February 2025 Research Roundtable: Inflammation with Alexandre Amato, MD, PhD, MBA

O vídeo apresenta uma mesa-redonda de pesquisa conduzida pela Dra. Karen Herbst, com a participação do Dr. Alexandre Amato, cirurgião vascular de São Paulo e especialista em lipedema. Durante a conversa, os dois médicos abordam:

• A Relação entre Lipedema e Inflamação:
  Dr. Amato explica como sua prática evoluiu do tratamento cirúrgico para um foco maior na identificação e eliminação dos gatilhos inflamatórios, que são fundamentais para melhorar os sintomas do lipedema.

• Gatilhos Inflamatórios:
  São discutidos diversos fatores que podem desencadear a inflamação, como intolerâncias alimentares (especialmente ao glúten), leaky gut (intestino permeável), alterações hormonais, estresse, sedentarismo, traumas e infecções (como a COVID-19). A ideia central é que cada paciente apresenta uma “assinatura” inflamatória única, exigindo abordagens personalizadas.

• Abordagens Terapêuticas:
  Além das intervenções cirúrgicas, são enfatizadas estratégias não invasivas, como dietas anti-inflamatórias e de eliminação, uso de suplementos e, em alguns casos, medicamentos como os agonistas do GLP-1 – os quais podem ser mais eficazes após a redução dos fatores inflamatórios. O tratamento foca na remoção dos gatilhos para que o corpo consiga reduzir a inflamação e, consequentemente, os sintomas do lipedema.

• Aspectos Diagnósticos e de Monitoramento:
  Os médicos comentam a dificuldade em medir a inflamação através de exames laboratoriais, destacando a importância do relato dos sintomas e do uso de questionários clínicos para avaliar o estado inflamatório dos pacientes.

• Considerações Finais:
  A discussão ressalta que, embora a inflamação seja uma resposta natural do organismo, a inflamação crônica pode desencadear problemas em outros órgãos e afetar a qualidade de vida. O lipedema, apesar de ser doloroso, pode funcionar como uma espécie de “escudo” que protege outros tecidos dos efeitos da inflamação. Os especialistas enfatizam a importância do autoconhecimento e da individualização do tratamento para alcançar melhores resultados.

Em resumo, o vídeo destaca a necessidade de identificar e tratar os gatilhos inflamatórios como estratégia central para o manejo do lipedema, defendendo uma abordagem personalizada que combina mudanças na dieta, intervenções clínicas e, quando necessário, o uso de medicamentos específicos.

Hi everybody, and welcome to the Research Roundtable with Dr. Karen Herbst. We have an amazing program scheduled for you tonight. And as you are logging on, please let us know that you’re there in chat where you are logging on from.

Our guest is logging on, well, it’s 10 p.m. where you are, Dr. Amato, where are you right now? I’m in Sao Paulo, Brazil. Sao Paulo, Brazil. Okay, now you taught me the proper way to say your first name.

Say it one more time. Alexandre. Alexandre.

I see, are you all impressed? Alexandre Amato is with us. But let me give you a little bit of the backstory. Dr. Herbst and I met back in the last quarter of 2024.

And I just said, give me your wishlist. Who would you like to have one-on-one conversations with in 2025? And we have quite a lineup scheduled for you all year long. The topic of inflammation came up and she said, definitely, I want Dr. Amato to join us.

So much happens in the world of lipedema and so many things change as the months go on. But this topic of inflammation is one that I know is of interest to both patients and clinicians. We do hope that you will put your questions in the Q&A.

And as the one-on-one conversation unfolds, Dr. Herbst will go to those questions as she can fit them in throughout the conversation. Dr. Amato is a prolific author, researcher, a vascular and endovascular surgeon and professor in Sao Paulo, Brazil. He worked in Italy and published several papers there with colleagues at the San Rafael Institute.

And in June of 2024, he published the essential guide to living with lipedema, discovering the truth and transforming the treatment of this misunderstood condition. And so without further ado, we get to be the flies on the wall, listening to a great one-on-one conversation about inflammation. I will disappear and I will say, Dr. Herbst, take it away.

Thank you so much, Brenda. And Alessandro, it’s so nice to have you on. I- Thank you.

It’s so nice to talk to you again. I’m always happy. So in order to start out, I know Brenda said a few things about your background, but can you give people an idea of what you do in your practice on a regular basis? What kind of patients do you see? What do you do? Well, I’m a vascular surgeon, so I do a lot of varicose veins and maybe a few years ago, a lot more arterial diseases.

