhealthy. So that is a big problem currently. Another thing is some studies will look at HOMA-IR. So they will be using an index of your fasting insulin and fasting glucose to categorize you as metabolically healthy or unhealthy. They won't bother with the blood pressure and the other like lipids. Then the most strict definition for metabolically healthy obesity, and this is what I'm going to use to describe metabolically healthy obesity in America from an NHANES study, which I'm like, wow, they have that, that makes my job so easy. I'm so glad that they have published this. But the stricter definition is no metabolic abnormalities. And this is those same traits: the blood pressure, cholesterol, and fasting blood glucose. So they're like, they got to have zero. They can have obesity, but they got to have zero to be considered metabolically healthy obesity. And so I will just describe what the NHANES study found regarding metabolically healthy obesity in America. So this is data where they're comparing from 1999, they're going from 1999 all the way to 2018. And they gather data from the whole country, so it's representative of the United States population. And they're tracking things like obesity, they're getting some, uh, biomarkers like fasting lipids and fasting glucose, and then they're getting some socioeconomic factors and things like your education, your employment, and things like that. And what they found was that in 2018, about 40%, there was 40% prevalence of obesity. And of that percent, so of the people that have obesity, about 15% were considered to have the metabolically healthy phenotype. And that leaves 85% to have the metabolically unhealthy phenotype. So just from that, it's good to know it's not the majority, it's not even half of the people that have obesity defined by BMI. So it's not half that have the healthy phenotype, it is still the minority. But that's not nothing, you know, that's not like less than 1% or something. So there's, this is still relevant to consider in the obesity field. And then when looking at things that were associated with metabolically healthy obesity, that tended to be, um, you had, how to phrase this, younger people tended to be more likely to have that phenotype, um, people with higher income and higher education tended to have metabolically healthy obesity. Um, and I think for racial and ethnic disparities, um, non-Hispanic white people were more likely to have the healthy phenotype. And so they really just commented on that, there's going to be things in the environment and maybe some individual level factors that contribute to somebody having the healthier phenotype for obesity. Which that in itself, just to make a little side point, right? We talked about, uh, causality, correlation, and causality, you know, the whole correlation does not equal causality. That's a perfect example, right? It's not, when you can't look at that data and say like, oh, if I don't want to be metabolically unhealthy, I need to go make more money, right? Making more money is not going to cure that, right?
Just to clarify here, well, money in and of itself does not directly physiologically, biologically, mechanistically cure or prevent disease. Money, having more of it, and financial status does allow for access to greater health resources, greater health access, greater healthcare that do lead to greater, better, improved health outcomes. So not to undermine the significance of money and financial status on health outcomes. Or, you know, being white.
I have to reverse my age. Yeah. Yes, yes. Exactly.
All right, sorry, continue.
Yeah. And one more thing from that study that I found very interesting was they were looking at the metabolic traits that contribute to like the definitions for metabolically healthy obesity, so like your blood pressure and your fasting glucose and stuff like that. And they were seeing how those changed over time from 1999 to 2018. So what they found was that among people with obesity, regardless of whether they're categorized as metabolically healthy or not, overall, and I'm going to remember, overall, the traits related to poor cholesterol decreased. So people started to do better about their cholesterol management. However, blood pressure did not change. So the prevalence of high blood pressure among people with obesity remained pretty constant. And then blood glucose control, that worsened. And so that kind of gives you an idea about like, across time, what was changing within this population. And it can give us an idea, like they comment, maybe people are getting better management through pharmaceuticals for their cholesterol, but something's going on with the blood glucose, and we got to try to tackle that still. So I thought that that was a really cool type of finding. I didn't expect when I just opened up the paper to get that insight.
All of that is is super interesting and I think not a lot of people appreciate that, right, right. And then, you know, that can have practical implications, um, you know, rather than just looking at a, a BMI chart that someone might be on the higher end, they're going to get treated, you know, just as, as someone who, uh, has worse metabolic, uh, dysfunction, even though they might be metabolically, uh, fine, right? And there's also the issue of ignoring people that have lower BMIs but are still not metabolically well. And I think one of, one of the papers you sent about this had that in the discussion about the risk for cardiovascular disease or for diabetes increases regardless of your BMI. It's going to increase the more metabolic problems you have. And like, if you don't do physical activity, that's not really really good either. So it's, it's a disservice to people on the whole BMI spectrum if they're just treated for the BMI and they're not being considered for like fasting glucose or their cholesterol, right?
