Sarcopenic Obesity

See this publication for more information on the diagnostic criteria for sarcopenic obesity: Donini 2021 Definition and Diagnostic Criteria for Sarcopenic Obesity

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And we also normally think that obesity and sarcopenia have different trajectories. And only very recently we noticed that obese subjects had nutritional problems related also to undernutrition. So this is a schematic biological pathway for the pathophysiology of sarcopenic obesity.

We know that aging process, inducing the reduction of metabolic rate, physical activity, and sex hormones may lead to reduction of skeletal muscle and to mitochondrial dysfunction and increase of oxidative stress and reduction of the anabolic pathway. The same way we know that obesity through the visceral and ectopic fat accumulation leading to insulin resistance and to inflammation may contribute to the pathogenesis of sarcopenic obesity. We know also that the combination of sarcopenia and obesity may increase the effect of both the situation inducing cardiometabolic diseases, increase physical disability, and increase mortality.

When we look to the prevalence of sarcopenic obesity, we can see, as it happens in this paper, that the prevalence is quite high. In this paper, the authors, they show in the population more than 13,000 people that the prevalence of high adiposity and low muscle mass was around 15% in males and of around 10% in women. But the data on the prevalence of sarcopenic obesity are not coincident in the literature.

Depending on the definition used, the prevalence goes from 4 to 20%. And even if we consider the same sample, just modifying the parameters or the cutoff, we can have an increase of the prevalence to 18% in women and to 43% in men and increasing with age. For this reason, EASL and ESPN, in 2018, they considered it was time to meet the challenge, in particular, to define diagnostic tools and diagnostic criteria for sarcopenic obesity.

The first step we performed is a systematic review of the literature that we published in 2019. We included 75 studies for a total number of participants of around 220,000 people. The distribution was 54% for women, mean age was 75 years, with a range from 20 to 92 years.

And the studies were conducted all over the world. But we found a great variability in the results. We found that among the 75 studies, we can see that there were 90 different measurements of sarcopenia, 10 different measurements of adiposity, and even for the cutoff points, we found a great variability with cutoff points coming from established guidelines for BMI, for example, or for population-specific cutoffs in other studies.

We found also a great variability among the diagnostic procedures that were used in the definition in the diagnostic process for sarcopenic obesity for the instruments that were used, DEXA in most of the studies for sarcopenia, but just in a minority of studies for adiposity, anthropometry, in particular, BMI for definition of obesity, muscle strength just in a minority of studies, gait speed in 12 studies, BIA or CT scan in just a few studies. For this reason, there was an initiative coordinated by ESPN and EASO. We introduced a certain number of researchers, 40 researchers coming from all over the world to define the sarcopenic obesity and to define also the diagnostic procedures that has to be used in this case.

So we followed the standard operating procedure for ESPN guideline and consensus papers based on a four-phase DERFI method using a five-point Likert scale and the statements that met a predetermined consensus threshold that was 75% for a positive result, agree or strong agree were brought forward to the following consensus step. And I will show you the results of this consensus that will be published just tomorrow, simultaneously in the Clinical Nutrition and in the Obesity Facts Journal. So the definition is that sarcopenic obesity is defined as the coexistence of obesity and sarcopenia, which means that it is characterized by the combination of high body fat, including ectopic fat and low skeletal muscle mass are combined by low muscle function.

In the definition of sarcopenia, we consider that skeletal muscle mass should be specifically considered rather than lean body mass and that we need probably to introduce the concept of adequate muscle mass to consider the amount of muscle mass that is necessary to people with a higher weight and higher fat mass. We consider also that the muscle functional parameters need to be included in the definition of sarcopenic obesity, since they are the main determinants of metabolic outcomes, cardiorespiratory complication, functional impairment and disability, reduced quality of life. Both altered body composition and altered skeletal muscle functional parameters should be present to assess the presence of sarcopenic obesity.

And at the moment, for clinical utilization, we do not have enough data to suggest and support an integrated index for sarcopenic obesity, which is one of the aims of the research in the future. But nevertheless, we consider that the two categories of obesity and sarcopenia should, however, be considered in the context of sarcopenic obesity that is a unique clinical condition. We know that sarcopenic obesity is more frequent in older adults, but not necessarily limited to this older age category.

And we know also that there is a difference between primary condition of sarcopenic obesity related in particular to the aging process and to sedentarism compared to secondary sarcopenic obesity related to the presence of acute and in particular chronic diseases. But this is another objective of the research in the future. So this is the algorithm we published for the diagnostic procedure of sarcopenic obesity.

It is a three-step procedure with a screening, diagnosis and staging. And now we will look more in detail these three steps. So for the screening, we consider BMI and waist circumference for the definition of obesity and surrogate parameters for sarcopenia, which means clinical symptoms, clinical suspicion or questionnaire.

Most of these are validated only in older subjects. Both conditions must be present to proceed with the diagnostic procedure. The screening must be performed in all subjects at risk, which means older adults with obesity subjects who have a rapid increase or decrease in weight and who have a comorbidity for chronic diseases by healthcare professionals, not necessarily experts in the field of obesity and sarcopenia.

And for this reason, as you can see, the tools we select are easy to find and use in any healthcare environment. We know that BMI could potentially exclude individuals with higher adiposity but with a BMI in the normal or overweight range. This is one of the open questions present in the publication.