But nowadays, I think my… I have 90 or 95% of my time dedicated to lipedema patients. So I became involved in treating lipedema out of necessity because of my varicose veins patients. They had the leg pain and I wanted to find the best way to help them.

So I do some lipedema surgery. I did the training. I trained with Dr. Rapprich in Germany and I came back, started doing a lot of lipedema surgery.

And then I noticed that surgery is not the solution. I noticed that we can get even better results doing the treating the inflammation. And nowadays only less than 10% of my patients goes to lipedema surgery.

So that’s my daily lipedema care. So you say less than 10% go to surgery. Is that your choice for them or their choice? At first, they come thinking about surgery and then they realize that they did not want the surgery.

They wanted a solution. And then we show another kind of solution that doesn’t require the surgery. Most of them doesn’t care about the surgery anymore.

And they don’t feel pain. They don’t feel the swelling. And some of them might want the surgery for aesthetical reasons, but not for the pain treatment anymore.

Okay. Are you using supplements or medications in your treatment regimen for lipedema? Yeah, I summarize the treatment in finding the inflammation trigger and then removing it for the patients. Anything else is trying to put down the inflammation fire.

Okay, we can use a lot of medications. There are many other treatment, other care we can do to lower the inflammation, but we can’t lower the inflammation and keep throwing gasoline on the fire. We need to remove the fuel.

So how do you, what are the most common causes of inflammation in lipedema that you find in your practice? Oh, there are a lot of triggers. It’s interesting because some of them are very common. And I think I need, I will say about the triggers, but I need to say that I see lipedema nowadays as a way to measure inflammation.

Everyone has inflammation, everyone, me and those who don’t have lipedema, but those who have lipedema, they will feel the inflammation differently. So it’s kind of a red blinking light in the panel of the car. So if you go to the mechanic and ask, please solve the problem with the red blinking light in my car panel.

And the mechanical says, okay, let’s remove the red blinking light, but that’s not the solution. We should see the motor, the engine, what’s going there and fix it and not removing the red blinking light. So I see lipedema as these red blinking lights for many triggers.

Some of them, one very common, it’s a small trigger, but age. Age is an inflammatory trigger. So as long as we get older, there is the inflammation.

So the inflammation goes higher, but there is a lot of food triggers. So sensitivities, the leaky gut change in the microbiota, dehydration, hormonal changes and trauma, varicose veins could be cause or also consequence, obesity, stress, anxiety, insomnia, even exercise. You see, if the exercise is so intense, it can also trigger inflammation, but the opposite is also true.

Those who don’t exercise at all, the sedentary, they are also higher in inflammation. So any infection, I saw a lot of inflammation with the COVID, but COVID is only one virus. There are a lot of bacteria and virus and fungi that could cause inflammation and mast cell activation syndrome, histamine intolerance and many autoimmune diseases.

So there are endless triggers, but I see your question was the most common. The most common, I think it’s food intolerance. Okay.

Food intolerance. Maybe leaky gut is second, but they go together. And when you say food intolerance, is that a true allergy, like an IgE mediated food sensitivity or is it just an overall inflammatory? And if that’s true, if the latter is true, how do you measure that? Or how do we, or is it just, you’re taking the word of your patient, when I eat bread, I get a very upset stomach, I get nauseous and I feel inflamed.

How do you figure that out? At first, I need to trust my patients. So I need to hear what they say. Maybe they don’t understand what they are saying 100%, but I need to think it’s the truth.

So, but that’s not enough. I need more. It’s not IgE mediated, most of them.

I see a lot of IgG mediated, but I even publish it about the HLA-DQ2 and DQ8. That’s the celiac disease genetic problem. Those patients, we have at least 60% of lipidema patients who carry these genes, and they are very, very, very sensitive to gluten.

They don’t develop the IgG or the IgE, but they have a super antigen that triggers inflammation higher than anything else. Those are the patients that if we remove gluten, and I say remove, not lower gluten, they improve a lot. They improve, we change their lives.

So, but the difficulty is that even small quantities of gluten can trigger the inflammation for 72 hours. So, I know many have tried gluten-free diet, but they did not remove everything. They lowered the intake of gluten, and so they don’t feel the improve of the inflammation.

