How Inflammation Changes Your Body with Philipp Scherer

James Hill:

Welcome to Weight Loss And, where we delve into the world of weight loss. I'm Jim Hill.

Holly Wyatt:

And I'm Holly Wyatt. We're both dedicated to helping you lose weight, keep it off, and live your best life while you're doing it.

James Hill:

Indeed, we now realize successful weight loss combines the science and art of medicine, knowing what to do and why you will do it.

Holly Wyatt:

Yes, the “And” allows us to talk about all the other stuff that makes your journey so much bigger, better, and exciting.

James Hill:

Ready for the “And” factor?

Holly Wyatt:

Let's dive in.

James Hill:

Here we go.

Holly Wyatt:

Today, we're going to talk about inflammation. And I know what people are thinking. Before you tune this out, you know, you think about inflammation like you have a sore throat, or your hands are swollen, or your knees are swollen. Just hang on. Inflammation is really much bigger or broader than that. For instance, if your weight isn't telling the full story of your health, if your labs are worse than expected and you're not sure why, or maybe you've hit a plateau that doesn't make sense, inflammation might be part of the picture.

James Hill:

It's not that inflammation stops weight loss, but it does change how your fat cells function and how your body responds to insulin and how your metabolism adapts. And that can influence your risk for diabetes, heart disease, and how your body responds to weight changes, whether you lose weight or not.

Holly Wyatt:

Here's the good part or the empowering part, Jim. Inflammation isn't just something that happens to you. There are real things you can do starting right now to reduce it. And doing so can shift your metabolic health, your energy, your future, no matter what the scale is saying.

James Hill:

Okay, Holly, you and I know a lot of things about weight loss, but there are areas where we're not an expertise in. And we've been able to bring some of the best scientists in the world to help us through these topics, and we have one of those today. Dr. Phil Scherer is our guest today. He's the professor of internal medicine, director of the Touchstone Diabetes Center at UT Southwestern Medical Center. He's also co-director of one of the 11 NORCs, the Nutrition Obesity Research Centers that we have here at UAB. Phil is one of the most respected scientists in the field of obesity, metabolism, and adipose tissue biology. He's helped redefine how we think about fat, not as just a passive storage place, but as a highly active organ that plays a central role in hormone signaling, information, and metabolic health. If you've heard of adiponectin, or the concept that fat tissue can promote or protect against inflammation, you've seen the impact of Phil's work. He's published hundreds of peer-reviewed papers and his research has shaped how we understand the biological differences between metabolically healthy and and unhealthy obesity. Phil, we're so glad to have you with us today.

Philipp Scherer:

Thanks for having me. Very much. Appreciate that.

Holly Wyatt:

So let's start at the beginning and kind of set the stage for our listeners. What exactly is inflammation and why should we care about it, especially in the context of obesity or metabolic health?

Philipp Scherer:

Well, that's a good question. So inflammation is something which is really integral to our health. Obviously, we get hurt, we get injured. There are many, many settings in which inflammation plays an absolutely essential role for wound healing, for any kind of acute response to injury, for instance. So that's a good thing. We want inflammation in that sense because it really helps us overcome all the negative aspects that are associated with environmental exposures or other internal injuries in organs. What we're really talking about today is similar factors, but it's kind of a different level of inflammation. We are not talking about the acute disasters that take place when you cut yourself out there. We're talking about a much more chronic, nagging inflammation that's at a very low level, but it never stops. It just keeps going always a little bit.

And many epidemiological studies have really linked that chronic, nagging, inflammatory response to all kinds of disease phenomena, particularly cardiovascular disease, has a very well-established component that inflammation is one of the underlying contributors to the negative feedback. So I think that's the setting that we're dealing with today.

So inflammation can be good or bad. There are some situations where it's really good to help acute injury, but the situation where you have this chronic low-level inflammation may not be so good for us.

It seems clear that this is not a good thing and we really have to get to the source of that chronic nagging inflammation that shouldn't really be there. And it's sort of a side effect of things going wrong at different levels in different types of tissues. And of course, you know, we like to think of our fat tissue as being one of the potential instigators of this low level of inflammation. That keeps sort of the flame, that low-level flame of inflammation going over decades almost.