And we know also that probably there is the necessity to include people with a lower cut point for BMI in the presence of comorbidities. And we know also that major diseases that can affect the body weight through, in particular, fluid retention should be carefully considered and assessed to avoid screening errors. The second step is represented by the diagnosis.

It will be performed in two steps. The first one is altered skeletal muscle function parameters, considering strength, which means angry strength and chest and test. If muscle function parameters suggest the presence of sarcopenic obesity, the diagnostic process will continue, considering body composition.

And body composition will be assessed considering fat mass percentage and reduced muscle mass assessed by appendicular mass to weight ratio by DEXA or skeletal muscle mass to weight ratio by BIA. And we stated that both altered body composition and altered skeletal muscle function parameters should be present to assess the presence of sarcopenic obesity. The diagnosis should always follow a positive screen, and it will be performed at the specialist level with access to technique, devices, and methodologies for body composition measurements.

Open questions are related to functional parameters. We know that we need to have functional parameter cutoff points validated as reference values for gender, ethnicity, and age. We provided in the paper a list of cutoff points for different reference populations, but it is not complete.

And we have also to consider gait speed and eventually to choose which test to be used probably in the future. For body composition, we need also cutoff points validated for gender, ethnicity, and age. We are not very sure if fat mass percentage is adequate for the definition of obesity.

Probably, we can imagine to analyze the role of fat mass index in this case. Distribution of fat mass should also be taken into account measuring waist circumference and probably also the visual fat analysis through DEXA. Anthropometry has been suggested to be used and limited to calf circumference in the absence of edema, and CT scan and MRI should be used when possible.

Other discussion points are represented by the limitation. We are aware that different instruments have in the evaluation of body composition, we have a limitation for BIA, for DEXA, and for anthropometry. And we have also the necessity to validate in other populations with different ethnicity if the proposed cutoff of 40% for female and 30% for male are adequate in our case.

And we suggest to use the same procedure, the same diagnostic tool for the patient during the follow-up to verify the efficacy of the treatments. The third step is represented by the staging. We propose a two-level staging performed based on the presence of complication resulting from high fat mass and low skeletal muscle mass.

First stage is no complication. The second stage is the presence of at least one complication attributable to sarcopenic obesity, for example, metabolic diseases, functional disability, cardiovascular and respiratory diseases. We point out the necessity to evaluate the disability since it represents a consequence of sarcopenic obesity with a strong negative prognostic value and it may be considered an aggravation or a perpetuation factor since it may exert a negative independent impact on the maintenance or recovery of an adequate body composition and function.

For the staging, we have some open questions. The first is that we know that it is at the moment arbitrarily assessed. We need some research to verify its validity and that we think that global functional outcomes need to be considered as markers of severity of sarcopenic obesity and in the staging of sarcopenic obesity, although they may not be necessarily associated with sarcopenic obesity as joint limitation and pain in some patients.

General future research questions will be addressed to devices. We need to develop and validate cost-effective techniques to measure body composition and skeletal muscle mass in clinical practice. We need to verify the validity of the cut-off points and the opportunity to move to T-score or Z-score as it happens for bone mineral density in osteoporosis.

And also, we think that cut-off points need to be validated as predictors of specific adverse outcomes like disability and mortality. There is a need for compromise between practicability and the precision as we need in research activity. We need also to discuss about the difference in the pathophysiology process and in the functional and clinical consequence for primary and secondary sarcopenia.

And we need also to study how to handle hybrid situations like obesity coupled with reduced muscle mass and normal muscle strength or with reduced muscle strength and normal muscle mass. There are some limits in the study. First of all, we have a self-selected panel of research mainly based in Europe.

So, we asked other researchers to contribute to the improvement of this consensus through research activity. But we have also some strengths represented by the fact that the research has come from different areas. We have nutritionists, experts in obesity or sarcopenia, gerontologists, and we think that this will has given the possibility to have a wide vision of coming from a different perspective of sarcopenia obesity.

So, in conclusion, we think that sarcopenia obesity represents a hard challenge from a clinical, functional point of view and we think also that the prevalence of sarcopenia will increase in the future. Definition diagnostic procedures for sarcopenia obesity have been specified by a consensus procedure promoted by ESPN and IASO. It is based in a three-step process, screening, diagnosis, and staging.

And we think that further clinical research is necessary to verify the validity of this schema. Thank you so much for your attention. Thank you very much indeed, Lorenzo.

That was comprehensive and very interesting indeed. I can, if you wouldn't mind unsharing your screen so that we can maybe see more people. That would be great.

If anybody wants to ask a question, please raise your hand and you can then unmute yourself and ask. But I see that we have a couple of questions already in the chat function, which I shall read out for you. So, the first one is from Feri Akbas in Turkey.

Is it mandatory to measure muscle mass to diagnose sarcopenia obesity or is it enough to measure muscle strength where diagnostic tools are not available? Good question. We decided that we had also the necessity to have measure of body composition. So, in the schema, there is an evaluation of body composition, appendicular skeletal muscle mass, or skeletal muscle mass through DEXA or BIA.

Thank you very much. And then another one, this is from Abtirani. How does the presence of sarcopenic obesity affect treatment choices? So, we published last year a systematic review on treatment of sarcopenic obesity.

