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The Four Pillars of Weight Loss Part 3

Sep 26, 2026 6:09 am
Dr. Catherine Bakewell 'Pharmacologic Treatment of Obesity': https://youtu.be/K8o0ZnqySZA Dr. Larissa McGarrity 'Psychology of Health Behavior Change in Obesity': https://youtu.be/v-rGrpjqh24 Dr. Elena Philippou 'Nutrition, Weight Management and Rheumatic Disease': https://youtu.be/2EOpgsS-EfA
Transcription
Hi, I'm Catherine Bakewell. I'm a rheumatologist out of Salt Lake City, Utah, and I have a particular interest in my practice on immunometabolic disease, and so it's my privilege and pleasure to talk to you today about the pharmacologic treatment of obesity. The ACR has given us guidance that for individuals living with overweight or obesity and rheumatic disease that we should be addressing this and they have said that weight management should be pursued through diet and physical activity which can complement but not replace pharmacologic therapy. We need to remember in rheumatology that obesity is a causal contributor for multiple of our rheumatic diseases including psoriatic arthritis, osteoarthritis and gout and that it can portend worse outcomes and poorer response to our therapies in all of these diseases including rheumatoid arthritis. Fortunately, we also have data that weight loss can improve outcomes and that individuals, for example, who can lose five to 10% of their body weight or more if they are at baseline living with overweight or obesity, they are more likely to attain low disease activity or remission.

So without further ado, let's talk about the pharmacotherapies available at CURRENT. I am going to spend most of the time talking about incretin therapy since they have truly swept the market. So a recent New York Times article estimated that one in eight Americans either is on or has taken in the past a GLP-one receptor agonist therapy. These or any pharmacologic therapy is indicated for individuals with a BMI of at least twenty seven with weight related comorbidities or a BMI of thirty or higher regardless of comorbidity status. So first I want us to talk about semaglutide, which is a GLP-one mono agonist.

This is given as a once weekly subcutaneous injection and in the initial phase three clinical trial program, individuals lost an average of 15% of their body weight. This is not counting the recent 2026 approval of a high dose, so up to seven point two milligrams subcutaneous weekly, in which individuals did lose up to 20 of their body weight in that clinical trial program. Tirzepatide I'll mention next. This is a dual agonist for both GLP-one and GIP with individuals losing up to 21% of their body weight in that clinical trial program. And I want to just touch on briefly a triple agonist which is currently under development that goes by the name of retreutide, so this is a GLP-one GIP and glucagon triple agonist.

And in the phase three clinical trials individuals have lost up to an astounding 28% of their body weight. This is approaching bariatric surgery levels of weight loss. This we will hope to see approved sometime in 2027, but by no means is this the only agent currently under investigation. There are multiple agents currently being looked at, for example amylin analogues, which may have a more favorable GI side effect profile, or myostatin inhibitors which can be used in combination with GLP-one or amylin therapies to reduce some of the sarcopenia that individuals on these therapies have experienced. There were two oral agents approved.

The first was semaglutide at a dose of twenty five milligrams once daily in 2025. This is a peptide and so is more delicate, if you will, has to be taken with a sip of water and not have anything to eat or drink for a half hour afterwards. Orfaglipron, which was approved in 2026, is the first small molecule GLP-one, non peptide though, so there's no food or water restrictions with dosing which may be a therapeutic advantage. When you have a patient in front of you that you're thinking about one of these therapies, you need to make sure that they don't have a personal or family history of multiple endocrine neoplasia type two or medullary thyroid cancer. Those would be considered contraindications.

You would want to have caution in individuals with a history of pancreatitis and you would not give it to anyone who is pregnant or lactating. Most common side effects are going to be gastrointestinal, what you would expect, nausea, vomiting, diarrhea or constipation. You can treat these things symptomatically. And bear in mind this is why we, you know, start low, go slow with your uptitration. Generally speaking, uptitrating only after about four weeks at any one given dose.