I think I answered your question. Yes, you absolutely did, and I’m gonna go to a question from the audience. Amanda Hadaway asks, since leaky gut or food intolerances are a huge cause of inflammation, is leaky gut actually reversible in lipidema patients? And she says, I ask because we have faulty collagen and defective connective tissue, so is it possible we will always have leaky gut or can we heal it? You know, yes, first of all, yes, the answer is yes, it’s possible.

Leaky gut is not easy to treat. I mean, it’s easy to get better, but it’s not easy to definitely solve the problem. Those who carry leaky gut, they have some kind of, they develop the leaky gut easier than others.

My personal experience with inflammation and everything else was leaky gut. I had an abdominal pain, and I thought it was appendicitis. So you see, I’m a surgeon, and I touched myself and said, oh, I have appendicitis.

I went to the hospital and said, you need to operate me. And I did all the exams and it was not appendicitis. I said, what I’m doing? I was going to operate myself and I was wrong.

So I did an exam and I found that I had a very large leaky gut. And then I treated and got better. And then I had another leaky gut, and then I got better again.

So it’s this go and come back and improve. But if you know how to treat, it’s easier the other time. One very important information for treating leaky gut is that gluten releases zonulin.

And zonulin breaks the tight junctions in the bowel cells, so in the wall. So it increases the leaky gut. So for treating the leaky gut, it’s imperative to remove gluten and then all the other food sensitivities and doing exercise and removing other inflammation and sleeping and everything else.

But it’s possible. And for fully treatment of leaky gut, I see maybe one or two years, but it’s possible to improve symptoms in less than a month. And do you, if you were to measure leaky gut, do you measure zonulin levels? Here in Brazil, it’s a little bit difficult.

I can do that, but it’s expensive and the insurance doesn’t pay. So I try to use other side products of the leaky gut. So there is the urinary Indicam and also the IgG tests helps a lot when we see a lot of food sensitivities.

It’s not a food sensitivity per se. The problem is the leaky gut. Michael, so if you do an IgG test and it’s got a hundred foods on it and your patient has a hundred food sensitivities, you are pretty sure that’s a leaky gut, right? Yes, yes.

There is no threshold number, but I use 10 foods as a threshold. If it’s more than 10, it’s probably a leaky gut, but it’s not written anywhere. Okay.

And let’s see, there was another question I was gonna… Oh, so that’s for measuring leaky gut, but what lab tests do you use to measure inflammation? What are your common lab tests that you use? That’s a very difficult question. You know it is because they are all negative. Yeah.

So how can we measure that? Yeah. Well, I use the symptom questionary. So I use the clinic.

I talk to the patient. So pain, swelling, bruises, and everything else that describes inflammation, I point them and I assume the points and I can measure the inflammation without using any lab tests. Okay.

I explained the red blinking idea, but I also see the lipidema as a shield for the inflammation. So the person who has lipidema, she has the inflammation coming from somewhere. And if she has the lipidema, the lipidema will be a shield that will absorb the inflammation.

And the inflammation- Like a shield. A shield, yes. And the inflammation won’t go elsewhere.

So won’t go or go less to other organs. So it’s not, I know everything here, everyone here who is hearing this presentation will say I’m crazy, but I don’t see lipidema as a bad thing. Lipidema is just the way the body adapts to a higher level of inflammation, but it doesn’t appear in the lab tests because of that, because it’s a way of lowering the inflammation for the body, for the other organs.

Yeah, I think I agree with you that fat is a great protector of the body and it can also suck up fluid as well, like a sponge and hold onto it until the body’s ready for it to release it. Exactly. Yeah.

So I agree with you. So somebody, Marilyn Lee would like you to unpack leaky gut. She wants to know like, what exactly is leaky gut? Wow, leaky gut is the break of the integrity of the bowel wall.

So everything passes through it. We should have a bowel wall that it’s very selective. So passes only nutrients and things that are useful for us.

But if this wall is broken, everything passes, viruses, bacteria, and endotoxins and toxins and everything. Even macro pieces of food. For example, if some macro molecule of any food, maybe, I don’t know, any fruit, lemon, for example, passes through the bowel wall, our immune system would trigger a response to remove this macro molecule.

So it needs to create an antibody. And this antibody is the IgG that will go there and remove this lemon molecule. That’s perfect for some time.

But if there is a leaky gut and there is more molecule, more, more, more, more, the body creates more antibody, more antibody. And when there is more antibody than molecules, those antibodies will go elsewhere in the body and attack any other tissue of the body. For example, the thyroid, that’s one very affected organ in the lipidema.

