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My name is Professor Barry Laird and it's a pleasure today to give this talk on cancer cachexia. Entitled to early recognition and compre Comprehensive Care is m disclosures. And the only objectives for this short talk are to trying to recognize and diagnose cancer cachexia earlier and consistently to apply validated diagnostic frameworks and integrated bedside and er tools, electronic medical record tools. So what is can say, well, you've all seen it, it's a condition that affects people with cancer, with heart failure, with end stage chronic obstructive ovaries disease and other conditions um usually towards the end of life and what it looks like clinically as patients become increasingly weak, fatigued and they have a reduced appetite and they become refractory. And that means the essentially will not respond to cancer treatment. And this was initially described by Hippocrates actually 2.5 1000 years ago. Um you know, kind of it comes from the great for, you know, wasting in bad state. So it really is a bad state and in terms of, you know, technically defining it well, efforts have been made over the years to try and bring together some, some form of consensus. So this study here um on this paper here um shows a nice figure of what is it goes from a pre cachexia stage, the cachexia stage and refractory stage. So a key point with this is that cachexia is not just one single point in time, it's really a transition that patients go from having very minimal or, or no weight loss. But they have the underlying metabolic change right through to a degree of cachexia where they have more great degree of weight loss or they kind of a low BM I and they often have reduced food intake with systemic inhalation and in the final stages, refractory cachexia. So this stage of cancer disease is usually proca not responsive to treatment. But at this point, survival is usually, you know, reduced to less than three months. So a key concept is that cachexia is, is a spectrum of of, of a condition. It's a technical um definition. Um Here is a multifactorial syndrome characterized by an ongoing muscle loss with or without fat fat loss. So this pause there. The key concept with this is it's ongoing muscle loss, but you don't have to have fat loss. And that's important because we know that loss of muscle will adversely affect outcome. So if you lose muscle, you lose the muscle in your leg, you lose muscle in your arms, you lose muscle in your, your chest, swallow, you lose muscles that help you to breathe properly. And you lose your heart or some muscle. So you start with cardiac tissue too. So this loss of muscle is potentially much more damaging than loss of system for fat. That's the first key concept. The second key concept is it cannot be fully reversed by nutritional support. Simply giving people who have cachexia, more energy or more calories is not enough to fix the problem. The final key comment is that it leads to progressive functional human patients become weak increasingly and unable to do their general household activities and interact with family members. So that's what it looks like. Weight loss, usually muscle plus or minus fat, you can't fix it just by giving people more calories and people become weaker to ultimately death. What's going on in the background of of this clinical phenotype? Well, it's an abnormal metabolism. Um it's a negative protein and energy balance. Essentially the body using up many more calories than it's than it's consuming and also combined that with reduced nutritional intake. So this has been sort of working definition for the past 4, 14 years and this was set up really as a sort of starting point to try and progress the cachexia research agenda. However, there's been various attempts to try and refine this over the years and this is quite a nice paper published um called cancer and cancer. What's in the definition and what they did here was they took a two different types of um Kie definitions. The one is the, the, the, the criteria which is the, the top top one you see here um Table A and the bottom one is the Evans criteria and both of these and criteria to use some and similar features we quite untranslated and the A criteria they include a marker of systemic inflammation. Now, I remember if the previously they talk about cancer being driven by an abnormal metabolism. So in the Evans criteria, they tend to incorporate this abnormal metabolism aspect by looking at systemic inflammation. And you can see here on these two survival K Meyer survival curves. The top one being the there's a clear difference in survival between patients who have no cachexia versus cachexia. However, in the es definition that this this disparity between the two groups is actually quite dramatic. So essentially including inflammation and the definition of cachexia is a, is a key component in prognostic outcomes. Now, we could take it even further than that. Um definition. This is a colleagues in Glasgow wrote this paper saying you listen to a simple objective framework. They developed a score called the Glasgow prognostic score which combines albumin. It's a marker of nutrition, c reactive protein, which is AAA marker of systemic inflammation and developed a simple framework going from a score of 0 to 2 the Glasgow prognostic score. So intentionally a score of zero, somebody has either um a a normal level and reduced um C reactive protein but look, it's all weight loss is not common in Germany. No metabolic upset. So no intervention is here for the next um group of people, they have a lower albumin slightly lower than the reference range. But again, they zero is normal in patients. They've got some weight loss, but there's no metabolic upset. In other words, there's a background, biological changes of cachexia haven't happened as yet in these scenarios. It's essentially just a case of trying to improve their um nutrition. Be a dietary, inform me dietary interventions. But once you got a score of one, when patients have a race c reactive protein, they were saying these patients are now are now um systemically inflamed. Then it's important, you know that they actually could consider some form of dietary intervention and also maybe some anti-inflammatory treatments. The final stage really is gastro prognosis score of two people are hypoalbuminemic and they're also systemically inflamed. And these patients, they have both severe weight loss often and metabolic upset. In these cases. Potentially the main treatments should be dietary intervention but also referral to important or palliative care or guidance. This is a very simple way of categorizing patients using it, a biomarker based approach. So really what you can see over the last 14 years from the Evans definite the the definitions through the Evans in this sort of simple cachexia framework proposed by Macmillan, et cetera. This is hard to inform the guidelines that are widely used. So the guidelines for cancer and nutrition, which the, the, the paper up here, these are the most highly CED guidelines in the area of co and nutrition. And they talk about um patients that a call to action for patients with cancer. So the key thing they say is they should screen all patients with cancer for nutritional risk and in the course of her care. So every single patient who get cancer should be screened for nutritional rest. And it shouldn't make a difference depending on the body mass index or weight. A even if somebody's overweight or has a high BMI I, they're still at risk because cancer cancer is predominantly loss of muscle. So it's important that we screen for these people irrespective of their body mass index, overweight. These some people, I would argue that body mass index is actually quite AAA poor measure. And it's also important to bear in mind that in the Western world, there's a lot of people who are overweight. So we have a thing called sarcopenic obesity patients being overweight but actually can still be losing muscle. They also say that we should increase nutritional assessment. And in that they are quite clear that we should include measures of systemic inflammation. In other words, the biological changes that are happening in cancer conia and they suggest the Glasgow Pro is that and then guidelines also say nutritional interventions should be individualized, suit that patient, their dietary needs also their cultural needs. Their socioeconomic needs, we should be focusing on increasing nutritional intake, decreasing systemic inflammation, hyperbolic stress, and increasing physical activity. And the reason we want to increase physical activity is because that helps maintain muscle or even promote muscle build up. And also if people are eating more as they're exercising more, you get post prandial anabolism, which is essentially the muscle building up after meals and that's a beneficial concept. So there we have gone from this a rudimentary definition to the importance of information and our clinical guideline if you take this in one step or the G group. So that's the global leadership initiative for malnutrition. I've approached, I produced it.