Chapters Video Allan Chipps 2022 Longer description of the video... Good evening, everyone, and thank you for attending today's symposium. My name is Patricia Kazan. I'm a gastroenterologist from South Australia. I would like to welcome you to this symposium entitled Leveraging the Multidisciplinary team to Care for Patients with inflammatory bowel Disease and Obesity. The symposium is based on an interactive format that incorporates case-based discussions, didactic lecture, and audience participation. I would like to give a special thank you for our grant supporter, Lily, who provided an educational grant for this activity. Now, please take a moment to scan the QR code or input the link to be able to answer the pre-test and the interactive calling questions. You will also be able to use your devices to ask questions during the Q&A portion of the program. Finally, we kindly ask you that you set your cell phone and pagers to silent during the presentation. These are our disclosures. And those are the learning objectives. So one is to describe the intricate pathophysiological interplay between the gut inflammation and obesity. Apply pharmacologic trials findings for both obesity and IBD to optimize care of each concomitantly, and develop a multidisciplinary team approach to the management of patients with obesity and IBD. The last objective is to incorporate an understanding of the comorbidities and negative healthcare outcomes associated with obesity in the care plan for patients with IBD. Pathological processes related to obesity and inflammatory bowel disease. So I'd start with the etiology of inflammatory bowel disease, but as many people in this room know, there is not a single road to IBD. There are many roads to IBD. It's a multifactorial disease. It's a complex disease. We traditionally say it's Crohn's disease and ulcerative colitis that are immune-mediated disease of the GI tract. Perhaps more mucosal and ulcerative colitis, although we know now it can be transneural from ultrasound studies and more transneural associated with complications with Crohn's disease. It they happen in patients with genetic predisposition and this is as well a complex area and we know from very early onset Crohn's disease, we have the um monogenetic associations, but later on we have genetic predisposition and we have um genes associated with higher uh um more difficult. no ty pe s in patients uh with uh genetic predisposition due to environmental triggers that can be as well um multiple environmental triggers such as um the diet, the food, the pollution, the um breastfeeding, etc. and it triggers the immune system disturbance. So the first case of ulcerative colitis was reported in the 18th century just before the industrial revolution, and the first case of Crohn's disease was reported by Sir Beryl Crohn's in 932. It was a case of severe terminal ileitis. And then since then we have witnessed a steady increase in The incidence of Crohn's disease and ulcerative colitis in the Western world until we have reached what looks like a steady state in terms of incidence. So the incidence of this disease seems to have stabilized in the Western world, but we are witnessing an increased incidence of IBD. In developing economies in growing economies, and this is as presented multiple times in the GDW and previously is potentially due to globalization, urbanization, as we are witnessing an increased incidence of this disease in rural India, in Southeast Asia, etc. etc. So now we have a high global burden of IBD due to the compound prevalence and the increasing incidence in uh newly industrialized countries. But this is a disease that affects people who are young, um, peak age of disease is in the, in patients' 20s to 40s, make those patients are quite productive at the peak of their, you know, work life, etc. and it affects men and women similarly. The CDC findings estimate around 3 million Americans, more than this, living with IBD and we have around 180,000 Australian patients who live with IBD. It is a progressive disease and we don't discuss IBD without putting the slide that I've seen everywhere. It's a very important slide to tell us that Crohn's disease and ulcerative colitis can lead to progressive bowel damage, can lead to um progressive fibrosis, strictures, and can lead to surgery and neoplasia. We have a window of opportunity, but at the early disease stage where we have an inflammatory predominant. component of the disease to try and modify this inflammation, decrease the inflammatory burden and slow the progression to a more aggressive phenotype, the stricturing phenotype, the penetrating phenotype, and more complications. Um, so, um, where the bowel function as well can deteriorate and ulcerative colitis. So it's really important to treat this disease at an early stage and to try and optimize um the therapy, um. Again, immunopathogenesis of inflammatory bowel disease. It's a complex interaction between the gut microflora, the gut microbiome, the luminal content of the gut, and the epithelial cells where epithelial damage can happen, and it's a point of entry for microbes activating a. Downstream immune response by activating antigen presenting cells and multiple different complex inflammatory pathways that can be different in Crohn's disease and ulcerative colitis, activating the T helper 1, T helper 2, TH17, and