Things to bear in mind are that any of your weight related comorbidities like hypertension, diabetes, hyperlipidemia, as the individual loses weight, you're going to want to peel back those therapies to avoid hypoglycemia, hypotension. Some individuals have had acute kidney injury if they got too hypotensive and were not drinking enough water. I'll mention also, touched on that sarcopenia, you need to absolutely advise your patients to be getting adequate protein in their diet, so anywhere from one to 1.2 grams per kilogram per day. So in general think about at least 30 to 40 grams of protein per meal, on average depends on the weight of the individual, but it's a lot. And they also need to be weight bearing exercising at least two times per week.

Again, I'd be remiss if I didn't mention Together PSA in a talk on obesity related pharmacotherapy. These were patients with psoriatic arthritis who were randomized to receive either ixekizumab or ixekizumab plus tirzepatide with a primary endpoint of simultaneous achievement of an ACR 50 and at least a 10% body weight loss. Needless to say, this was a statistically significant difference between the combination versus monotherapy. Ixekizumab is not a weight loss drug, but of interest to us in rheumatology is that there was a sixty four percent relative increase in the percentage of patients who were able to attain that ACR 50. They're showing a significant difference in our pure rheumatologic outcomes for in this case addition of incretin therapy to our standard of care.

So I'll leave you with three basic thoughts. Number one, obesity is a causal contributor to multiple of our rheumatic diseases and it can portend worse outcomes for these patients. Number two, fortunately this is something that we can reverse with weight loss. And so my hope is that addressing overweight and obesity will be a part of all of our systematic approaches to individuals with rheumatologic disease. Thank you for your time and attention.

Hi, I'm Larissa McGarity. I'm an associate professor and clinical psychologist at the University of Utah, and my specialty is psychological health for patients with severe obesity. And I'd like to today just share a few thoughts about health behavior change really from a psychological perspective. One thing that I always tell my trainees is that understandably, every discipline tends to look at obesity through their own lens. So a dietitian is going to think about the specific nutrition changes that are most likely to optimize health.

Physician who say is treating diabetes is going to think about the medications that will be most helpful to the patient or the lab values or the amount of carbs per meal for diabetes management. And exercise physiologist will think about the amount of physical activity that's associated with the greatest kind of cardio metabolic benefit. And all of those perspectives are absolutely important and they matter. My role as a clinical psychologist is to think about something a little bit different. And that is in this case, can this patient actually do the things we are asking them to do?

And maybe more importantly, can they keep doing it and keep doing it really long term? Because health recommendations only improve health if they actually become part of someone's life over the long term. So from a psychological perspective, behavior change is really less about identifying like what would be the ideal recommendation for this patient and more can we help patients to find meaningful changes that they can realistically sustain. One challenge in doing that is that the typical patient we see with severe obesity has often spent many years, sometimes decades, trying to lose weight. Many have tried restrictive diets, intense exercise programs, may have done commercial weight loss, and they've often lost substantial amounts of weight before.

This is usually not the first attempt and they've experienced that really common cycle of what we call the yo yo diet or weight recurrence over time. And over time, many patients have internalized a pretty specific message, the idea that I failed. That message often comes from close loved ones, family members. It comes from the media, social media, health care experiences, and eventually internalized or from themselves. So, when a patient walks into your office, they may come with years of discouragement, self blame, and reduced confidence that change is even possible.

And it turns out that's not the best starting point for behavior change. So one question I like to ask, especially when meeting patients for the first time and beginning to discuss this is help me understand, help me understand your journey with weight and health over time. Very open ended. The answer is often much more complicated than people expect. And sometimes you'll hear about pain or stress or depression, caregiving responsibilities, maybe financial constraints.

Understanding those barriers allows you to then work on a tailored plan for that patient that really addresses their needs. And that brings me to kind of a second point. As health care providers, including clinical psychologists, we spend a lot of time identifying risk factors and pathology, but we really should spend just as much time identifying resilience and patient and family strengths. And one thing I've learned from working with this population over the years is that many patients with severe obesity are remarkably resilient, and that flies in

the face of some of

the common stereotypes that I think we sometimes see. These patients have spent years managing health challenges, stigma, setbacks, yet they continue showing up and trying again. Research from my team supports this. So we've actually found in our studies that levels of resilience for patients with severe obesity are comparable to primary care norms, and higher levels of resilience are not surprisingly associated with better psychological functioning, improved health behaviors, and quality of life. So I often ask patients, what has helped you get through difficult situations before?