And is there any data showing, um, you know, what, what maybe the impact or influence physical activity has on that phenotype? Like, is regular exercise, regular physical activity a causal factor of that phenotype?
I saw in one of the review papers that they did not really have too much evidence on it. And while they can kind of believe like, yeah, exercise is good, you know, like, yeah, it's probably good if you have obesity to exercise. But I don't think like in NHANES and in these, uh, epidemiological cohorts, they don't really collect too much on the physical activity, with the exception of the one you sent. And it's self-reported. But that's okay. I mean, you know, they got, they kind of got to do that for for that level of, of a study. Um, but I do want to just briefly touch on the paper that you brought, that you sent. And it showed the risk of having metabolically healthy obesity versus other types. So is metabolically healthy obesity benign? And some of the studies that I went over are showing that it's not benign. But there's kind of like a tier list. So I don't know if you've seen like those tier lists or it's like S tier and A tier and all that.
I've seen them, but I'm 37 years old. I have no idea what the letters mean.
Yeah, okay. I, I was literally making a tier list, but then I was like, no, I should stop. Okay, the tier list is just simple. It's like A, B, C, D, like the top is the best. So yeah.
Why is S at the top though? I don't know what S stands for, honestly.
I don't know. I'm sorry. I'm Gen Z, but I stay off TikTok. Like, so yeah, like I'm Gen Z, but I'm doing a PhD, so I'm kind of, I'm kind of different. But yeah, yeah. Like, like I am, I am giving a lot of grace to obesity and to the nuances and like, not everybody with obesity is going to be unhealthy. However, I will, I will admit, the S tier, the highest tier, as far as like, you know, preventing your risk for different cardio-metabolic disease, is going to be metabolically healthy normal weight. Like, yeah, yeah, yeah. You got me. But as we go down the list, then it gets more tricky because it's like, if you have metabolically healthy obesity versus metabolically unhealthy underweight, like, it's like sometimes it seems that metabolically healthy obesity wins. But it's very complex. It depends a lot on the specific comorbidity. As one of the studies that we read showed it, it's like, I don't even remember these comorbidities to be honest, like peripheral vascular disease versus cardiac something, because I don't study those things. But it's like, one outcome could be that having obesity is protective, but another one, it's not good to have obesity. So I'll say like, yes, the best one, according, you know, on a population level, is the normal weight without metabolic issues. But then it gets to be more like individual level and what does the metabolically healthy obesity look like? Because is it the zero comorbidity, the zero issues one? Or is it the, they have two, but they got classified as healthy? So that's where it gets very nuanced and it's hard to make generalizations about what's the best phenotype to be.
Yeah, yeah. And I think, you know, from a, from a real-life practical practitioner, uh, standpoint, you know, those things are, are good, good to.
Know, right? But then even applying those things in into practice. So, like, you know, I don't know if you remember, but I've have done personal training for a very long time, um, and still do a little bit of it now. Um, but if you have someone who, you know, say has a couple of cardiometabolic, um, conditions, you know, high blood pressure, insulin resistance, it might be type two diabetic, or, you know, dyslipidemia, uh, whatever, whatever the case is, you know, and obesity.
From a practical standpoint, if they're training, if they're exercising, and they're not losing weight, that's still not a bad thing, right? You're still going to have improvements in those outcomes, in those health outcomes, which overall is going to be, you know, lower your risk of many, many chronic, well, more chronic disease and and premature death, right? So even though someone might not be losing weight, they still definitely could be improving their health. Now, ideally, you know, in most cases, you know, you want to see both because again, generally speaking, as ad, as obesity goes down, you know, better health outcomes. But even despite that, you know, you, you want to encourage people to not be discouraged if they're exercising to try to be healthy, but they're not seeing movement on the scale. Like that, you're, you're, you're not wasting your time. You're definitely getting some, some big-time health life benefits.