leading to a severe inflammatory burden in the gut wall. I move to talking obesity now, and there is no question that obesity is a global health issue, and we are witnessing an obesity pandemic mainly in the Western world, but the epidemiological patterns as well are getting there in the growing economy. So at this stage, around 1 in 8 of the world population are affected. With around 41% of all Americans and 31% of all Australians living with obesity, but still there is no consensus on the definition of clinical obesity with arguments between two groups, both very legitimate about whether to medicalize or not medicalize clinical obesity. And to try and settle this debate, a Lancet Diabetes and Endocrinology Commission just a few weeks ago published a definition for clinical obesity. It's a chronic systemic illness characterized by alterations in the function of tissues. Organs, the entire individual or a combination thereof due to excess adiposity. The problem is adiposity, no question, and the the visceral adiposity is the main problem in there leading to the insulin resistance and all the complications, metabolic complications. A very good. Definition is an elevated defended fat mass set point where the body is unable to down regulate the set point basically, regardless of what of what a certain individual can do. We use the body mass index quite a lot in our therapeutic approach, in our diagnostic approach, but it is a surrogate measure and it is important. It's simple and it's usable, but it's important to acknowledge its limitation. It's unable to differentiate between the muscle mass, the fat mass, and the distribution of the fat, the visceral fat, and the subcutaneous fat that are important determinants of the metabolic health. So it is a screening tool and it is as well affected by age, sex, genetics, and ethnicity. The causes of obesity are complex. The cause of the obesity pandemic is perhaps the food environment that we live in, where we have a nutrient rich, energy-rich food which is very calorie dense, very highly palatable, easily accessible, easily available, and the lifestyle associated with this food pattern. As well, that is as well the marketing industry for the food, the ultra processed food, the, um, so and the lifestyle. But it is important as well to mention that the gene there are genetic factors for obesity. So we know from genome wide association studies that multiple genes that are associated with eating. Patterns and behaviors and associated with the neurobiology of obesity have been identified and an important role for epigenetics as well as during World War II where there was a food barricade to Holland, we have seen that the babies of starving women were born with type 2 diabetes and overweight. So obesity is adiposity and visceral adiposity, but the adipose tissue is a source of marvel for many, but of misery for many others. It's not a single organ, it's a collection of tissue depots, and each of them can have an independent functionality. Just to be very basic, the white adipose tissue is the um tissue for the energy storage, and that's where I say it's a, it's a source of marble. The brown of adipo adipose tissue is um responsible for heat production or non-shivering thermogenesis. And in between, we have the beige adipose tissue. Now, the white adipose tissue is an Theocrine organ by itself with important immunometabolic functions, it can it does secrete actually multiple adipokines such as leptin which has a pro-inflammatory role, adiponectin, an anti-inflammatory role, estrogen adipocytokines as well, such as TNF alpha. So in obesity, we see a preferential expansion of the white adipose tissue due to genetic dysregulation, as I've already said, and potentially hypothalamic dysfunction. Due to the excess fat, that there will be um adipocyte hypertrophy, and we understand now that a single adipocyte can increase in size up to 100 to 1000 times. And will include the triglycerides, free fatty chains, and um they increase in the size of the adipocytes, the ballooning, it will compress the surrounding vascular milieu. It will promote tissue hypoxia. The tissue hypoxia will promote an inflammatory cascade with a differential gene expression and cellular damage and inflammation. I'll be talking about this a bit later as well in a bit more details. The food intake control again, very important to mention that it is not as simple. It's not only energy in energy out. It is mediated by central the central nervous system, the hypothalamus, the brain stem, and the endocannabinoids and peripherally by the stomach, ileum, colon and the adipose tissue. Three types of hunger, again, I, I'd like to keep things simple. It's the nutrient hunger, which is more for protein, the energy hunger more for carbohydrate, protein and fat. And the hedonic hunger, and the word hedonic comes from the Greek word hedon, that is the Greek god of pleasure. This type of hunger can eating actually associated with the hedonic hunger can activate a dopamine release and activate the cannabinoid and the opioid receptors in the brain. So we move now to measuring the problem of obesity. I will be discussing some data from the states and and a preliminary data we have from Australia. We know from adult studies that 15 to 40% of patients with IBD suffer from obesity and another 20 to 40% are actually