So there is the Hashimoto’s thyroiditis and then develops the hypothyroidism. Yes, yeah. So we know clearly, and it’s been, there’s a number of papers that have been written that the gut and the thyroid are intimately linked together.

So it makes perfect sense that there would be a lot of thyroid disease in a population in which inflammation is prevalent. A big problem with the leaky gut is that we absorb everything that’s not useful and what is useful, we don’t absorb. For example, iron, the iron goes down.

Yes, yeah, that’s one test that I think a lot of, or that women with lipidema should have is iron testing. There seems to be a lot of low iron in the population and iron causes, low iron causes hair loss. Vitamin D is low, yep.

Two questions, why would, if somebody, I mean, I’ve had leaky gut in my life too, just like you have, but I don’t have lipidema. So why don’t you and I get lipidema, but other women do get lipidema when they have leaky gut? How does that work? Do you know? That’s a body response for, I can explain in another way. Okay.

Imagine in the old cave, when we lived in caves very early, a long, long time ago, and there were the woman and the man, they had different roles in the society. So the man would go outside to hunt and the woman would stay to take care of the kids. Okay, let’s simplify.

Nowadays, very more complex. But in that time, the woman would need to leave to take care of the kids, even if there was no food, no water, they need to hold to the energy as possible, while the man would need to go outside and spend the energy to be able to hunt some animals. So when the woman get the first period, they are not a child anymore.

They would not be cared, but they would care about others. They would take care of the kids. So after the first period, they need to be able to have a very effective way of storaging energy.

And that’s the lipidema. And the man, no, that energy need to be released fast to hunt. So that’s why we hold this energy as visceral fat.

It’s faster to use them. While the peripheral fat, it’s very slower to lose because that’s the way it’s done. That would explain why I don’t have lipidema, but wouldn’t explain why you don’t have.

I think I could explain why I don’t have it. Please. Yeah, and it goes right along with exactly what you were saying, because I’ve been looking at genetics and I think that I veer more towards making androgens.

So I don’t have PCOS. I don’t have congenital adrenal hyperplasia, but I make more androgens than normal. And it would be more subclinical.

I have to do a lot of deep testing on myself, which I haven’t done. But it could kind of explain why I could build muscle as a younger person. I could, I mean, I was so muscular, I was embarrassed because I looked more like a guy, right? But I’m obviously very female and I wanted those skinny little girl arms, but I had these big muscles and I used to, I could pick up those water bottles in the lab.

I mean, they’re huge, they’re like a hundred pounds. And I would, I’d say to the guys in the lab, would you put that up on the shelf for me? And they were like, no, you do it. So I’m like, okay.

And so I would just push and put it up. So I was extremely strong. You know, that’s changed over time as I went through menopause.

But I think that I don’t, a lot of my energy goes out into the environment and I don’t have a lot of visceral fat either. So I do have female fat, but it’s different and it’s probably different and it’s related to a little bit more connected tissue issues. But my androgens prevent me from developing lipedema, I think.

And I could be wrong. That’s my guess. Would love to hear from, you know, other people.

Yeah, probably that’s the reason. Maybe we know how, but we don’t know why. Yeah, don’t know why, but I’m pretty sure that’s, you know, cause, and there’s some, there are some ladies who have had lipedema and they told me that they used to be very muscular and involved in lots of sports.

So it’s not consistent with their life, you know? So, but we’re different people and it would be, it would be really great if we could figure that out. I do know some ladies with lipedema who take androgens and they work with practitioners to monitor their testosterone levels. And, you know, I don’t have any data.

We don’t have any data on their body composition before and after, but you know, that would be something interesting to do. I can say something about that. We have a big problem here in Brazil because we have the beauty ships that are hormones and they are using hormones to everyone.

Yes. And they think that the lipedema is a hormonal problem, but it’s not. No.

The hormones are what make woman, woman. Yes. I mean, that’s what I was saying about the caves.

The hormone triggers the function of the woman in the society. So after the period, the hormones, they have another role. And after the pregnancy, another hole.

So the hormones just make woman what they are, woman. Yeah. And they are trying to change the woman to a metabolically a man.

Will that improve lipedema? Probably it will improve some symptoms of the lipedema, but it will also carry all the problems of the androgens for the man. You know, I’m going to die earlier than everyone who is hearing this presentation, just because I’m a man. And that’s okay.

I know that. That’s the testosterone. That’s how it’s done.