Yeah, and I think that that's really great to have that practical, real-world experience working with people too, 'cause then it gives you those insights of like, how, how would you try to encourage somebody if you're trying to focus on health but not necessarily weight? Because in a lot of people's minds, like, they've grown up being told, you know, they got to be smaller to be healthy, or they always got to lose weight. So what is kind of the way that you try to communicate that it, it may not all be focused on weight all the time? Sometimes there's other benefits for the exercise.
Yeah, uh, I would, just to be honest with you, one thing that is really useful and goes a long way with most people, and it's not even really say physiological or clinical, but it's just like, hey, don't you feel better, right? You can do more, you can get up easier, you can do things without getting fatigued, you can, uh, you know, get up and down, you're not out of breath, you can move, right? Even some things as simple as that from a practical, like, perspective in communicating, working with the individual. You're not even measuring, okay, what's your blood glucose, right? What's your blood pressure? But even just that, there is like a very obvious and impactful indicator that some positive effect has gone on, right?
Now, you know, if, if you do have access to some of those measures and you have been working with someone long enough to see changes, uh, occur over time, right? Then, yeah, you want to sort of ask and like, okay, you know, show me your, your, your markers, right? Show me your, your blood, like, show me your, your glucose, right? And, you know, generally speaking, if they've been consistent and they've been, you know, um, you know, been doing it long enough to see change, like you should, you should see some changes. And and highlighting those things, you know, and, yeah, kind of disentangling the, the connection, the colloquial connection between health and weight. Even though we're not saying it doesn't exist, right? But those two things can be independent of each other. And just showing, see, look, your glucose went down. Or another one is, you know, you, you have halved your blood pressure medication, right? You're not taking as much insulin, or your, your insulin dosage is down, or whatever medication you might be taking, you're not taking as much, your dosage is down. And those sorts of things are, are really important to, uh, to highlight to again, not, you know, try not to let people get discouraged and not let them think that all their work in time is, is all for naught. And highlighting not just the implications of the, the effects of, of those things now, but like over five years, 10 years, 20 years, or whatever the case may be. Those have big-time implications.
Yeah, that's, that's a really good point that I think in science we forget just some of the basic, I don't know, basic, but some of the motivators of like, oh, are you having fun? Are, do you feel good? Like, do you feel confident? And I, I know that there's research in those areas where they would like intellectualize like each, you know, what is fun in an academic context or self-confidence. But yeah, I think when you're talking with normal people, when I'm talking with normal people, I try to just always remember to be like, normal as well and just connect on like, a more human level. And, you know, not be like thinking about their fasting insulin or whatever else I spend all my days reading. So, yeah, that's good.
Yeah, no, it, it's, it's really, uh, interesting and, uh, useful. I think especially like, we just got done with the holidays, right? So like, you know, you probably went back back home, I went back home around, you know, friends and family and whatnot. And, you know, they might know that you're in nutrition and in health or whatever. And, you know, people ask you questions. It's like, and the level of question is just so different than what we might be used to in in the lab or the classroom or in Academia, right? And it's just important to, to, to have that, I think, juxtaposition. Because ultimately, what are we studying these things for, right? Is to help people get healthier, help people and improve, you know, their metabolic health or whatever, whatever the case is, get fitter, get stronger, right? Reach their, their fitness goals. And, you know, we might have a huge intellectual, in-depth, mechanistic discussion, but it's like the type of information, like that's good to know, right? But the type of information that you're communicating, you know, with a, with a non-scientist, physiologist, nutritionist person is just like, is very, very different. So be able to communicate those things is, is super important.
Yeah, I mean, I, I found sometimes, and it might be because of social media, where people will ask me questions that are very, like, I'm like, you watch a TikTok and now you're asking me about like, glycemic load. Like, so they'll be like, oh, you study nutrition, so, so I got this question from someone. They're like, so does the order of eating this matter? Or does, um, if you freeze rice, then does it reduce your? And they're using academic words, but I know that they're not in this field. And then what I do to them is I'm just like, it doesn't matter, bro. And like, I just don't take the bait. Like, I'm like, I know the answer. Like, I'm like, well, yeah, like your insulin response is going to be impacted by this, but I don't get into that. Like, I'm like, you're not a professor, ask me questions at my defense. So I just go like, like, dude, like, why are you worrying about that, right? And so I don't know, I just like to troll them 'cause I'm like, I have this knowledge, but when people are asking it in a certain way, I'm just like, dude, just like, touch grass, man. Like, it's not, it's not a big deal, like, if you froze rice before you ate it or not. So even though yes, I read those papers, I'm not going to tell them, well, yeah, here's the, here's the breakdown academically, you know?