There are not so many papers that have been published. So, we are not very, very, it is not very clear what we can do. Anyway, it is very difficult to reduce fat mass without affecting lean body mass or at least in increasing the lean body mass.

We can probably learn from the studies that have been done in sarcopenia to improve the lean body mass using oral nutritional supplements or increasing physical activity. But we don't know exactly which type of physical activity is the most effective in this case. Thank you very much.

And now I hand the floor then to Bridge who has his hand up if you could unmute and ask away. Dr. Lorenzo, wonderful presentation. I think, you know, most of the time when we talk of sarcopenic obesity, we refer to elderly people who have, you know, loss of muscle mass and more of fat.

Within the spectrum of obesity, we have an entity called metabolically obese normal weight individuals. Does that also represent something like sarcopenic obesity according to you? In some cases, probably yes. If we use the schema that has been proposed by Yaz and Aspen, probably we can involve some people in, we can consider some people with normal weight of the subject as sarcopenic obese.

In fact, through the screening process, we exclude people with normal BMI. And this is one of the open questions that I've mentioned in the presentation. But we have the necessity to be as precise as possible in the process of the diagnosis.

This is a very good question. Another important question is, do we only look at the muscle function in terms of the physical strength? Or should we also look at the metabolic dysfunction resulting from low muscle mass and high fat mass, which happens in this particular case? So, we consider just muscle strength in the schema. One of the open questions is if we have to consider also a gait speed as another parameter.

But we try to combine easy to use parameters for clinical practice, leaving more precise and more sophisticated procedures to research in the future. Probably the metabolic consequences of sarcopenia in obese subjects is very important to be considered. Thank you.

Thank you very much. And I see that Lisbeth Van Rossum has her hand up as well. If you could unmute and ask.

Thank you. Thank you so much for this great presentation. Very, very informative.

I was wondering, you suggested to do proper diagnostics, and you had a beautiful scheme for that. I was also wondering, one of the main causes in my clinical perspective as an endocrinologist is also that people are using critical steroids, which can induce proximal muscle atrophy, as we know. Well, in the Netherlands, 10% of the population is using critical steroids, but in people living with obesity, we found 28% is using any type of critical steroids.

And that's also in a clinic what I see the most, if people have obesity, that's a major cost. Do you think it's useful to do diagnostics also towards the causes, as you suggested? And does it have, maybe it's an extended question of what Apturami asked, does it have consequences for treatment? And then I'm thinking of maybe, for example, combining muscle strength exercises with metformin use, like it's known to protect for cardiometabolic side effects, would it be beneficial for muscle strength? So do you think this type of cause is important to diagnose during the process of diagnosing sarcopenic obesity? I think that we have to consider all the treatments that people use during the diagnosis process. But when we look to the literature, looking at the treatment of sarcopenic obesity, we found very few papers.

And in most cases, the definition of sarcopenic obesity was different. So we don't have at the moment any clear idea about what to do in every people. And there is also a great variability in the clinical situation of people with sarcopenic obesity, in particular when they become elderly subjects.

So we don't know exactly what to do. We imagine that protein, supplementation, certain branch chain amino acids, essential amino acids, physical activity may be effective in treating sarcopenic obesity. But we don't have at the moment any clear data about that.

Okay. Yeah. Because one of the things you said in corticosteroids related to sarcopenic obesity, then it will be more proximal muscles.

So does it matter whether it's the proximal muscles versus the more distal muscles, for example, so more, yeah, more what? Sarcopenia or... But it's maybe further research and to explore. And the first step is to diagnose it anyway, the sarcopenia. We try to give to everyone just one schema for the diagnosis, just to have data that are comparable around the world.

Yeah, perfect. Thank you so much. Very much, everybody.

Miriam, has your question been answered in the chat? How could we induce weight loss without losing muscle mass too? I know that we discussed that a little bit, but perhaps we could refer to it again. Yes, it is a $1 million question. And probably physical activity will be the best way to preserve muscle mass, lean body mass during the treatment of sarcopenic obesity.

But as I said before, we don't have at the moment any clear protocol of intervention, any clear results from the literature. Thank you very much. Well, in this case, we shall move on to the second speaker, who is Andrea Curin, who is an associate professor at the endocrinology specialist at the Department of Endocrinology at the University Hospital Valdebron, which is in Barcelona, Spain.

Andrea is also very extensively published in obesity, diabetes, hypertension and cardiovascular disease. And today she is going to talk to us about sarcopenic obesity, even in younger ages. So, Andrea, thank you very much for joining us today.

Thank you for giving us this presentation. And I hand the floor to you, if you could share your screen. Thank you very much.

And thank you for this initiative. It's really very nice to have these sessions and to virtually meet and share opinions. Actually, my presentation will also bring some polemics and answer some of the questions that have already been commented or bring more polemics, if possible.

So, I expect some discussion after that. So, I'll speak about sarcopenic obesity in younger ages. There's not much data to count, but I'll try to do something.

So, I come from… Andrea, could I just ask you firstly to put your presentation mode on? Yes, right now. Perfect. There you are.

Thank you. So, I come from… Thank you. I come here in Barcelona from the Valdebron University Hospital.