If you just change that, you’re changing the problem. You’re changing the target of the inflammation for the legs and they will go to the inflammation. We will go to the visceral fat.

That’s the worst that can, that exists. Yeah, I agree. I think exogenous androgens, especially, you know, I was recently in Brazil and I was pretty surprised at how extensive the treatment of women with lipedema and hormones was.

And a lot of these were androgens, some of them that are not available in the US. And there’s no long-term studies on androgen administration with lipedema. Even short-term studies.

Or short-term, yeah. It’s just that- There are no studies. There’s no studies.

That’s right. There’s no studies. So that’s a little, that is very concerning.

I am okay with women getting measured for testosterone. And if it’s, they have none to get some back, but it has to be monitored. I don’t want anyone with really high testosterone levels.

I don’t want anyone with really high estrogen levels either. So, and that’s why I don’t take care of hormones in my practice because it is, there’s extensive monitoring. And you also have to make sure you’re keeping up on your cancer surveillance.

So I tell women, you know, you need to go find a practitioner that’s gonna monitor you and care for you. And I do give out names of people that I know, but I can’t, I can’t do lipoedema and mast cell and hypermobility and do research and, you know, and do bioidentical hormone replace. I can’t.

Would I like to? I really understand you. Yeah. Yeah.

So I have a question for you. What is inflammation? What is inflammation? Inflammation is something that’s very poorly understood even though we know about it for a long time. Inflammation is not by, it’s not bad per se.

Inflammation is just the response of the body for any harmful, something that happens to the body. So if we get hurt, if we touch a bacteria or something like that, the first response is the inflammation. So that’s how the body sends all the army to try to fix the problem.

But there are two inflammation, the acute inflammation and the chronic inflammation. The acute is what we want. So we have some, we have flu, we need an inflammation, we kill all the viruses and then we get better and there is no inflammation anymore.

The chronic inflammation is that keeps going all the time and never goes down, but it’s not high enough to bring a lot of symptoms. This chronic inflammation is the cause of a lot of chronic diseases like even diabetes, Alzheimer, a lot of cancers, atherosclerosis and many, many, many others. So if we don’t take care of our chronic inflammation, we will develop something worse than the lipidema.

That’s why I don’t see lipidema as a bad thing. If we have the blinking red light saying that we have the chronic lower inflammation, we can do something to change it. I don’t have it.

I don’t have any symptoms when I chronically inflamed. I need to guess, am I good today or am I not good today? I don’t have the red blinking light. So inflammation is not bad per se.

Inflammation is just immune response. I can’t hear you. Sorry, my dogs were barking.

So inflammation probably has like a thousand different components to it, maybe 5,000 different components. How many functional studies can we do to assess somebody’s immune system? Well. Functional, like how does your, can we say like, oh, let me just do a functional test on you to make sure your immune system is working correctly? Wow, okay.

I like to do some genetic testing, including interleukin-6 and TNF-alpha. I know it’s not functional, but then we know the basis how the patient would work. We can measure a lot of inflammatory, indirect biomarkers.

So like homocysteine and PCR, and even the ferritin and some others. And then we can know if it’s, if there is some kind of inflammation or not. But we couldn’t rely only on that because lipedema is very prevalent in the population.

There are a lot of women. In my first paper about it, we found in Brazil 12%, 12.3% of women with lipedema. That’s a lot.

So how can we have a disease with 12% in the population? First of all, it’s not a disease that will kill and remove the genes from the genetic pool. Second, it should be many different genes and not only one. If it were only one gene, it would be a very rare disease.

So if there are a lot of different genes, there are a lot of different lipedemas. So one lipedema that improves with something and another that improves with other things, one lipedema that has one inflammatory trigger and other. So I think we have a bag with, no, another analogy, an umbrella with a lot of different problems under this umbrella.

When we say lipedema, we have a lot of different lipedemas under this umbrella. I agree. And really, I was being really facetious about the functional testing because there’s very, very, very few tests, which just makes figuring out inflammation a lot harder.

And it’s just so complex that I don’t know if we’ll ever have functional testing. Maybe we will someday. It’s interesting because clinically, it’s so easy to see the inflammation.

And I don’t see in the lab something so easy to find. I mean, if I touch a patient and see her color and see if she has pain in the touching, I can see if she has inflammation or not, but I can measure everything. There will be some- One, maybe two, and then that might change.

Yes, yes. And that’s very difficult for the science. It is.