Yeah, yeah. The, the level of impact in real life can get blown out of proportion and really distorted, you know, when it hits people's ears on their, their algorithm or, or whatever. Yeah, yeah. You got to, you mean, there's a lot of stuff with exercise, but I think nutrition's even worse. Beans are [ __ ] coffee is borrowing tomorrow's happiness today. Coffee is [ __ ] not or broccoli. I've never eat this garbage. That's total [ __ ]. I ate a green banana. Oats are a grain. Grains are seeds. Seeds are highly defended. They are full of plant-defense chemicals. This is complete [ __ ]. People often ask me if I use deodorant in these pits. Absolutely not. I use nothing. 'Cause everybody eats, so everybody thinks about their food in a certain way. And I think there's times when people will ask me 'cause they just want me to affirm their beliefs. They'll be asking me about nutrition and they're like, oh, you studying nutrition and carbs. I don't tell them I study like carbs and insulin 'cause then, oh God. So they'll just be like, so it's bad to eat carbs, right? And I'm like, no. And then they're just like, oh, well. And then they start treating me like I'm just wrong. And I'm like, right, but if I had said what they agreed with already, they would have been like, yes, queen, like you're an expert. But if I disagree with them, they're like, oh, never mind, we don't care about you anymore. So that's why I try to just keep it to like, the big picture of, you know, don't worry about it, is my answer most of the time.
Yeah, and there's, there's a lot of that. And especially, you know, I, I try not to get, uh, exposed to it too much because it's, it's irritating. But, you know, as a, as a, a male, uh, my algorithm will send me certain things. And there's, there's, um, like the whole biohack manosphere adjacent type stuff, you know? It just, it just gets so people get hooked on stuff for emotional reasons. And almost it's like, you know, I, I, I know what the truth is. We're, we're the right ones, right? We're going to do this really obscure, minimally impactful, minimally scientifically efficacious practice. And like, this is, this is the thing because so and so said it, right? And there might be some data to it, but again, the, the, the efficacy or the efficaciousness or the effect size, right? The actual impact that this one thing might have is going to be so minuscule compared to just the basics that are not sexy, right? Right. Eat a balanc, eat a balanced, uh, diet. Eat some fruits and vegetables. Right. Touch grass. But, you know, getting hooked on some of these super esoteric, uh, biohacky type type things is, is, I think, more psychological than than health, than health. But, you know, no, I totally agree. And I, this is, this is not really a hot take, but it's kind of like the whole omics and personalized and precision, like medicine and stuff. Um, it has been something where I'm just like, I, like, like, and I'm not trying to be like, we just need to focus everything on public health and, and, you know, like social determinants of health are everything. But I worry that we will try to like think like every single one of us requires a unique solution. And it's true that while we're not one size fits all, and in obesity, they'll say it's not one diet fits all, but as my mentor, Dr. Gower, says, you're not going to get your personalized nutrition readout that says you get to eat Froot Loops and Twinkies and that's going to solve your problems. Like, no, it's probably going to be, eat fiber. And whatever, there may be some things where some people could tolerate a higher carb, you know, more refined diet and they're not going to experience, um, I don't know, effects that cause them to overeat. So some of that research is being done, like who responds to ultra-processed diets with like, you know, overeating, who's not going to be affected by our current food environment today. But as a whole, like, some of these messages that are one size fits all would be good if people were able to follow them. And so it's not about like, like, I'm, I'm here, like, I don't know if there are significant gaps in knowledge. This is, I don't know, I think this is just my belief. I don't know if it's a fact, but I'm like, are there really big gaps in knowledge to be filled that would change people's lives in health? Or is it the implementation and the resources and the politics that, you know, we, we can't solve through scientific questions? And that's hard to cope with as scientists. So we just come up with new, new ideas and methods.