Holly Wyatt:

Are you kind of saying this low level of inflammation, how is body fat playing a role in that?

Philipp Scherer:

It's clear that when we progress from lean to obese and we are coping with that excess weight in various ways that the fat tissue is one of the tissues that's initially affected and that continues to contribute to the systemic elevation of some of these pro-inflammatory factors. I guess most of us don't fully appreciate the complexity of our fat tissue. We think of it as flubber, you know, we carry too much around. There's basically fat cells, but no, there's actually so much more to it than fat cells, basically, because unlike almost any other tissue in our body, we have every conceivable immune cell that likes to use the fat tissue as a playground.

And as we gain weight and as our fat cells become less and less functional, the complement of immune cells that reside in adipose tissue changes for the worse. And again, that's a good question. How do we get that negative feedback started in the first place, but the role of fat tissue as a central player in systemic sort of immunity and inflammation is by now well-established, and we have to appreciate it that if we face what I guess we conventionally call angry, insulin-resistant, and quote-unquote inflamed fat, that this is the package that comes with weight gain with most of us.

James Hill:

So, is inflammation always associated with weight gain? And is it a feedback loop? Does the inflammation actually contribute to sustaining the obesity? Or do we know about that?

Philipp Scherer:

It does look like there's a feed-forward mechanism in place. Critical question is, how do we get that process started in the first place? And one of our favorite theories for which there's a fair amount of evidence is that if we compare an expanding fat path, perhaps in a first approximation to an expanding tumor lesion, to a cancer lesion, one of the most critical factors that a tumor needs to thrive is the appropriate vasculature. So the infrastructure to deliver the nutrients and the blood has to be an integral part of tissue expansion. Our fat tissue has the ability, is perhaps the only tissue that we have, with unlimited expansion potential without being cancerous. But the basic requisites for that expansion remains the same. So if we expand our fat tissue, we need the vasculature to keep up with it. And one of the things that happens when we gain weight in initial stages is that the vasculature just isn't keeping up. And that means that fat tissue in this context lacks the appropriate oxygenation and it becomes what we call hypoxic. And when it becomes hypoxic, there's a whole response that kicks in within the cells, particularly in the adipocyte. Because then they're prompted to make more of these fibrotic components in the extracellular matrix that makes your fat tissue increasingly stiff and inept at adapting. And that stresses the fat cells because now they're encaged in this in this extracellular matrix component. They're trying to push because they're being asked to expand and accommodate more lipids. And the combination of this hypoxia, the subsequent extracellular matrix formation, that leads to an increased rate of stress and perhaps even cell death and it's not a good kind of cell death then that means when you have cell death, inflammatory cells have to come in sort of the there's a lot of garbage to be taken care of and the main cells that are in the business of disposing of this garbage will be macrophages and these macrophages fall again in many different categories we have good macrophages and bad macrophages. And as we go along in our obesity path, they become increasingly of the worst kind that we call the M1-type macrophages. They are inflammatory macrophages that then contribute to that local microenvironment of inflammation.

James Hill:

Gotcha. How would someone know if they have low-grade inflammation?

Philipp Scherer:

There's a couple of clinical markers that can be almost part of your routine workup. They're not always there on the default panels, but things like high-sensitive C-reactive protein and CRP is a very unspecific marker, but it does give you a little bit of an idea what your level of basal inflammation is in the system. I think we're all working hard to find better markers for that that will be a little bit more specific, one which you cannot measure at this point clinically, but which bears a lot of promise is a fat. We call it a fibroinflammatory marker because it combines both inflammation and the fibrosis aspect. And that's a marker called endotrophin. And it turns out that is, at least in clinical studies, we'll have to see how that develops over the next couple of years. In clinical studies, it serves as an excellent marker for trouble of all kinds: cardiovascular disease, kidney disease, diabetes, obesity, it's all in there.

James Hill:

So right now, our listeners could talk to their doctor when they go in for the annual checkup and ask if they're measuring markers of inflammation. And if not, those could be added. The physician could request those.