overweight. We've seen similar trends in pediatric patients. Um, this is based on a paper published in 2017 by Dr. Milly Long and her colleagues. So the pediatric obesity is a problem and pediatric obesity and IBD is a problem. We are about to publish some results from our work in Australia, the prevalence and impact of obesity in an Australian, actually a New Zealand cohort of people with inflammatory bowel disease. This is through the Crohn's colitis cure data insight. Programs and we have observed the same pattern, around 25% of our patients are obese and 1/3 are overweight. Or just to be uh to use a patient first term, I say suffer from obesity and suffer from overweight. This is a in submission and the slightest courtesy of Dr. Gold, but this is a this is an American data, the obesity again, this is newer, so 2025, uh high prevalence in patients with IBD with 33% of patients being obese, 65% being obese or overweight. The obesity rates vary by sex, ethnicity, and geographic regions, with African Americans suffering more than Asians, for example. So we spoke about IBD, we spoke about obesity. How about obesity and IBD? It looks like it's a tale of two epidemics that we see there is an increasing global rate of IBD and increasing rates of obesity as well. Do we have a causality effect between obesity and IBD in the modern world, or do we actually have to think about A unifying route, which is, you know, the current dietary environment, is the Western diet, or what we call the standard American diet, causing those two epidemics. I don't know the answer, but in one of the papers I published with my colleagues in Australia a year and a half ago, we looked at the impact of obesity on IBD, and we went through some epidemiological data and it Quite conflicting where the nurses health study suggests that the BMI, more than 30 kg per meter square is predictor of developing Crohn's disease. It wasn't associated with ulcerative colitis. The Copenhagen school health records register showed that childhood obesity increases the risk of Crohn's but not ulcerative colitis, but the EPIC study from Europe showed no association with both. It's very hard. Those are, uh, basically, uh, population-based cohort studies. It's very difficult to pin down a causality effect, but that's a space to watch, um. This is that was published only a few weeks ago and when I was reviewing my slides, I thought I'm just gonna add this, this is again a population-based study from um from uh Spain.s Severe obesity is a susceptibility factor for developing IBD. um I won't go through the slide in details, but this is very similar to I've just to what I've just discussed before. So now talking about obesity-related inflammation. There is a lot of things that we understand, but similar to the IBD related inflammation, there are a lot of pathways and a lot of things that we don't understand. So I've, you know, done a huge amount of literature review and I find, you know, a lot of very impressive, informative things, but we are, we don't know the full story yet. I will try to summarize what we know with the adipocyte hypertrophy basically that where the adipocyte increases in size and it's got a lot of lipids inside just to uh it will produce this uh compromise of the vascular milieu and um um induces hypoxia. Where the hypoxia is induced, a pro-inflammatory cytokine called the osteopontin is secreted and that will help the pre-adipocytes to develop um and to progress actually into B cell, monocyte, and macrophages. Now, on a lean person, in a lean person, the visceral adipose tissue can have up to 10% of macrophages. In obesity, in mouse model, we've seen 40% of the visceral adiposity occupied by macrophages and in human studies, we think it's around 40 to 50%. So those are those are obviously immune cells. There are, um, that can get polarized to two types, and this is very interesting, the M1 macrophage and the M2 macrophage. The M1 macrophage has a very pro-inflammatory activity and actually it induces the glycolysis within the microphage and it induces the secretion of um cytokines such as the TNF alpha. That seems to be that the TNF alpha was discovered 30 odd years ago and we are using TNF alpha blockers in a lot of disease now because it's involved in many diseases such as IBD rheumatoid disorder, dermatological disorders, and obesity. It's one of the main cytokines that we see in, in, in obesity in the adipose tissue. Interleukin 6, interleukin 12, and interleukin 23. And the downregulation of the M2 macrophage pathway and the M2 macrophages actually are anti-inflammatory. They play an important role in tissue regeneration, collagen production, healing through oxidative phosphorylation. That gets down regulated, the M1 pathway gets up regulated. There will be more recruitment of macrophages that will form what we call a crown-like structure around the dead adipocytes. So the adipocytes that undergo apoptosis or hypoxic deaths. And we believe those are responsible for the insulin resistance and all the complications that Dr. Gold will be discussing later during this talk. So I'll start with a case study. I like to keep things very simple. Um, I have Jim. He is a 28 year old male patient with intermittent periods of abdominal pain, with bouts of diarrhea and loss of appetite. He is single, works as a paralegal, in a desk job primarily, and