Yeah, and I think some of them can be legitimate and, uh, driven by by literature and, and, and research. But then a lot of it can just be, there's a market. Mhm. There's a market. I'm going to sell a product. A lot of this stuff is not regulated, right? And I'm just going to, I'm just going to cash in, um, on that, you know, on that confusion, on that gap, on that, um, I don't know what the word is, right? Desperation at some point, at sometimes, right? And then, you know, you mentioned like the omics type stuff. I'm not, uh, super familiar with all of that, but I know like the, the general, um, idea of it. But it reminded me of, you know, again, kind of going back to like the biohack manosphere adjacent type stuff, where it's like all of these strategies, protocols, therapies, you know, sauna, infrared red light, cold plunge, um, you know, I don't know, blue light blocking, um, all of these compression, you know, all, all of these things. Yeah, the supplements, right? The supplements. And, you know, to me, and, you know, I probably to you as well, like that's for people that got money like that. And so when I, you know, and that, that made me think of the omics type stuff because that stuff costs money. If you're going to go get some sort of like blood test printout, genetic type thing. Like all of these things, even if they are efficacious, a lot of them are are overblown. But to me, like it just rubs me the wrong way because it's just like, that's not, that's not going to help the type of people that, one, I'm from, and the type of people that need the most help, right? Mhm.
Yeah, and one of the issues is also when we consider health disparities, that could be racial or ethnic. It can also be by income. But if we have these treatments, and that includes obesity medications like the GLP-1 receptor agonists, when they're not available to the poor people, if I'll just use a non-academic word there, um, then the health disparity is going to worsen. And it's just like, do we even care? I know we care, but it's just like, do the people that generate these solutions care? And it's like, maybe not, right? So, yeah, they're, they're only going to care if for the people that can pay it, you know what I mean? Yeah, yeah. Um, that's, it's what it is. One thing that was interesting from the paper that I sent, the Peterson et al. 2024, that was a study from Samuel Klein's group. And I had the, uh, honor of meeting him at Obesity Week this past year, and he gave a presentation about this paper. And that was one of the things that really inspired me to think more about metabolically healthy obesity. So that lab does a really, really in-depth work in like metabolism. Until they'll do tracers and biopsies and probably what would be considered omics. But what he found really was characterizing like different organ systems and comparing the metabolically and healthy obese group, the metabolically healthy group, and then like lean people. Um, I think lean was normal BMI, but that might not be true. But they, they were just the, you know, they didn't have obesity. And what they got more information about was the adipose tissue and the skeletal muscle kind of like variables, hormones, um, you know, secretome. Well, I don't know if secretome is the right word, but you know, secretions that can be associated with the health or the lack of health. And one thing that is very interesting is like adipose tissue is a very dynamic organ. And so some of the things that could differentiate someone's metabolic health could stem from what the adipose tissue is secreting that could be inflammatory factors. And it could be hormones as well. So getting back to like our conversation about, you know, getting really super into the weeds versus like the big picture. I think what's going to be interesting to see is if these little molecules that are able to differentiate someone's healthy adipose tissue and unhealthy adipose tissue, if we can find some things that correlate with those that could be assessed on a population or like in a medical setting, for example. So do they associate with HOMA-IR? Then we just look at HOMA-IR. We don't have to spend a bunch of time collecting adipose tissue. But if these are super unique and we can't actually assess them any other way, then trying to figure out like, what are ways of trying to feasibly screen for these adipose or muscle factors, right?
Yeah, yeah, definitely. And I, and I don't want to be characterized as, uh, not supporting the omics research. Like the, the research and the, the scientific stuff is, is one thing. And then the predatory, at times, we'll say suspect, um, sort of practices of, of for-profit entities or individuals is, is, is something different.