Or what supports you or who supports you when things get hard? Asking about the support system, asking about resources and strengths already available to them. These answers frequently then become that foundation for behavior change. And many patients with obesity don't need more education about what healthy behaviors look like or what they're doing wrong. Some do, but many have heard this many times before.

What they do need is help translating your recommendations into sustainable action within the realities of their own lives. So one of my favorite questions when we think about getting at bigger picture values for patients that drive behavior change is if you could achieve the goals that we're talking about here today, what would look different for you and your life five years from now? That again really gets at underlying motivation, intrinsic motivation, and anything that we can do to help patients remind themselves of those bigger picture values supports the likelihood that they will make sustainable behavior changes. The third point I'd like to make is highlighting weight stigma. It's been a major focus of my research where team has identified that improvements in weight stigma from before surgery, bariatric surgery, to about two years after surgery was actually a stronger predictor of many psychological outcomes than the amount of weight that people lost.

In other words, the change in stigma was more strongly associated with psychological distress, dysregulated eating, some of the things that we hope to change for patients than anything about the change on the scale. And I think that is a powerful finding because it really suggests that when we reduce the stigma patients experience or anticipate or internalize, we're not simply being kind to them. Reducing weight stigma is in itself a clinical intervention. So sometimes that starts with small changes in how we communicate instead of just being one more provider to tell the patient to just eat less and exercise more. We can be a provider who acknowledges complexity and chronicity of obesity.

We can validate their experiences and feelings. We can highlight their unique strengths, and that allows us to engage in truly patient centered care. And finally, when I talk with patients, I try not to focus primarily on weight, which may sound a little odd when what we're talking about is weight management. Most patients have already spent years focusing on weight. So at every possible opportunity where you can focus instead on function, quality of life, sustainable behaviors, you're more likely to get that momentum with patients.

So I might ask, how can we help your body and mind function at their best? Or what change could realistically fit into your life this week? The goal is not about perfection. It really is helping patients identify those changes they can realistically sustain. A modest change that they maintain consistently will almost always have that greater impact on long term health than any perfect plan that a patient abandons two weeks later.

And with that, thank you so much for your time and for the work you do supporting your patients living with obesity. If you want more information, check out resources through RheumNow.

Every meal represents a small, repeated exposure that may influence inflammation, body weight, metabolic health, physical function and ultimately quality of life in rheumatic disease. Hello, I am Doctor Elena Filippo, a registered dietitian and associate professor in nutrition and dietetics at the Universi Unicosia in Cyprus. In clinical practice, we often hear the question What should I eat to reduce inflammation? And while it sounds simple to answer, the scientific response is more complicated. Firstly, we should establish that diet is certainly not a substitute for disease modifying therapy, but it could certainly be a modifiable lifestyle factor that can play important direct and indirect roles in Rheumatic disease management.

This is because what we eat does not only have an influence on body weight and composition, but it also supplies a combination of nutrients, with potentially beneficial or even detrimental effects on overall health. Diet also influences cardiometabolic risk, of course, bone health, pain and physical function, as well as mental and other outcomes. Today, I will briefly cover three areas: the evidence on diet quality and dietary patterns in relation to rheumatic disease, the importance of excessive deposit and sarcopenia, and how we can translate this evidence into practical advice. So, let's start with the first point dietary quality. A 2025 systematic review and meta analysis found that healthier dietary patterns were associated with a low risk of developing rheumatoid arthritis, although of course the evidence was observational and a bit heterogeneous.

Similar associations between greater Mediterranean diet adherence and more favourable disease related outcomes have been reported in systemic lupus erythematosus, psoriatic arthritis and idiopathic inflammatory myopathies. So the signal is fairly consistent overall diet quality appears to matter, although causality cannot be assumed. One way of examining dietary quality is through the dietary inflammatory index or otherwise referred to as DII. In the six year Japanese Tomorrow study, people with RA whose diet shifted towards a more anti inflammatory DII had approximately three point five fold greater odds of maintaining low disease activity. Associations between a more inflammatory diet and poorer outcomes have also been reported in osteoarthritis.