has no past surgical history. His mother has a history of type 2 diabetes. He's currently on no medication. He doesn't smoke. His BMI was 25 kg per meter square in his teens and currently it's 32 kg per meter square. He was referred to the gastrointestinal clinic for ongoing abdominal pain. So 12 months of intermittent abdominal cramps and diarrhea, no blood or mucus in his stools, some sensation of urgency to open his bowels, no trigger factors to his pain. The diet include his diet included random meals, takeaway mainly to his job demands, and he doesn't exercise. He lives a bit of a sedentary lifestyle. Given Jim's symptoms and background of obesity, what investigations do we order for Jy? So we started with a full blood examination that was quite normal. We did an electrolyte test, urea and creatine and normal as well. A liver function test that showed an elevated ALT of 120, otherwise normal. And we've done a stool called Protectin that was 200. Then we decided let's try and perform an intestinal ultrasound on Jim. OK, here we go. This is the intestinal ultrasound and I'm depicting a similar loop from the terminal ileum. I've done his ultrasound and I found it a little bit more challenging due to the visceral adiposity. So overcame the challenge by increasing the probe pressure in the right iliac fossa, and we've just actually as well published a review about small bowel imaging in Crohn's disease with a special focus on patients with obesity, pregnancy, and post-surgical assessment. Um, that shows that patients who suffer with obesity can have difficult, uh, access to, um, radiological investigations. So, um, I'll leave this ultrasound. This is how it looks like. I won't describe it, just I will go ahead and um to the um MCQ. So please engage in a table discussion with your peers to explore and respond to this question. Based on the available investigation, what's Jim's most likely diagnosis? irritable bowel syndrome, Crohn's disease, celiac disease, or small bowel lymph lymphoma? I'll give you a few seconds to choose a diagnosis. One more, one more second and we will move to the next slide. So 70% of the participants think that he has Crohn's disease and around 30, 33% says it's IBS. OK, um. So The right answer is Crohn's disease, and I'll this, the patient has. Abdominal cramps. He has a mildly elevated fecal calprotectin, but on his intestinal ultrasound, I'll go back to it, we can see in the terminal ileum, there is an increased bowel wall thickness in the TI. I don't have the Doppler images in here, but there was as well a Dopplerta, more vascularity in the submucosa. So this is my working diagnosis. I might be wrong. How would you confirm Jim's diagnosis? Do we do an ileo colonoscopy, and MR enterography, and endoscopy, or there is no further investigations required? OK, that's great. So we will aim to do an ileo colonoscopy, intubate the terminal ileum if we can. Very important to see the ileoshecal valve is the stenos, can we get in there, take some biopsies, confirm the diagnosis. So we did this and the diagnosis was confirmed. The patient had active terminal ileitis based on histology. So what would be your management plan for Jim? Gut hypnotherapy, gluten-free diet, and obesity management, biological therapy, plus or minus diet therapy, plus obesity management or lymphoma therapy. Perfect. OK, that's great. So we will be discussing this a bit more in details and how to manage the obesity in somebody who has an active active Crohn's disease, illegal Crohn's disease. So the applica uh approach and therapy for obesity, from my perspective, first and foremost, it should be a patient-centered approach. The stigma associated with obesity in the community is one of the major obstacles to addressing it, to preventing obesity as well. It can be as simple as reducing the net negative energy balance by reducing food consumption, but I'd be very cautious as well about what to tell patients. So we label the diets as low calorie diet, very low calorie diet, restricted calorie diet. We, we just sometimes can give the patient a approach of blaming, you know, or punishment. Can we go to something more like a healthy diet, a tasty diet, a Mediterranean diet, etc. So it's a, I have a biopsychosocial approach to obesity. It depends on the risks for the specs. It's a different, it's a case by case, obviously different for every patient, but what are the factors. Associated with the increased food intake on a for a certain patient, that is the power model that was published quite a few years ago, but that works extremely well. So we do the obesity assessment, we initiate the weight loss therapy, we try to maintain, you know, the weight loss, and we try to make sure the patient doesn't regain weight. Doctor Gold again will be discussing more details her cause she runs the IBD and obesity clinic. The multidisciplinary team approach she, she does, but the psychological interventions are very important, behavioral therapy is important. I always send my patient to a dietician who has a special interest in both obesity. And IBD, um, and that works quite well. Um, that is always social and environmental factors, food triggers, behaviors that is that we live in a stressful environment where a lot of us are subject to what we call strain, which is our inability to cope with our day to day stress, and