Philipp Scherer:

Absolutely. Particularly if there is reason to believe that something is sort of sweltering in the background there that you have maybe, you know, borderline diabetes or you're inherently overweight, or there are some markers out there that would suggest that your cardiovascular profile may not be ideal, your lipid profile is not there, it might be worthwhile to actually look at more than two inflammatory markers.

Holly Wyatt:

So am I hearing this right? You could be overweight and not have this low-grade inflammation, or you may have it. Or does everybody who carries extra body weight have this low-grade inflammation?

Philipp Scherer:

I think that's a really important point because even though the maturity of people that will be overweight obese may be prone for an elevation in inflammation, not everybody is. And not everybody who's lean is necessarily completely free of inflammatory responses. So this has sort of created a very interesting concept that people really discuss at, you know, very heated and emotional level. They call them metabolically healthy obese individuals. So I think it is clear that there are people out there that might be overweight, that might be people with high degree of obesity, very high BMI, they don't have any signs of cardiovascular disease. They do not have diabetes. They haveby all accounts, they're perfectly fine. So these are the people that have found a way to expand their fat tissue mass in, I guess, for lack of a better term, in a healthy way without all the negative side effects. And that gives rise to this group of people that we refer as metabolically healthy obese. And we want to study those because we really want to find out what is the magic behind that expansion.

Philipp Scherer:

Importantly, the reason why people don't like necessarily to call it metabolically healthy obesity is because it almost sounds like an endorsement for obesity, which it isn't. It is simply the fact that not all of us are created equal, and some of us carry our weight a little better than others. And we want to know why that is. Again, much of what I said is seen in these patients. They have a better vascularization of their fat. They have a reduced level of this fibrosis in their fat. And indeed, they have a reduced level of inflammation locally produced in that setting. So it really checks all the boxes for a healthy fat tissue. In contrast, of course, if you have an inability to expand your fat mass, you're lean, but gee, you're a type 2 diabetic. How is that possible? Yeah, well, that just means you have some problems with respect to having your fat cells absorb the lipids. They might end up somewhere else. They might end up in the liver, and that's when you start to have that inflammatory response as well, despite the fact that you're not even overweight or obese.

So weight alone is not necessarily the deciding factor, even though for the vast majority of individuals, it is. But we all hear about the BMI not being perfect.

It remains a very easy parameter to measure, and it serves its purpose in many different settings. Even though it's not the right measurement for everybody, particularly if you have a high muscle mass, you may have a high BMI despite the fact that you're not obese. We have to take and interpret these values with caution, but for the most part, they still end up being very useful parameters to look at.

James Hill:

Phil, we know that people put on excess body fat in different places. Is there evidence that maybe excess visceral fat is more likely to lead to inflammation, or is it overall fat?

Philipp Scherer:

I think that's a very important point. We like to say if you're fat, it's like real estate, right? It's location, location. So there is no doubt epidemiologically, again, when you look at large populations, that for a given body mass index, if your fat distribution leans more towards the visceral fat, and of course, that's our more male pattern belly fat, right, that we carry around, that this has very significantly more negative consequences compared to the subcutaneous fat. And this is apparent in almost every population. When we focus, for instance, on the Southeast Asian population that has an inherently, I think, quote-unquote healthy BMI by all accounts compared to a Caucasian population, they suffer a much higher incidence rate of cardiovascular disease because their fat distribution is much more leaning towards that unfavorable visceral, particularly in males, Southeast Asian males, the visceral distribution. And because these visceral fat pads do drain directly into the liver, there is direct communication access of those inflammatory, markers that the fat tissue produces and affects the liver directly, leading to fatty liver disease and more.

Holly Wyatt:

I'm getting a little depressed here because it sounds like there's this inflammation and we don't even know how to measure it exactly for sure. And it's causing all kinds of trouble. Is there anything we can do about it? So are there any behaviors that maybe we think we have it, what do we do?

Philipp Scherer:

Well, that is the big question always. I mean, there are certainly ways by which you can fight against that low-level inflammation.