And as we know, observational studies demonstrate associations rather than causation, and dietary intervention trials remain challenging because of issues such as adherence. Nevertheless, in our 2021 systematic review of 70 dietary intervention studies in rheumatic arthritis, we found promising signals for omega-three fatty acids, vitamin D, sodium restriction and the Mediterranean diet, particularly where shared mechanisms such as chronic inflammation are involved. So, which dietary pattern should we recommend? The Mediterranean diet is probably the most clinically defensible. It is rich in legumes, fruits, vegetables, nuts and seeds, whole grains, of course extra virgin olive oil and fish, and less red and processed meat and highly processed foods.

I would also add that the evidence suggests an extra intake of omega-three fatty acids, either from more frequent consumption of oily fish, such as salmon, sardines, sea beams, sea bass, walnuts and chia seeds, or through supplementation, or a combination of both. Importantly, randomised trials in rheumatoid arthritis support this approach. Some examples include the SCALDSTUM trial, which is a twelve week Mediterranean diet in patients with RA, and this produced a 0.56 reduction in DAS28, together with improved physical function. Another example is the Adira crossover trial, which was an anti inflammatory diet rich in fatty fish, whole grains, fruit, vegetables and nuts, and this study produced a modest improvement in DAS28 DSR among those participants that completed both dietary protocols. And more recently, the MEDRA trial found better physical function and quality of life following a Mediterranean diet intervention compared with healthy eating advice, although importantly both groups improved.

So, my message to rheumatologists and patients is very simple: the Mediterranean diet has emerging evidence in rheumatic disease, substantial wider cardiometabolic benefits and is a sensible pattern to recommend alongside effective rheumatological treatment. Now, let us move on to talk about body weight. Obesity is not simply another cardiovascular comorbidity in rheumatology. In The UK ERAs and Iran cohorts, among the longest running and most substantial rheumatoid arthritis inception cohorts involving more than two thousand people with early RA, Doctor. Nighifora and colleagues showed that obesity was associated with approximately half the odds of achieving low DSA28 at two years, as well as poorer function and physical quality of life.

Interventional studies also suggest that weight reduction can improve clinically relevant outcomes. We have evidence in psoriatic arthritis, RA, osteoarthritis and others. So, excess adiposity deserves our attention for sure. Body mass index is a useful starting point, but it should not be the whole assessment. We need to add a measure of central adiposity for sure.

Waist to height ratio is particularly practical, and a ratio above 0.5 suggests excess central adiposity. And here the simple patient message is: try to keep your waist below your height. If weight loss is appropriate, a sustainable energy deficit with an initial target of approximately five-ten percent weight reduction is a reasonable target. But in rheumatology, we should ask not only how much weight is being lost, but also what tissue is being lost, because muscle matters. Sarcopenia is relatively common in RA with meta analytic estimates of approximately twenty four to thirty percent, depending on the diagnostic criteria used.

And sarcopenic obesity is particularly important because BMI can miss it completely. It is also associated with poor physical function. So I would ask three questions. Does this patient have excess adiposity? Do they have adequate muscle?

And are they functionally strong? The sarcath is a very quick screening tool covering strength, walking, rising from a chair, climbing stairs, and falls. Therefore, when weight loss is recommended, protecting muscle must be part of the prescription. In older adults and particularly those at risk of sarcopenia, around one point two to one point five grams of protein per kilogram per day is recommended, but of course individualized according to renal function, nutritional status and body size. Together, of course, with resistance exercise at least twice per week and aerobic activity as tolerated.

All of this is also where multidisciplinary care matters. Patients requiring individualised dietary treatment, weight management or sarcopenia assessment should be referred to a registered dietitian, and manage This approach is broadly consistent with recommendations from EULAR, the French Society for Rheumatology and the American College of Rheumatology, which support healthy dietary patterns including Mediterranean style eating and appropriate weight management as components of rheumatological care. So, I will finish with four key take home messages. The first one is improve overall diet quality, which with support from a registered dietitian where needed. The second is that the Mediterranean diet is a sensible evidence based dietary pattern to recommend.

Third, identify and manage excess adiposity where appropriate. And lastly, when patients lose weight, protect muscle through adequate protein and resistance exercise. Ultimately, the goal is not simply weight loss, it is a healthier diet, healthier body composition, less pain and better overall health. Thank you very much for your attention.

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