For example, if I want to measure the inflammation in ultrasound, that’s a great idea. But I need to compare it with a golden standard and there is no golden standard. Right, that’s true.

So there’s the Strohmeyer paper that came out of Austria. They showed that if they grew up a liposuctioned tissue in a Petri dish, and then they just collected whatever the fat cells and other cells in that dish secreted, they could take that fluid and put it onto normal endothelial cells and they leaked. And so that shows that there’s some sort of, in my opinion, an inflammatory mediator.

You know, it could be something as simple as histamine. It could be a bunch of different mediators. And that means that there’s things, there’s inflammatory stuff floating around in the body of a woman with lipedema.

And it’s amazing how many women, at least in my practice, that have brain fog and chronic unrelenting severe fatigue. And that suggests to me that it’s affecting the brain as well. What are your thoughts? I am 100% sure that happens and happens a lot.

You said the leaky gut, and we have the leaky brain, and now we have the leaky fat. Yeah. Yeah, there’s leaky, leaky every, right? I mean, it’s not just the gut that’s leaky.

It’s the tissue, when there’s inflammation in there, it’s damaging. And so what I am concerned about is just, long-term cognitive changes. And maybe, and this is all maybe, because we don’t know for sure, but maybe a higher risk of dementia in women with lipedema, but women with leaky gut too, right? And men with leaky gut, right? I think that’s a high risk for dementia.

I have another idea about that. I cannot prove that, but I really feel this way. I think most of the women with lipedema, if they don’t have the lipedema, they would have a worse disease.

I mean, if you see a woman with a brain fog or any cognitive difficulties, probably an encephalitis, and she has lipedema, the inflammation goes most to the lipedema, but it’s more than the lipedema can deal. So some of the inflammation also goes elsewhere. For me, I think that if this woman didn’t have the lipedema, all the inflammation would go at first to the brain or any other organ, and she would get even worse.

I think some of them, it’s so much inflammation, so much inflammation that if they didn’t have the lipedema, they would have died earlier from another disease. Like diabetes, they would have gotten diabetes or heart disease, stroke. Diabetes, cancer, many, many, many diseases that are related to inflammation.

So that’s how I feel. So I am very, very worried about removing lipedema fat surgically, because as I said, I see as a shield. If you remove this shield, something will happen, and no one is looking what will happen to those patients after they remove this fat, because no one cares about that.

I can say no to that, because I just spent the weekend at a conference, and you know who Wei Chen is? I don’t know if you know Wei Chen. I mean, you’re in Brazil, we’re here in the US, but Wei Chen is a lymphatic microsurgeon at Cleveland Clinic, and he’s interested in lymphedema, and he does surgery for lymphedema to treat it, and he also does surgery for lipedema, and he said that after surgery of any kind, that cognition improves in women with lipedema, and he’s busy working on that to write it up. So he thinks that, and it’s just, we don’t have the answer, so I’m not saying it is the answer, but we’re looking at this from two different ways.

One, the lipedema fat acts as a sponge, but then the Strohmeyer data suggests that lipedema is secreting something bad, like maybe from mast cells, and again, there’s women with lipedema who have mast cell issues, there’s women with lipedema who don’t, so it doesn’t apply to everybody, but he thinks that if you do any kind of surgery, you could do a lymphatic surgery, you could do a liposuction, it removes a lot of that inflammation, removes the burden on the brain, and women’s cognition improves. That’s his thought, that’s his hypothesis. I only believe seeing.

Yeah, you’re waiting to see the data, but what about, for example, there’s a lot of GLP-1 use, you know, GLP-1 agonist use in the U.S., with hempic, Wacobi, Menjaro, ZepBound? It helps a lot, a lot, a lot, a lot. I really think there is no need for bariatric surgery anymore if we use it in a proper way. It’s possible to treat almost all kinds of obesity with those medications, and they have some anti-inflammatory indirect effect, so they also help.

But what I see, if the, I need to say something before. Here in Brazil, we see a lot of pure lipedema without obesity, and I think in the U.S., there are a lot of obesity plus lipedema. So using the GLP-1 with pure lipedema, and if we don’t remove the inflammation, they don’t lose weight.

That’s incredible. They keep complaining, they spend a lot of money, and the medication doesn’t work. If we just lower the inflammation, then the GLP-1 works a lot.