There are anti-inflammatory diets that people are told they can eat. I am not the biggest fan of selling them that way because when you look at the composition of an anti-inflammatory diet, it is really just common sense what everybody tells you to eat. You know, focus more on plant-based diets. Stay away from processed food, meat. You want to have healthy fats and not unhealthy fat. So stay away from the trans fats, the saturated fats. So all of these have been shown both in preclinical studies in cell culture. They cause inflammation. Yes, those are the contributing factors. But there's not necessarily that one unique magic anti-inflammatory diet that selectively targets inflammation. That's a secondary effect with every healthy diet. And if you follow the general nutritional guidelines, which we all try to do, but most of us are weak and we fail as we go along through the week and if you're stressed. But certainly the basic suggestions of eating a healthy diet is an integral part of that. There are interventions, pharmacological interventions that can target that to some extent.

Holly Wyatt:

Well, one thing on the diet, is it diet or is it weight loss that's associated? Can you change inflammation and not change your weight just by what you eat?

Philipp Scherer:

That is probably possible with a healthy diet. There's not an integral component to it that invokes weight loss as the necessary driver for the anti-inflammatory components. But, and that's a very important but, I do not want to de-emphasize the benefits of weight loss in this context. And particularly when it comes, for instance, to the new magic weight loss interventions on the incretin side, I mean, who isn't on Wegovy at this point? We learn a lot from these interventions. And one of the things that we learn from these interventions is that if you want all these benefits that these incretin drugs give you on the cardiovascular side, on the liver side, on the kidney side, on the diabetes side, that almost all of it depends to a large extent on weight loss. So, yes, you want to try to reduce your weight, even though just on the basis of reducing your inflammatory response through a nutritional intervention is beneficial unquestionably as well.

James Hill:

What about physical activity, Phil? I always bring that in as important along with diet. Do we know anything about physical activity and inflammation?

Philipp Scherer:

It's an interesting issue because we do appreciate that when you go on prolonged sort of endurance exercise that there is in fact a little bit of a pro-inflammatory sort of response built into that. However, the long-term benefit of exercise there's no question that that has to be an integral part and unfortunately, you know, I'm probably preaching to the converted, that's what you've been told all along. Eat less. Exercise more.

Philipp Scherer:

It doesn't work for most of us in terms of having a consistent long-term goal in mind. We have to bear in mind when it comes from anything, inflammation, diabetes, obesity, we got to remember that it took us, most of us, decades to get to the weight where we are right now. The idea to go on a crash diet by going on an anti-inflammatory diet, by stop eating, by losing the weight within weeks and months, that, in my opinion, is doomed for failure. Because A, you're not able to stick to it over the long term. And B, it's actually physiologically probably unhealthy to embark on such a rapid weight loss. It's got to be gradual. It's got to be over the years. And with that come the long-term benefits of really losing weight and everything that comes with it.

Holly Wyatt:

So the obvious question, I think, is what about taking an aspirin or ibuprofen? We have a lot of anti-inflammatory drugs. Why don't we just take one of those every single day? Would that solve the problem?

Philipp Scherer:

Not a really good point. And the fact is that the literature has shown now for many, many years that anti-inflammatories not only do not help you lose weight, but they also don't improve your insulin sensitivity.

Philipp Scherer:

So I sort of, even as a researcher, I go through these various stages where we were all excited about inflammation and then we get somewhat depressed because, yes, none of the anti-inflammatories that we are using really help. And the question then is, is inflammation the instigator of the whole problem or is it simply an integral part of the response to it? Now, more recently again, I would say the last one or two years, certainly on the research side, the idea of fighting inflammation has come up again through various new pathways. There is something called an inflammasome that can be targeted, the NLRP3 side of things. That's far from being implemented clinically, but they are very promising results, actually, with respect to targeting very specific components of the pro-inflammatory pathway in very specific places. But the generic anti-inflammatory approach through the conventional, you know, over-the-counter pills, no, it will not improve your insulin sensitivity, and it will not help you lose weight.

Holly Wyatt:

Yeah, so maybe those drugs are more working on some of the acute aspects. We use them when you have an acute illness. You have acute injury. We prescribe those and they work. But this low-level kind of foundational just always in the background sounds like it's a whole different pathway, maybe, a whole different animal.

Philipp Scherer:

Correct.

James Hill:

So, Phil, you're at the cutting edge here. Where is the science taking us over the next few years? What kinds of things can our listeners maybe anticipate in terms of learning more in a way that will help people better manage their health?