So, two things about the muscle, right? Because the classical function was that the muscle is important for the physical movement, for the postural condition, the respiration. So, the logical question is, therefore, if I do not intend to move, I do not need the muscle, right? Well, this is not true, because the muscle now is considered an endocrine organ, because besides the structural function, also has metabolic functions, like the main protein storage, like glutamine synthesis and storage, the main organ involved in glucose-level homostasis, and also is important in a disease, because the muscle is a metabolic endocrine organ, which is very important in malnutrition, for instance, because it supports the tissue structure and function, the organ structure and function, the immune responses, the skin integrity, the neural function, and the muscle deficiency will leave the person unprotected for energetic storage and defense during a disease. So, the muscle mass is important.

Sarcopenia, as was mentioned before, was a definition which comes from two Greek words, sarco, which means meat, and paenia, deficiency, was registered as a condition in the International Classification of Diseases, and is a complex syndrome characterized by low skeletal muscle quantity and or function, right? And as we saw in the previous presentation, there are criterias and consensus, and it seems that is more important, the quality and the function than the quantity of the skeletal muscle. I would just like to comment on the European Working Group on Sarcopenia, which was published the first consensus in 2010, and I highlighted here that is the Working Group of Sarcopenia in Older People, because until recently, sarcopenia was considered a condition of the older people. The consensus was revisited in 2019, and here we have a paragraph on sarcopenic obesity, which says that was most often reported in older people, and just below, they say that sarcopenic obesity is a distinct condition, which is beyond the scope of the article.

So there's not much data. So this is my, the topic that I will try to explain today, sarcopenic obesity, even in younger ages. Just two things about the BMI.

This parameter was invented by a mathematician in the 19th century, based in one subject in France and Scotland, and was not designed for health outcome, but to demographically describe the characteristics of the common person. So in 1998, the World Health Organization decided to classify, depending on the body mass index, not on the way normal range of weight and obesity, but with the years, we saw that BMI is the main criteria for bariatric surgery. Nevertheless, we have patients that do not respond to bariatric surgery or have complications.

Also, obesity paradox was described, for instance, in heart failure and cognitive decline, which now we know is false, because the BMI has limitations, because there's no data on the body composition, and here you can see that for the same BMI and or body weight, the muscle mass can vary by 30 kilograms. Okay, so we are losing a lot of important data on the metabolic condition if we only use the BMI. Sarcopenic obesity is the interaction of the two epidemics, of the obesity and the loss of muscle mass, and if we take into the account the new definitions of obesity that are proposed according to the percentage of fat mass of total body composition, we can see that we have different scenarios, that people with obesity and low lean mass, which will be sarcopenic obesity, people with obesity and normal muscle mass, or people with obesity and high muscle mass, and also BMI can be normal and still have sarcopenic obesity because you have a disbalance in the body composition, increased body fat and low muscle mass.

You can have anthropometric measurements that can also be normal, as you can see here in this picture, and also the muscle mass in kilograms can be normal but with poor quality. Here you can see some pictures of a study that we are conducting here at my site, where you can see that within the same muscle mass, you can have different qualities. Here you can see the myostatosis, the fat infiltration in this muscle mass, okay, so this is a poor quality.

Obesity and sarcopenia share common mechanisms like insulin resistance, inflammation, oxidative stress, hormonal changes, and they potentiate each other and the consequences are important. Besides dyslipidemia, type 2 diabetes, cardiovascular disease, hypertension, frailty, I have added new conditions that were associated with sarcopenic obesity, like cognitive impairment, even in younger ages, like prolonged hospitalization, osteoporosis, worse surgical recovery, mortality, low life quality, and so on. We saw this picture before, and just to highlight that these alterations like insulin resistance, ectopic fat accumulation, visceral fat accumulations are present in younger ages in people living with obesity, and the key between the insulin resistance and sarcopenia is very simple.

When you have a normal insulin pathway signaling, you have protein synthesis, but when you have insulin resistance, you have proteolysis, so you are losing muscle weight. We saw the diagnostic algorithm, then the clinical suspicion, the SAR questionnaire, and then all the tests, DEXA body composition is still the gold standard method, but what happens in younger ages? Actually, in the literature, there is very few data and very heterogeneous, a lot of variability in the methodology. Here we see a study performed in children between 4 and 14 years of age, and they used the bioimpedance and defined the muscle fat ratio cutoff of sarcopenic obesity as two standard deviations below the third BMI quantile, and then they proposed a new biomarker by using the hand grip test.

But the prevalence of sarcopenic obesity in these children varied between 7.2 in boys until 9.3% in girls, and I think that this is a lot if we take into the account that these children should be moving the whole day, right, and have a healthy muscle. Then moving to young adults and middle-aged adults, this is a study that used body composition, DEXA for quantity, the hand grip test for strength, and used the ratio strength and muscle mass for the quality of the muscle. And they saw that depending on the criteria that they used, the prevalence of sarcopenic obesity was different.

For instance, in females, if they use the appendicular skeletal muscle mass by weight, they found the prevalence in women ranging between 8.8% between 20 and 40 years until 12% between 40 and 60 years. We can see that in this study that the age is also important. The prevalence of sarcopenic obesity is higher when the patient is older.