sometimes we just go home after a long day at work and we decide we want to have a very rich, nice meal as a um treat. OK. I, I won't go, uh, I'll leave those guidelines, we can leave a copy for everyone. Those are good guidelines, uh they were published in 2016, so we have a lot that's happened since then. Um, for the management of obesity, again, they rely heavily on the BMI, which is not necessarily a bad thing, but I like was the wasted conference as a better, uh, measurement of clinical obesity, and I think we should start integrating this in our obesity clinic and our IBD clinic because it will help us understand things better and conduct better clinical research. So the currently approved obesity medications as you can see here, and I will probably be focusing on the last 3. I've got an experience in, in prescribing the GLP1 receptor agonist more than the first medications. So the luagglutide, the semaglutide, and the tisappatide. We had a a few studies published in 2020. and 2022 um about the weight loss effect of the GLP1 receptor agonist wegovisemaglutide, and the GLP-1 GIP receptor agonist isapetide mujaro where people patients achieved a significant weight loss. So what are GLP ones? Those are incretins and those are hormones secreted in the endo endocrine cells in the gut, mainly in the ginum and the ilium throughout as well, and they basically are secreted in response to a meal and they can activate the beta cell in the pancreas to secrete insulin and that will help. That will help people glucose uptake in the cells, and that's where the problem is in type 2 diabetes. Perhaps those GLP-1 memetics, they are very similar in cretins. I think the the pharma only change one amino acid, so those are not cut by the DPP-4 enzyme and so they can, you know, stay in the serum. And they have a very robust weight loss effect. So tiapetide, uh, that was a Sermon one study published in the New England Journal of Medicine in 2022, and we can see that there's a huge, uh, delta between the placebo and the tisapetide medication that most of the patients lost a significant amount of weight, around 18% um. Of the baseline weight over the study period, which was I think 772 weeks and very similar to the semaglutide, the overall percentage of weight loss was a bit smaller, but very significant as well. And those are both approved for type 2 diabetes. For example, in Australia, we can't access them through the PBS for treatment of obesity, but when needed, they're very important and I've been prescribing them. Any patient with a BMI more than 30 or the BMI. More than 27 with obesity associated metabolic complications, those medications are suggested as adjunct therapy. We don't, we don't prescribe those medications and tell the patients to eat and not exercise and eat excessively, but they can come, they should come in adjunction to diet therapy, to lifestyle changes, including, um, uh, um, including aerobic training and resistance training at least 3 times a week. OK, this is, this is a bit of a challenging slide, and it's very hard to talk about modern management of IBD in one slide. So I'm gonna ignore the slide and just talk. Uh, basically, it's complex and it depends on the IBD type and phenotype. Is it alternative colitis? Is it Crohn's? And in Crohn's disease, is it ileal Crohn's disease? Is it perianal Crohn's disease? Is it colonic Crohn's disease, all of this. And whether the patient has extra intestinal manifestations, um, and which one. So I don't, I don't like summarizing it because each of them needs a whole talk, but basically we have very uh uh simple therapies or like 5 ASAs uh for mild ulcerative colitis. We have non-targeted immunomodulators that can work for both ch. An alternatives. We have targeted immunotherapies nowadays, biological therapies, TNF alpha pass, the TNF alpha pass where that's um that's involved in the obesity related inflammation, but we have as well other um anti-integrans, lymphocyte sequestering therapies, uh, small molecules, etc. The issue is that in most of the cases. There is a plateau, and 1/3 of the patients don't respond to initial therapy up to this, up to 40% sometimes, and another 1/3 subsequently have a secondary loss of response to therapy. So on top of us trying to find novel therapies, which is, which, which, which is heading, which what we're doing, we should try to optimize the, the therapy that we have. And in patients with obesity. City we have realized that the biological therapy don't work as much. We have some prospective data from Andrea Aroor here showing that higher infliximab levels may be required for patients with higher visceral adipose tissue. That was a prospective observational study of 142 patients, and he measured the quartiles of visceral adiposity. Um, and he found that the infliximab trough levels associated with remission outcomes varied based on the VA vis adiposity burden. The higher it is, the lower, the higher the levels of the infliximab that we need. He published a similar study later on looking at 4 approved biological therapies with similar um results. So what we need to do is to try and shrink the visceral adiposity. Um, and to try and recapture response. This is what, what I think at least, um. So the role of GLP1 receptor agonists in inducing anti-inflammatory response while treating obesity. Now, the mechanism of the TNF