So you try and reduce the inflammation with diet and maybe some supplements beforehand, before GLP-1? Some supplements, there are a lot, maybe curcumin and others. It helps, but the most important thing is find the trigger and removing it. Yeah, okay, yep.

That’s the most important. It doesn’t matter if I give all the anti-inflammatory drugs that are in the world, and if she keeps putting inside her body what gets her inflammated. So that’s the most important thing.

For example, treating the leaky gut. We need to focus treating the leaky gut 100%. If not, the wall will pass everything and we’ll get inflamed by everything.

There is no anti-inflammatory drug that will be enough. So just to reiterate, you think it’s really important to look for inflammatory triggers in women with lipedema. Get rid of the triggers, reduce the triggers, treat the triggers.

And then if they’re not responding to a GLP-1, then try a GLP-1 again and they may respond to it. Yes, I have many patients that tried GLP-1 before alone and it didn’t work. And afterwards, removing the trigger, using any anti-inflammatory supplements, it starts working better.

And so are you saying that lipedema tissue can respond to a GLP-1 agonist by decreasing? Yes, it can. It is not as fast as the visceral fat, but it can improve a lot. And do you think it just takes a little bit more time because of the structure of the tissue, the fibrotic structure? Can I show one image? Please, please.

Let me share my screen here and I can show wherever here. Okay, are you seeing my screen? Yes. Okay, I have one patient here that’s very easy to understand.

Okay, she did use GLP-1, but you can see this is three months, she lost 18 kilos. Sorry, I can only say in kilos. No, we’re good.

And after six months, she lost 32 kilos. And then she started gaining muscle without surgery. Okay, but coming back here, what’s the most important thing that happened here? She lost the redness.

She lost the inflammation. She’s not red anymore. She’s not inflammated anymore.

She tried GLP-1, she tried all kinds of anti-obesity drugs before and nothing else worked. But now she lost 18 kilos in three months. Why? Because we removed her trigger.

Removing her trigger, any drug would work. Can you just tell us what her trigger was? Was it gluten? For her, was the gluten. Okay.

For her, was the gluten. But this one, so no surgery. She lost 20 kilos and then she improved muscle with exercise.

Any exercise works if she is not inflamed. For example, maybe this one, this one here. In three months, she lost six liters.

And then in six months, eight liters. And then 11 months, she lost 11 liters without surgery. And this one, it’s a long time ago, she did a keto.

She improved a lot with keto. And this one, it’s the symptoms. She improved symptoms in 78%.

And she had one trigger that was the Brazilian nut. Removing the Brazilian nut, she didn’t have pain or any other inflammatory trigger. Is that an IgG test that you showed? In the IgG test, yes.

Okay. For everyone, Brazilian nut is very good, don’t. Don’t worry about that.

I only use this example because as it’s a common anti-inflammatory food here, I want to show the other side. It can also be inflammatory for some people. And well, this one here, she has Ehlers-Danlos.

She has mast cell activation syndrome. She has gluten intolerance and removing all the… She never lost weight before. She never did exercise.

She never gained any muscle. She improved this way, removing the triggers. And then I can show what happened to her.

That’s the same patient. She lost all the volume without surgery. And then she started doing exercise.

She became a triathlete, started gaining muscle. And that’s it. Wow, that’s really impressive.

That’s a really great surgical outcome. But I know it’s not surgery. I mean, that’s a great before and after picture.

But that’s surgery, that’s it. And no GLP-1, right? You just remove the triggers. For her, removing the trigger and a lot of exercise.

There is one rule that we can change. If there is inflammation, you won’t lose fat and won’t gain muscle. Remember the caves.

Why would I gain muscle if I need to absorb energy and keep alive? There is no need. So I need to tell my body that I don’t need this energy. So there is no stress.

There is no lack of food or water or anything else. I am in peace. If everything is in peace, even our inner self, our inner inflammatory, I don’t know what, the body understands that we don’t need to hold to this energy and we release that easier.

You put everybody on a keto diet? No, keto is not so easy. It’s not for everyone. But I put everyone in some kind of anti-inflammatory diet.

And for those who agree and are willing to, we try the keto at least once. There are many anti-inflammatory diets. There is the removal.

We keep removing the food, test how the patient is and put the food back again. There is the food map. There is the Mediterranean diet.

There is anti-histamine diet. So as I said, I see lipidema as an umbrella with a lot of different necessities. We need to understand what each patient needs.