If they use the appendicular skeletal muscle mass by BMI, the prevalence was higher, about 27%. And when they combined the muscle mass with the strength or quality, the functionality, the prevalence was different, ranging between 1.8% in younger females until 12% in older females. The same happened in males, but here the prevalence was higher, between 25-36%, even 63% if they used the appendicular skeletal muscle mass by BMI.

Nevertheless, it increased with age. So, this paper highlights the importance of the muscle quality, but the need for specific criteria for people living with obesity for sarcopenia, and the need for a more homogeneous criteria for the diagnosis, as was commented before. Then I found some indirect data because the papers, the studies were not designed to look for prevalence of sarcopenic obesity, but for instance, this is a paper published in Obesity Surgery that looked for the impact of sarcopenia in the outcomes after bariatric surgery.

This author used mathematical equations for the muscle mass evaluation, and no objective tests. They found no impact of sarcopenia in the post-bariatric surgery outcomes. Nevertheless, the prevalence of sarcopenia was about 33.3%, but they used mathematical equations, which we know that are not really the best option to evaluate the muscle mass in people with, living with obesity.

Then another indirect data extracted from this study was that in people with about 45 years of age, the previous study, sorry, also the age was about 45 years, so there were younger, younger persons. Here in this one, they used the skeletal CT scan, only evaluated for the quantity of the muscle mass, not the quality, and they found the prevalence of sarcopenic obesity between 32.2%. The important conclusion of this study was that the presence of sarcopenic obesity had a high impact on the post-surgical complication like the gastric leak, for instance. This is to answer the one previous question in the chat, that if the basal condition, if we should treat before applying any treatment, I think that we should do it.

Then this is a study from my group, when we wanted to see the impact of bariatric surgery on the muscle mass in patients with obesity, but here we have some indirect conclusions, also people with mean age of about 45 years of age, we used bioimpedance and also evaluated the phase angle. We found a pre-bariatric surgery prevalence of sarcopenic obesity of 37% in these young persons. Then we found that after the bariatric surgery, the muscle mass was continuously dropping, even after two years, while the fat mass started to increase one year after the surgery.

And then regarding the muscle quality evaluated by the phase angle, we saw a very, very significant deterioration, even one month after the bariatric surgery. And then the major determinants of the post-bariatric surgery muscle mass were the insulin resistance and the muscle mass before the surgery. So the basal condition, I think that is important for the outcomes after the losing weight intervention.

In order to shed light on this issue, we have right now ongoing clinical study financed by the government here in Spain, in order to find out which is the prevalence of sarcopenia in patients with obesity older than 60 years of age. And at present, I do a little bit of spoiler of the presentation that the oral communication that I will give in the Congress in Maastricht, but we found a prevalence of sarcopenia of 37.6% in these people with 43 years of age. Nevertheless, we, and I'm sorry for this professor, we did not follow the diagnosis algorithm and we did the DXA in all the patients and we found that the questionnaire for the screening would have identified only 24.6% of the patients with risk of sarcopenia while we found the high prevalence with the DXA.

The conclusions, there is at present few reliable data in young people living with obesity, but the sarcopenic obesity can have a high impact on clinical outcomes and costs in the health system, about 30% of prevalence, but the methodology is not homogeneous. There are no standardized methods for people living with obesity and sarcopenic obesity also is a hidden disease because the muscle quality is difficult to evaluate. Here is just an example for the study of us that for the same muscle mass, you have different qualities of the muscle with different impacts in the outcomes and the evolution of the patients.

The more red color we see, the better is this muscle health. Okay. And yes, the sarcopenic obesity, time to meet the challenge.

I think that we have a big challenge and a lot of things to try to solve and the floor is open for discussion. That's all because there is not much data in the literature. Thank you.

Thank you very much, Andrea. That was very, very interesting indeed and very nice to hear from your very direct clinical experience and from the studies that are ongoing now. I don't see any questions in the chat, but I wonder if anybody has any questions and they want to raise their hand and ask a question.

Brij, you were very quick there. Over to you. Dr. Henry, a very good presentation and you, you know, basically touched upon the point that I asked with the previous presentation.

So very interesting slides and one of the slides you showed that insulin resistance leads to proteolysis and, you know, further worsens sarcopenia. So is it the insulin resistance which is worsening sarcopenia or it is sarcopenia which is further worsening insulin resistance? You know, it is a big question. So is it that we get fat mass leading to lipotoxicity, insulin resistance and sarcopenia leading to a sarcopenia which is the primary culprit here? Well, that's a very good question.

I think that depends on what kind of people you are thinking about because if we think, if I refer to young people, I would say that first we have insulin resistance because they do not have another cause for the sarcopenia. And then the insulin resistance, yes, is one of the major determinants, right? Then they'll have myostatosis and so on. And then the relationship is bidirectional.

One condition worsens the other. In older people, I'm not so sure because if we have aging also playing here, I'm not so sure if insulin resistance is so important as a trigger for sarcopenia. Another very important observation you showed is the post-bariatric surgery that, you know, despite two years follow up, despite the fat still, you know, coming back, the muscle is still going down.

Yes, this is really preoccupying because the insulin resistance, I'm sorry, my webcam is okay. The insulin resistance became normal six months after the bariatric surgery, but now we are looking at the biomarkers. One of the hypotheses is that maybe the the insulin resistance before the bariatric surgery left some important damage in the muscle, you know, and then the rapid losing weight very quickly only worsened the condition.