Yeah, no, I think that's a, a, a very good point to make of, you know, adipose tissue, like skeletal muscle is a functions as like an endocrine organ, right? Releasing hormones, releasing chemical messengers to other systems, to other tissues. Um, and that can be modulated by things like obesity, right? Or exercise. Um, and so finding the, you know, having those right inputs into those tissues to release positive biochemical signals, um, you know, goes into, goes into all that. I do want to ask you one, I do want to ask you one last thing because you do study nutrition and you do seem to be somewhat aware of some the stuff that is out there on the social media YouTube, uh, circuit. Were you mentioning, uh, were you referencing Glucose Goddess? No, I, okay. No, no. I know of that account because of a different account I follow that critiques them. But I do not follow them. I don't, yeah, because she had come out talking about, and again, I, I came across her because I follow someone that critiqued critiqued her as well because she had come out with something with, uh, meal order of eating a meal, things like that. Here's what we see. We see that if we eat the consistance of a meal in a specific order, we can reduce the glucose spike of the meal by up to 75% without changing what we're eating. God, that's so, like, these numbers are really impressive. Yeah, but if we change the order, we reduce to spike so significantly, which means less inflammation, less aging, you know, better hormone balance. I mean, we just feel much better. So the correct order is, she makes some extreme claims about glucose. Every time you have a glucose spike, it's increasing your biological age and all this kind of nonsense. Blood glucose increases in response to a meal are completely normal. They are not unhealthy. If you gain too much body weight and you become insulin resistant where your blood glucose remains elevated, that is very unhealthy. But let's stop demonizing short-term changes in blood glucose because they do not reflect long-term changes in blood glucose regulation and insulin sensitivity, especially not based on the data we have now. And I mean, of course, as any marketing genius will tell you, the best way to sell something is to create the problem, make people afraid, and then sell the solution, which of course, she sells a supplement that is supposed to blunt postprandial blood glucose excursions.
Yeah, it, I think it's not just that person, but I do, I do think there's that, there's like the meal timing misinformation. There's the glucose, like wearing a continuous glucose monitor, um, yeah, misinformation. There's like, this is just my knowledge, this is not academic, like this is just from like social media exposure, um, seed oil misinformation. What is the, uh, not keto, uh, meat only diet, carnivore? I could not remember the word. Carnivore. I was like, meat something with meat. Yeah, carnivore misinformation. Yeah. We, we'll end on this. What, what are your thoughts on carnivore as a nutrition PhD student? Do you think your ancestors got excited about eating pond scum, the newest superfood? Seashells? You think your ancestors got excited about garbage like this, like algae, pond scum, and seaweed? No way. Listen, I love my cholesterol. Celebrate your high LDL cholesterol. Which of these two diets is sexier? Sometimes people ask me if I take cheat days. I never take cheat days. I'm at this conference talking about the Maha movement and I brought raw milk. This is what's up. Brought a container of meat with me. I'm living it. You guys, this is legit. I'm not, I'm not [ __ ] around. Don't do it. Don't do it. Eat, eat some, eat some vegetables. Eat some fruits. Um, for most people, just, just eat, eat the balanced diet that the government prescribes. And like, that's probably okay. Yeah, for most people. Yeah, yeah. So, no, I'm anti. I'll go on the record. I'm anti carnivore. But I think you can still eat meat. You can eat meat. That's fine, right? Yeah, yeah. It's 'cause you're not Alpha. I'm not. I'm a beta. Yeah, I'm a woman, so I don't know if I can be Alpha. Yeah, yeah. Okay, well, hey, uh, Amanda, thank you for, thank you for your time. This was a interesting, uh, conversation. Nice to catch up with you and and hear about what you're doing and talking about some, some cool science and also some real-world, uh, impacts because ultimately that's where hopefully the, the research, uh, ends up being useful. And so I appreciate, appreciate it. And, uh, we should, we should do this again and talk about some, some other things. I think that would be, uh, I think that would be good.
Yeah, definitely. Thank you so much for having the conversation. But, you know, even if this wasn't for like a podcast, like it was still a good, a good use of time and, you know, developing ideas and my kind of science communication, um, and, you know, processing some of these things out loud is helpful for when I go back to the lab and have to talk about them again for your defense.
Yeah, yeah, yeah, yeah. If you can handle YouTube comments, you can handle your PhD committee. H. Yeah, I would rather handle my committee every day. Don't worry. We, I, this, this thing doesn't get comments. Oh, no. I wouldn't look. But yeah, no, this one's going to get comments. The algorithm, G, it's just going to be like, yeah, screw them. Yeah, we triggered. We triggered some, uh, internet circles. You called out Glucose Goddess. That wasn't me. Glucose Goddess, that was you. Yeah. So, hey, it's on sight. It's on sight. Yeah. Okay. All right, Amanda. Well, uh, thanks and we'll, uh, talk again soon. Okay. Thank you. Stay safe. [Music]