Yeah, so it’s very personalized medicine that you’re doing. You’re finding each individualized trigger and then you’re finding food that she would like to eat that’s anti-inflammatory, right? Exactly. And let me just, there’s an anonymous attendee that is asking what research or science supports a GLP-1 impacting lipidema tissue? Or you’re just saying it’s removing lipidema tissue or just reducing inflammation, therefore lipidema tissue? I haven’t seen any paper about GLP-1 and lipidema connecting directly and only about that.

But all the papers on GLP-1 have studied lipidema patients mixed in other patients. Yes, yeah, yeah. I agree with you.

Dr. Herbst and Dr. Amato, oh my goodness, we have opened up a big old can of worms here. We have so many brilliant questions. I want to acknowledge at this less than five minute mark left in our program, thank you to all of you who have logged on tonight.

Your brilliant questions and your genuine caring about this topic with these two experts means so much. This is why we do these programs. And we realized that we didn’t get to all of your questions.

Yeah, sorry. I do want to say, oh, well, you did a brilliant job, what you did. I do want to acknowledge one thing because it was a pain point when it was said lipidema is not a bad thing.

We certainly understand how painful it is to live with this condition. So while we’ve discussed how it can be a protective mechanism in the body, we are in no way glossing over the pain that you deal with day in and day out. Yeah, the reason we do these programs is because we care and we acknowledge.

And I see great hope in the chat about conservative measures. Of course, Lymphopress sponsors this program tonight and the pneumatic compression can certainly help deal with the inflammation and the pain. If anyone who has logged on tonight needs that kind of help, we would be honored to help you.

This program tonight will be, has been recorded. It will live on the Lymphopress website because I know you’re going to want to watch it again and again and again. And I think one of the underlying questions overreaching this conversation is got to find out what our triggers are because they’re different for every person.

And so Dr. Amato, how would you for next steps tell our audience how to do that elimination trial to find out what their particular trigger is? You can try an elimination diet. So remove some foods for a week or two, see if you improve symptoms and then try to put the food again and see if the symptoms get worse. So that’s the first attempt I try.

It’s easy if you think about the, you start with the most common ones. So wheat, gluten, milk and others. And it’s not so difficult, so impeditive.

But for some people who don’t have the most common ones, it will be a little bit more difficult. And I would like to say, I never underestimate the pain and the feeling my patients have. But I want to show them that’s not only hate, I hate, it’s a love and hate, it’s an equilibrium.

The nature doesn’t care what you feel. The nature just responds to some stimuli. So if you have inflammation, your body will respond to that.

If you like this response or not, that’s what is keeping you alive. But I always care a lot about the pain. So the pain is my main focus.

Sometimes they came for the aesthetical reasons and they feel pain. I always change that. I need to treat pain before I get worried about the aesthetical.

So with that, Dr. Herbst, do you have any closing comments? And Dr. Amato, your closing statements to our wonderful audience tonight? I wish we had a whole nother hour because I think we could have easily filled it. This has been just a brilliant conversation. I think we brought up kind of some new points.

And I do want to also echo that, I want a t-shirt that says lipidema sucks because it does. And I’m like Dr. Amato, we’re detectives. We try and figure out what you have and what we can do to calm all that down so that your lipidema tissue can realize I don’t need to be here and it can go away.

So I think we just don’t understand female fat very well. There’s a lot more research that needs to go into female fat and lipidema is a great start. And so I think lipidema is really paving the way for us to better understand the connective tissue of women.

Excellent, thank you. And Dr. Amato, your closing words to our audience. I agree with Dr. Karin, and I thank a lot for everyone and this opportunity.

But I would like to say that self-awareness is the key to understanding and managing lipidema effectively. So we need to understand ourselves and use lipidema for better understanding greater good, at least to improve yourself. I think that women with lipidema are extremely self-aware and everyone comes in and they’re extremely well educated about what lipidema is.

And I think you should all just applaud yourselves because you are such an informed population. We just need more tools, right? In order to find all these triggers faster and get rid of them. And amen to that.

And with that, we are out of time. Dr. Amato, Dr. Herbst, amazing conversation. I know a lot of people are encouraged tonight and more questions, but we’ll have more answers because we are not giving up.

Thank you everyone for joining this Research Roundtable. Mark your calendar for next month. Shelley Crescenzi, salt and physiology, a one-on-one with Dr. Herbst.

It’s gonna be on fire, awesome conversation. Have a wonderful night, everybody. We’ll see you next month.

Thank you. Thank you, good night.