I do not have the answer right now, but I think that because the muscle is going down two years after that, despite of normal insulin resistance levels right now. Thank you very much. I see a hand raised by Abt Tirani.

Abt, if you could unmute and ask your question, please. Hi, and thank you very much for giving me the chance to ask the question. Thank you for the presenter for a great presentation.

I want to be a devil advocate here and say, if muscle mass is that important, and you've just shown us that muscle mass is being lost after bariatric surgery, despite the weight loss, why do I have all these great outcomes long term after bariatric surgery in terms of type 2 diabetes remission, reduction in cardiovascular disease, reduction in mortality? So maybe, and I'm just being here really very provocative, maybe the loss of a lot of fat mass, then the loss of muscle mass becomes less important for hard endpoints. Wow, you are a great advocate. No, I do not have the answer yet, but what is really true is that the muscle is important in the glucose homostasis, but is not the only factor, because as you know, we have also the gut hormones, the cytokines, and so on.

Maybe this muscle, which mass is going down, has a better function. I do not know, but it seems that when the body is trying to recover and increase the muscle mass, what it gets is increasing the fat mass. And maybe this, you know, the problem with the muscle is not the type 2 diabetes, but is that the resting energy expenditure is going down.

So there's a higher risk to weight regain after that, you know. That's why it's not just the muscle mass is just the effector, you know, but the hormones and the cytokines are the ones that are actually acting on the function in type 2 diabetes remission. But on weight regain, I think that is crucial, this muscle mass loss.

Thank you. If you are coming to ICHO, we can have a discussion about that. It would be nice to have that.

Yes, yes, yes, I'm coming. Thank you very much indeed. Some very interesting discussion there.

So thank you, Andrea. Thank you for your time and an excellent presentation. So we've heard a couple of times that there is not a huge amount of evidence and not a huge amount of research.

So that might make Marwan's presentation a little more challenging because Marwan is going to be the third and final presenter, giving an update on research through the latest publications. So Marwan Elgoh is a clinical professor and head of the nutrition and dietetics department at the Beirut Arab University. He was trained and worked for many years in Italy and he is the author of nearly 100 papers in the field of medicine, clinical nutrition, dietetics, etc.

He's also the co-editor in chief of the Journal of Population Therapeutics and Clinical Pharmacology and on many other editorial boards. So Marwan, good luck and I hand the floor to you. Thank you very much for your time today.

Thank you for this nice invitation as well and for the difficult task to handle, presenting the last publication on the topic. Actually, I really thought a lot before preparing my presentation and I have focused my presentation. I don't know if you're able to see it.

Here it comes, yeah. Yeah. Perfect.

But it was a difficult task to think about how to present the last publication and data that can be shared with people who are dealing with and treating obesity. As we can notice here, the topic of sarcopenic obesity is not that new. As we can notice, the study of this phenotype has started in the late 90s of the last century and there is a growing interest in this field reaching the 2022.

In fact, a considerable research has been conducted on sarcopenic obesity, especially in elderly with my understanding and understanding of the audience that there is a big problem regarding the screening, the definition, and as Professor Donini have underlined, I think that any definition that we would use or any tool we would use can be arguable to define or to screen sarcopenic obesity in patients with obesity. In fact, as my colleague Andrea have underlined, that there are very few data that has been published in non-elderly population with sarcopenic obesity, especially during a weight management setting. I would like to invite you to consider the data that I will be presenting as pilot studies that can leave us with a sort of brainstorming or to think a little bit about the impact of what can be the impact of sarcopenic obesity on our treatment, the treatment of our patients as well, and on the other side, how can our treatment, the so-called weight loss, whatever it is, can impact sarcopenic obesity.

From this perspective, I've tried to prepare my presentation, reporting some studies that will be focused on the association between sarcopenic obesity and the weight loss determinants, namely resting energy expenditure and the physical activity, and the relationship between the sarcopenic obesity, perhaps on the baseline of any weight loss treatment and the weight loss outcomes in the long term. Namely, I'm talking about the dropout, the interruption of the treatment, the weight loss rate, and the weight loss maintenance. And finally, I would like to present a very preliminary results about new strategies for improvement of sarcopenic obesity during weight loss in terms of diet, physical activity, and whatever.

The studies that I will be presenting right now are dealing with non-elderly patients with sarcopenic obesity. Well, in the first part, I will be talking briefly about the association between sarcopenic obesity and energy expenditure, where a research question has been reported in a couple of studies, where two patients with sarcopenic obesity, when compared to patients without sarcopenic obesity, may have a lower resting energy expenditure, I mean on baseline, or they may be prone to have a more sedentary lifestyle. In fact, this study has been published in 2020 on a sample of nearly 90 patients of both gender, of a mean age of 40, 41 years, and BMI of 34.5, 35.

The resting energy expenditure has been measured by the indirect calorimetry. And as you can notice here, that patient with sarcopenic obesity seems to have a lower resting energy expenditure. In other words, patients with sarcopenic obesity appear to have nearly 150 kilocalories per day of resting energy expenditure when compared to patients without sarcopenic obesity.