alpha, for example, the loss of response to TNF alpha or the poor response in patients with obesity can be explained by multiple mechanisms, but we think that the TNF sync phenomenon where the TNF alpha blockers that we are given neut uh is being neutralized by the act. cytokine of the visceral adiposity and not working properly in the gut perhaps, but the GLP1 receptor agonists have receptors in the gut. We have seen from mouse studies that in um induced colitis mouse model GLP1 receptor. could treat the scholitis. So we don't have any prospective human data, but very reassuring retrospective data. It has a strong anti-inflammatory effect through the NF k Kappa Beta pathway that's strongly as well involved in the IBD pathogenesis, and it can decrease the pro-inflammatory cytokines. So I'm aware of two big Prospective studies, a randomized controlled trial that is being that is about to start called the commit Crohn's disease and commit ulcerative colitis. It's by Lily as well, uh, which is a combination of medikizumab andti appetite for Crohn's disease and one is for Crohn's and the other one is for ulcerative colitis for patients who have a BMI more than 30 or more than 27 with a comorbidity. In terms of the safety data uh for GLP1 receptor agonists in IBD, there's clinical data for uh the GLP one through nationwide registries mainly and mainly for patients with diabetes. Um, so there was no apparent difference between IBD and non-IBD patients in terms of the efficacy of the GLP1 receptor agonists for weight loss. In terms of safety, the data is so far quite reassuring, um, as well, it's all large database studies, similar side effects to non-IBD population. Uh, the side effects are all dose dependent, and we know this from non-IBD patients, but typically mild to moderate and usually within, they will resolved within the first few weeks and if they don't, we stop the medication. Uh, the most common cause of cessation of this therapy is the cost. So that's one of the biggest obstacles, I think. Um, in terms of the gut side effects, nausea, vomiting, diarrhea and constipation. The discontinuation rates 5 to 10% in trials, but as I said, it's higher in the real world because patients have to self fund this medication, at least in Australia. OK. So I move to my second case study. 335 year old female patient with left-sided ulcerative colitis, diagnosed 7 years ago, works as a part-time copywriter. No surgical history. Her mother has a history of breast cancer and father passed away in an accident. She's on infliximab 500 mg 8 weekly. Started a year ago after an episode of acute severe ulcerative colitis. Her BMI is 30 and her weight is 105. Despite initial response to therapy, the patient experiences recurrence of bloody stools, urgency, tennisness, fatigue, and mild abdominal cramping. Those are her investigations in one slide. Her hemoglobin is 122. She has normal white cell count, a mildly raised CRP. The albumin is 33, so mildly low. The fecal calprotectin was 3,872. That's a very high fecal calprotectant, and her trough level for inflexima was 3.3. The flexible sigmoidoscopy shows a male two colais. Those are not ulcers. This is mucus, and her intestinal ultrasounds show some transmural. This is activity in the sigmoid. You can see those little flecks of uh Doppler, the red ones in the submucosa. So she does have Mao2 disease in the left colon. Given the clinical and endoscopic findings, what's the most appropriate next step in managing Lisa's condition? Short course of steroid therapy and continue with the same dose of inflixima, short course of steroid therapy and switch to a DAC inhibitor, colectomy, a short course of steroid therapy, intensified inflixima regime, and anti-obesity therapy. OK. Now, I'm not any, I'm not sure if anyone has any comments, but I would like to ask, how would you treat the obesity and our GLP1 receptor agonists useful in patients with active IBD? Do we prescribe them? We have some good safety data so far. If a patient has active colitis or active Crohn's disease, is it safe or is it OK to prescribe GLP ones? If anyone has a comment, please let me know and I can discuss with you. I mean, as I just said, there's no prospective data, there's no prospective study, so, um, to reaffirm the use of GLP one in active IBD, it's my personal practice that I've been using them, and I have started roughly a year ago, so I do have some. Some follow up data and I find especially with patients who have a big like a significant visceral adiposity, a high waist circumference. This is the way of my way of measuring it. Uh, I prescribed both imaglotide withgovi and Monjaro recently and I've had reasonable effects, and I think in two cases, both perianal Crohn's disease on infliximab, I could recapture response and improve trough levels. But again, there's no data that is a big grant that was given to one of the American centers to conduct a prospective study, and that is this randomized control study that's about to start. Um, sadly, we're not involved in Australia in the study, uh. How should obesity be managed in patients with active IBD? And what's the role of GLP1 receptor agonists in this setting? OK. You can engage with your peers to explore these questions and maybe Stephanie can take over and discuss a bit more. Thank you. Published Created by Related Presenters Allan Chipps, MD