Philipp Scherer:

Well, I suspect that the next couple of years, they will not reveal any new dramatic insight in terms of the magic new diet that you should hop on. I think we've learned everything we need to learn. Fewer calories, better calories combined with exercise would be the way to go. Research, of course, right now is very much revolving around the pharmacological interventions.

James Hill:

Yes.

Philipp Scherer:

On the incretin side, the GLP-1 receptor agonist side, and it's quite remarkable. I think we've all just come back from the American Diabetes Association scientific meeting in Chicago. It's remarkable how much activity is really going on in that area. And given the very, very large number of people that are now embarking on these drugs with reasonable success across the board. And with relatively minimal side effects, I think we can look forward towards having better and more effective versions of combination therapies with these.

At the same time, I think this is not for everyone. It is clear that people differ in their response. Not everybody loses the weight. Not everybody copes with outside effects. And of course, the big deal on the gastrointestinal side, a lot of people have nausea, they might have diarrhea, constipation. I mean, that's the very basis on how these drugs kind of work.

And we have to continue to find better ways to basically combine maybe some of these drugs with additional interventions that will help us lower the doses to avoid some of these side effects. And that's certainly where research is heading right now, where we accept that these incretin drugs, these Ozempics, Wegovys, Mounjaros of the world, that they offer an excellent baseline to help people overcome some of the obstacles that are just inherent in lifestyle changes. We have a hard time sticking to these lifestyle changes, and the drugs help us stick to it a little better. We have to use them, I think, organically. We again race too much towards new versions of these drugs that promise even faster and even more effective weight loss. I think that's nonsense because that's not a race we want to embark in. We want to think long term. We want to think losing that weight over one two three years steady, slowly, not two pounds three pounds a week. No, do take your time. It's going to be easier to keep them off and it's going to keep your side effects at the much lower level as well. That's basically where the research arena is dealing with right now. Combination therapies add-ons to the incretins, I think that will be the name of the game. And hopefully, there will be more readily accessible in the future at a price that is economically responsible for a large number of people and for health insurance providers as well.

James Hill:

We've talked a lot on this podcast about the new medications, and we agree. These are wonderful new tools that are very, very welcome and are wonderful at producing weight loss. What we think is a real need is the long-term weight loss maintenance, where it's some combination of medications and lifestyle. And to me, that's going to be the major thing. We know now most people can get the weight off, but at least some of the data coming out is that people aren't staying on them that long. And I think we really need to have better strategies for weight loss maintenance, might include drugs, might include lower dose, might include intermittent use, might include lifestyle. To me, this is the exciting part. We now can help many, many people reach their goal weight. We have to figure out how we keep them there and keep them in maximum health.

Philipp Scherer:

Jim, yeah, I think I couldn't agree more. Absolutely. You summed it up very well. And yes, you're on the drug for a year, for two years. You are and have achieved your goal, your weight goal, basically. What now? I mean, do you keep going? Do you decide to lower your dose to a maintenance dose? There's no question that hopefully over that two-year period that you embarked on that weight loss regimen, that you have acquired certain habits in terms of lifestyle changes. Nutritional changes, maybe you've stayed away a little bit from these nasty fats and were opting to sort of change it. But because you've taken these steps very slowly, I think it might hopefully be easier to maintain them. To completely get off the drug is probably a bit of an illusion because we've seen now in many instances that while the weight regain is not instantaneously kicking in, many people kind of drift back up despite all the efforts and the goodwill and sticking to it.

One of the interesting aspects about weight loss, which goes maybe a little bit too much in detail, but we all appreciate that if you go on a diet, you lose the weight. But even though you stay on the same number of calories, all of a sudden, the weight kind of creeps back up again. And that's because our energy expenditure, the amount of calories that we kind of use goes down somewhere inside of our network that says, okay, food is scarce. I'm going to use the calories that I eat much more effectively. And really, that is the crux of weight loss is. We do not really fully understand how to avoid that. There is a new flavor.