In the same direction, a study published nearly one year, one year and a half, in the frontiers of endocrinology, composed of 111 patients of both gender, with a mean age around 37 years, and a BMI of 36. Authors in this publication have measured physical activity by mean of a pedometer as well, I mean the steps. What they have noticed in the study, they've noticed that patients with sarcopenic obesity are more likely to be sedentary, I mean to have a daily step less than 5,000, plus they've noticed also that these patients, namely the patient with sarcopenic obesity, seems to achieve a lower mean of daily steps.

For this reason, the patient with sarcopenic obesity conclude that the patient with sarcopenic obesity were more likely to be sedentary and to perform nearly 1,500 steps per day less than non-sarcopenic obesity. Well, these two studies conducted in the early 2020 have led to a clinical question to say that, well, the patient with sarcopenic obesity are more likely to have a lower resting energy expenditure, plus they are more sedentary, and they perform lower number of steps. For this reason, the question was, do these disadvantages, I mean the baseline disadvantages, as reduced resting energy expenditure and more sedentary lifestyle in individuals with sarcopenic obesity when compared with non-sarcopenic obesity patients, may have a negative impact on the clinical outcome, I mean on the weight loss clinical outcomes.

Well, before talking about that, all of us, I mean under the IASOCOM, we deal with patients with obesity and we know very well that the main clinical outcomes in an obesity treatment during a weight management program are the early dropout, it's one of the major causes of failure of weight management program for obesity, with a rate that reach in certain type of treatments the 80%. The second outcome is the weight loss in the first six months, and last but not least, the third outcome, which is the weight loss maintenance, I mean 12 months and more, we know very well that 50 to 70% of patients during the treatment of obesity usually return to their baseline weight after three to five years, and this is really a big problem for us clinicians and people who deal with the obesity. So the research question was, do patients with sarcopenic obesity when compared with the patient without sarcopenic obesity during a treatment are in higher risk to interrupt earlier the obesity treatment? And to this aim, a study has been conducted in the late 2020 on a sample of 103 patients of both gender, of a mean age of 35 years, and a BMI of nearly 35, and authors in this study noticed that there was a significant higher prevalence of sarcopenia or sarcopenic obesity among droppers when compared to completers.

I mean, the patients who early dropped out had nearly a prevalence of sarcopenic obesity of about 51% against the prevalence of sarcopenia, of sarcopenic obesity on baseline of the completers, I mean, which was nearly 26%. This relationship between the dropout, the early dropout, and a sarcopenic obesity was confirmed by the regression analysis that showed there was an increase of the relative risk of dropout in the patient with sarcopenic obesity by nearly 150%. Well, in another study that had the research question, I mean, two research questions were, do patients with sarcopenic obesity when compared to patients without sarcopenic obesity achieve lower rate of weight loss at six months of follow-up? This was the first question.

And the second question was, do patients with sarcopenic obesity when compared with patients without sarcopenic obesity may face more difficulties in maintaining weight loss in the longer term? And in this study, the follow-up was on a period which exceeds the 12 months of follow-up. Well, this study was composed of 46 patients with obesity of both genders having a mean age of 44 years and a BMI of 35.71. 21 patients of the sample was affected by sarcopenic obesity. 26 were patients with obesity but without sarcopenia.

And as you can notice from this table, as well as from the figure, that the weight loss rate on the six-month follow-up did not differ between patients having sarcopenia or not having sarcopenia. However, on follow-up, it seems that the patient with sarcopenic obesity used to have more difficulty to maintain the weight loss achieved in an earlier stage when compared to the patient without sarcopenia. Well, in this setting, we've noticed that patients with sarcopenic obesity may have lower resting energy expenditure, more sedentary lifestyle, and it seems that, between brackets, that these patients, I mean patients with sarcopenic obesity, may have two difficulties mainly during the treatment of obesity.

The first one is being on higher risk to drop out in the early stages, and this is one. And another difficulty that can be noticed from this pilot study, that they have more difficulties to maintain weight on the longer term. From the opposite side, the other question here, also that we have introduced initially, what is the impact of the weight management program or the weight loss, between parentheses, on sarcopenia? And I'll be presenting the data in this recent study with a recent question, what is the impact of weight loss on sarcopenia? It may improve or worsen the weight loss.

For sure, it depends on the type of treatment. For sure, it depends on if it's pediatric surgery or not. It depends if it's a lifestyle modification or not.

However, in this study that has been published a few days ago, in a sample of 41 patients of both gender with a mean age of 43.6 years, BMI of 36. And it has been noticed that with a significant weight loss, which was around 9% of weight loss, a decrease of the prevalence of sarcopenic obesity from baseline to follow up, it was by nearly 12% was noticed. And the regression analysis showed that a significant weight loss, which is superior to 5% combined to a lifestyle modification program, to an active lifestyle, in this term, I mean, 8,000 steps, a model was created as well, seems to decrease the risk of sarcopenic obesity.

So, in conclusion, in a weight management setting, patient with sarcopenic obesity appears to have a lower resting energy expenditure and more sedentary lifestyle, plus a higher rate of early dropout and more difficulties to maintain the weight loss in the long term. Here, we are talking about a follow up that exceeds that 12 month follow up. It seems that an effective lifestyle program can improve the sarcopenia related indices in this population.

And thank you. Thank you very much, Marwan. That was very interesting, indeed.

I'll go to the chat function first, because I see that there is a question already. And it's from Abt. Thank you for a nice presentation.

The relationship between sarcopenic obesity and sedentary lifestyle, is this a cause or effect or both? That's an excellent question as well, because we don't know who arrives before as well, but it seems that they interact between each other. I mean, I don't know if the sarcopenia or the sarcopenic obesity may lead this patient to have a more sedentary lifestyle, or the contrary. In my modest opinion, I think that they can interact between each other, and they can, I mean, one can lead to another and vice versa.

I think it's a bidirectional relationship. Thank you very much. Any other comments on that? From the other faculty? No, seems okay.

Would anybody else like to ask a question? I don't see any more in the in the chat. So if anybody would like to ask anything, you could raise your hand. I just have one for you, Marwan, and it would be, okay, there is some research being done now and some more evidence is being gathered.

But it's not a huge body of evidence there. If you had, if you were in charge of the, let's say, the EU Commission's funding protocol, what would you divert your money towards researching first? The question is for me. Yeah, yeah.

I mean, if you had, if you, let's say you had a limit, limitless amount of funding, and you wanted to look into something very specific in this field, what would you, what would you, what would you prioritise? Actually, the main problems, as we have noticed from the very nice presentations of my colleagues, we have the main problem on how we can define a precise criteria to say who is having sarcopenic obesity and who's not, because I think this is a very important variable. Second, once we establish this, we need screening tools. I mean, cheap, simple, that any clinician, any dietician, in any clinic can use it in order to identify who is having or on higher risk of having sarcopenic obesity.

Actually, once we've established these, and we find that patient with sarcopenic obesity may have a worsened outcome during a treatment, our resources should be focused on the strategies that we have to adopt in this patient in order to have better outcomes. And by the way, what Andrea has said, that the prevalence of sarcopenic obesity in her practice is nearly 30 to 40%. I completely agree with her because this is also my impression.

With the dilemma that we have on the definition of sarcopenic obesity, but also in my clinical practice and the studies that I published in the four, five years, I found and reported a prevalence of sarcopenic obesity, which was around the 40%. And to be honest, I've received many criticisms about that. It will be nice to clarify this issue.

And I think it should pass through an accurate definition in order to say yes or no. As we have the criteria for type 2 diabetes, 126 for instance, is having diabetes or not, even if it's not that accurate. But we need a unique measure that we can apply in Italy, Lebanon, UK, wherever, to say that this patient is having sarcopenic obesity or not.

And this is, in my opinion, is the hugest problem. Wonderful. Thank you very much.

I see your fellow presenters have both put their hands up. So I think Andrea was just first and then Lorenzo, if I could unmute yourself, Andrea, and please take the floor. Thank you.

Thank you, John. Thank you, Marwan. Now we are two of us with the criticised for these conclusions.

I think that the answer, whether this condition is relevant or not, I totally agree with you that we need the same criteria in all countries and so on. But I think that the answer, whether this condition is relevant or not, and we have to put our efforts in order to better this condition, are the outcomes of these patients. You know, what happens with these patients during the follow-up, they regain weight, they lose less weight than the other ones, they are more diabetic, more cognitively impaired and so on, you know, even in children and younger people, because we do not have studies on the outcomes of the younger people.

Completely agree. Thank you. Thank you very much, Andrea.

And Lorenzo? Yeah, I agree with Marwan and Andrea that we need precise definition and diagnostic criteria for sarcopenia obesity. If you wait till tomorrow, you will be able to find our proposal. It is a not a defined definition and criteria.

And what we think is that it would be interesting to review all that are based, including the criteria that have been proposed by EASO and ESPN and verify using the same criteria, the prevalence and the clinical and functional consequences of sarcopenia obesity defined in a shared way by all research. And then we can go through and verify the validity of this proposal in the future. But the proposal, the aim of the proposal is just to have a year zero for the research on this topic.

The results I've shown you that we consider 75 papers in the first systematic review with 19 different ways of defining sarcopenia means that we don't know at the moment anything clear about the prevalence or the treatment of sarcopenia obesity. So, if we can review our database and our data on considering the new criteria, we probably will be able to put together this data and have a more clear vision of the situation. Thank you very much.

Thank you very much. I think that will be very helpful for everybody. And we'll share the publication when it comes out tomorrow.

It's going to be jointly published in Clinical Nutrition and Obesity Facts, and we'll share it with the Collaborating Centres Network as soon as the publication has been confirmed to us, together with the recording of the discussions in the presentations today. So, I guess if there are no further questions, I give you a few seconds to raise your hand if there are. OK, if not, well, I would like to thank our three presenters today for giving wonderful presentations and facilitating some really interesting discussions.

And thank you, everybody from the Collaborating Centres Network for participating again in this session. I think these are really nice sessions in a very relaxed atmosphere where we can have good educational presentations and discussions amongst the network. So, thank you for participating.

We'll contact you with the recordings and further information as soon as we can, and we'll communicate with everybody about the next sessions, which will be on Tuesday the 29th of March, so the last Tuesday of every month. And then it's NAFLD is going to be the topic for the next session. So, we will send information about that.

And so, with that, I close the session and thank you all again for your participation, your presentation and your enthusiasm. And we'll keep in touch and we'll be in contact very soon. So, have a lovely evening and continue to stay safe.

Thank you. Thank you. Bye-bye.

Bye-bye. Bye-bye. Good night.