You know, we started out with a single incretin, then we added a second to it. There was a GLP-1, GRP, and the most recent one that will be, my suspicion is, maybe available in the clinic as of next year, has a third component to it, glucagon. And what people talk about with the glucagon component is that it helps you avoid that drop in energy expenditures. So you lose the weight, but you prevent your system from adapting to the weight loss and still use the same number of calories that you were using initially. And that is something to look forward to, see how that happens. That might be one way of keeping the weight off long term by hoping to avoid that lowering in energy expenditure, which is really the crux of any weight loss.

James Hill:

We've talked about that many times. That's really the problem in regain.

Holly Wyatt:

So one of the other things I think with these drugs, which I agree is the huge tool, they're pretty much working by decreasing your appetite, decreasing the amount of food that comes in. They're not encouraging you to move more. They're not necessarily helping with your sleep or stress. And we know sleep and stress, there's more than just food and body weight that's impacting inflammation. So how do you think about that? So what if you have lost weight, but you still don't sleep well, you have a high stress job, you're totally sedentary. What do you think your inflammation is going to be in that scenario?

Philipp Scherer:

Oh, that's very clear that stress is an instigator of low-level inflammatory responses, absolutely. And again, it goes into that chapter of lifestyle changes. Not everybody has the luxury of that lifestyle change, of course, and that's really the problem, of course. You have a stressful job. You may not have the option to quit and say, okay, from now on, I'm just going to make goat cheese in Vermont and cater to the Manhattan. That is an issue which obviously each one of us has to cope with, of course. And we have to bear in mind that we need to maybe just chill, relax, and not take everything that seriously. And that brings down the inflammatory state a little bit as well. But that's more easily said than done.

James Hill:

Now, that's a great advice for our listeners. Chill a little bit here. Holly, it's time for some listener questions. So, how might inflammation affect my blood sugar levels or my cholesterol if I'm losing weight?

Philipp Scherer:

Again, research shows us very clearly that if you expose a fat cell to an inflammatory challenge in the form of adding a cytokine to them, they become insulin resistant. So, basically, insulin resistance means that tissues and cells don't do the proper job. The insulin-resistant muscle doesn't take as much sugar after a meal. The insulin-resistant fat cell releases too many fatty acids into the system. So, it is clear that there's a direct impact on many different cell types with respect to an inflammatory exposure.

Holly Wyatt:

We've talked about this a little bit, but I got multiple questions. How do I know I have inflammation? If I feel totally fine, can I feel assured that I don't have it? And if I want to make sure I don't have it, is there a test? I think people are really wanting to say if there's something they can ask their doctor for that really will tell them whether they have this low-grade inflammation or not.

Philipp Scherer:

Well, bear in mind, you can feel perfectly normal and still have hyperglycemia. You can be a borderline diabetic. In fact, we always say a lot of people are type 2 diabetics and they don't even realize it. So everything is fine. Maybe I got to pee a little more often than usual, but, you know, who doesn't? I think we got to make sure that we do do these annual checkups. And during those checkups, you will have a pretty good insight into how you're handling the glucose, the sugar, your hemoglobin A1c. And yes, there is usually an integral part of an inflammatory readout, including that high-sensitive CRP measurements that really is on most of the panels.

Holly Wyatt:

Okay, so that's the test they should look for, that CRP.

Philipp Scherer:

Yeah, they should look for that. But also bear in mind that if you have your annual checkup and you happen to have some form of infection, this might artificially put the CRP level up. So that's why it's not a perfect measure, but it will do for a start and repeat measurements will show you what's going on.

Holly Wyatt:

Nice.

James Hill:

All right, Holly, we need to do some vulnerability questions.

Holly Wyatt:

Okay. I'll start. I'll start with this. So Phil, what's something you used to believe about inflammation or maybe the fat cell that you now see differently? Something you maybe you got wrong or that's evolved over time in terms of what you thought it did one thing, but actually it did something completely different.

Philipp Scherer:

Well, it doesn't do something completely different, but I had to kind of revise my sort of the model in which we think of it. Is inflammation really at the beginning of it all and does it kick it all off or is it a secondary response to something which is already wrong to start out with?

So at this point, I am leaning a little bit more towards the fibrosis, that stiffening of the tissue as being the instigator of a lot of it. And then the inflammation follows as an integral part that is sort of in a feed forward mechanism kind of sets it all off. So I used to think of inflammation truly being the initial instigator of it all. But when you think about it, you need more than that, basically, because you go through these waves of inflammation in response to X, Y, and Z. I think the order of events is a little bit different. That doesn't de-emphasize the importance of inflammation at all, and it doesn't de-emphasize the relevance of inflammation as a contributor to the pathology. But to me, that was my sort of researcher hat-based kind of change of view as to what gets the whole thing started with more and more excitement on my side, personally, on the fibrosis stiffening side of tissues. That's relevant not just for fat tissue. It's relevant for your kidneys. It's relevant for your livers and also for heart failure.

That's a fibrotic disease as well. So every age-related phenomenon that we struggle with in these tissues is a fibrotic disease to start out with, followed by inflammation, and hence, we call them fibroinflammatory diseases that are really driven by this underlying combination of fibrosis and inflammation.

James Hill:

Okay, I have one. If you look at the epidemiology data, obesity rates in the U.S. Have risen pretty consistently since the 1980s, a big increase at first and then continuing to increase. What's your optimism, Phil, that we're going to be able to eventually reduce these rates in the population?

Philipp Scherer:

Since we're going through this revolution on the pharmacology side, so with these weight loss drugs, I think we see a little bit of a dip already. Hopefully that will sustain as these drugs become more accessible. And it's really about accessibility. They're out there. And if you have enough money and you have a good insurance plan or whatever, but they need to be accessible for everybody as a basic right for health care, basically. And as they become more widely used, I think this will be one of the ways to curb that further increase, stabilize it at least. And hopefully, over the next five to 10 years, actually see a bit of a decline in that area.

James Hill:

Yeah, I hope you're right. Okay, Holly, let's do some takeaways here. We've learned a lot in this episode about inflammation. A couple of things. One is you aren't necessarily going to feel bad with inflammation. And one of the ways that we recommend our listeners is next time you go in for your checkup, ask your physician if they're measuring CRP and what they think about inflammation. That could really help. The best way to address it is weight loss, a healthy diet, physical activity. As our guest said, it's a slow process. Don't expect that this is going to change overnight. But I think what we've learned in Phil's work has been critical in this is we used to think of fat cells as just a place you put energy in, it wasn't very useful. But they're endocrine organs, and I think they're playing a huge, huge role in both inflammation in our general health. Phil, did I get it okay?

Philipp Scherer:

Excellent summary. Thank you very much.

James Hill:

One message you would leave our viewers with regarding inflammation and health.

Philipp Scherer:

Big question. My key thing is just to remind everybody, take your time with these changes. Do not rush. No crash interventions. Don't get ready for that wedding or for that thing in a matter of two months. Does not make sense. You will not sustain it. Keep it up over a prolonged period of times in baby steps, baby steps. Remember how long it took you to get to your weight. You're not going to lose it overnight. But if you take your time and you take advantage of the tools that we have available now, I think weight loss is a possibility for everyone at this point.

James Hill:

Right, right. Well, Phil, thank you so much for joining us. Your work reminds us that what's happening inside our bodies is often as or more important than the number on the scale.

Holly Wyatt:

Yeah, I love this. So many more things for us to think about, which is really what this show's all about. Weight loss and fabulous stuff. Thank you for being on.

Philipp Scherer:

Thanks for having me.

James Hill:

And we'll be back with the next episode with more real science, smart strategies, and conversations that connect the dots because weight loss is just the beginning. Thanks, everybody.

Holly Wyatt:

Bye, everybody.

James Hill:

And that's a wrap for today's episode of Weight Loss And. We hope you enjoy diving into the world of weight loss with us.

Holly Wyatt:

If you want to stay connected and continue exploring the “Ands” of weight loss, be sure to follow our podcast on your favorite platform.

James Hill:

We'd also love to hear from you. Share your thoughts, questions, or topic suggestions by reaching out at [weightlossand.com](http://weightlossand.com/). Your feedback helps us tailor future episodes to your needs.

Holly Wyatt:

And remember, the journey doesn't end here. Keep applying the knowledge and strategies you've learned and embrace the power of the “And” in your own weight loss journey.