ECPO 2019: Complexity of Obesity & Q&A session Jon Hazelhurst


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Hello everybody. My name is John A. Woodhurst. I am a clinical lecturer in endocrinology and diabetes in Harvards Hospital, which is an AASTO centre for obesity management.

Excuse me, could you speak a little bit slower? Oh, sorry, yes. Do you know what, I’ll move your mic a bit. Let’s try, yeah.

Yeah, sorry, you’re quite right. And I have that in my head as well, because obviously lots of people here are of different languages, so I’ll try my best to slow down. If I do start talking quickly again, if somebody can just shout at me, it will be very well received and it will be fine.

Okay. So, as I say, my name is John. I’m a clinical lecturer in endocrinology and diabetes.

I work at the Centre for Obesity Management, which is at Harvards Hospital in Birmingham. And I’m also an academic at the University of Birmingham. And I’m really pleased to be here today to support this group and ACPO in particular for all the great work that it does.

It’s really nice to be here. And actually the introduction, I think, was key. We’ve heard lots already about what the idea today is to share.

And I don’t feel I’m here to teach. I also feel I’m very much here to learn. That said, I am obviously going to cover a lot of information today.

Hopefully in a slightly clearer way than you might have heard before. So lots of people in this audience are fairly expert, and I’ve met lots of people in this audience before at different meetings. And I know that you’ll have heard some of these kind of talks before, or at least some people will have done.

But I also know that there will be other people who haven’t heard this kind of talk before. And I’m going to try and make this as clear about the message that I’m going to try to convey as I possibly can. And I would be wearing my people-first ribbon, but I haven’t got anything to stick it to.

But I’m pleased to have that on my initial slide. So I don’t really have any significant disclosures. Some of my professional training is supported by Novo Nordisk, but I haven’t had any money off them for speaking engagements or anything like that.

I invite you to ask me lots of questions. If there is anything I say that isn’t clear, or I’m speaking too quickly, then please shout at me. That’s fine.

I will ensure that I use people-first language and non-stigmatising images throughout the presentation. If I say something that is not people-first, accidentally, when I’m talking about data, I invite you all to tell me and to shout at me, and that would be very well received. So don’t worry about that, but I’d be surprised if it happened.

So I guess the framework of the talk today is about obesity as a disease. And of course, obesity is a disease, and I’m going to cover why that is in the coming time. And we’ve got quite a long slot, so there’s plenty of time for discussion as we go.

I have obviously written a presentation to be the framework for this session, but do feel free to ask me questions as we go. That’s not a problem. There’s plenty of time for that.

But as part of thinking about obesity as a disease, and to help as part of this event, and this kind of empowerment training, I’m going to try and provide some responses to why some people say that obesity isn’t a disease. Now, just to be very clear, that’s not my position, and that’s not my outlook, and that’s not represented by the centre I work in or my colleagues, but it’s my job to try and provide you all, I think, I hope, what my brief is, some answers to what some people say. And that’s how I’m going to frame the talk.

Now, this is obviously a very mixed audience. I imagine there’ll be people from every profession in this audience, and every walk of life, because that’s the nature of obesity. Obviously, some of you will understand scientific data very rigorously, some of you will be slightly unfamiliar, and I’m going to try and walk you through some of the data that I’m going to show in a fairly accessible manner.

As I say, if there are anyone who’s unsure, please do tell me. What the slides are mostly going to look like, and this might seem like a strange thing to do, but just to prepare you all for what you’re about to see, is you’re going to see quite a bit of data. That might be some graphs, it might be some diagrams, all sorts of things.

In a yellow box, you’re going to see the kind of design of that study. So I think some of what we, kind of in the obesity community, get criticised is people say, oh, that study was only done in however many people, or it’s not relevant to a wider population. So all the research I’m going to talk about, I’m going to try and explain who that was applicable to, and why it matters to certain populations.

And then in the red, you’ll see some hopefully very clear take-home messages, which I hope are very consistent. And then when we see these academic talks, the bottom little bit in the black that’s always tiny and too hard to see, is the people that did the work that I’m going to talk about. And actually, all the science that I’m going to talk about today, all of the data that I’m going to talk about today is all, I think over 90% of this is freely accessible information.

You don’t need to pay any subscriptions to any academic journals, or there’s no paywalls about what I’m going to tell you. So if you want to go away and do further reading around anything I talk about today, everybody in this room has access to that information. So I don’t want you all to necessarily agree with everything I say.

I want you to think carefully about what I have to say. And if you don’t agree with me, that’s absolutely fine, and I kind of welcome that discussion. Equally today, I might say some things that resonate with some people, because I’m obviously going to present the kind of wider data.

And if something resonates with you, or you find it upsetting or distressing, and that’s obviously not my intention, then we can obviously talk about that as the day progresses. So, as we’ve all talked, lots of aims. What’s obesity? And that’s going to sound like a very strange thing to this audience, but it’s actually hugely important in the classification of obesity as a disease.

Does medically or perhaps metabolically healthy obesity exist? That’s another really important area, thinking about obesity as a disease. How common is obesity? What causes obesity? What are the consequences of obesity? And that will be in the framework all of, is obesity a disease? A little bit around some interventions. I’ll have a bit of a focus on whether diet is effective.

I’ll talk a little bit about some medications, and I will obviously talk a little bit about bariatric surgery, and I will also cover some of the data and science around stigma as well. So, I was going to start at the end with some conclusions, in case everybody decides to fall asleep, and that’s fine. It is an early start, after all.

Now, obesity has clearly got a major adverse impact on people at an individual level, the healthcare system, and also to an extent the economy as well. Preventing and treating obesity is a public health priority, and you’ll see that I said and treating. This can’t be either or.

We mustn’t focus all our efforts on prevention or all on treatment. It has to be a kind of a joined-up strategy. There are obviously some things that are aimed at prevention that might benefit people undergoing or seeking treatment as a kind of follow-on, but we must think about these things joined up and slightly separately as well.

Now, obesity is, I’m going to show you lots of data shortly, is obviously a multifactorial chronic relapsing disease, and that word relapsing is key. It’s caused by complex genetic, environmental, and biological interactions. If anyone doesn’t believe me, I’ll be convincing you of all of that shortly.

It’s not caused by failure, a lack of willpower. Weight regain, which is an extremely difficult area, and you’ve heard about some of the studies already from IASO, is driven by biology. It’s extremely difficult, and I’ll explain why that is shortly, and it’s not related to willpower.

Recognizing obesity as a disease caused by a combination of genetic predisposition, as well as some what we call modifiable risk factors, so things that we can try and change to an extent, can lead to policies addressing the obesogenic environment as well as increasing access to treatment. So, what is obesity? That feels like a strange question, but actually this is crucial, because it’s answering the question, how can obesity be a disease when we don’t always know what it is? I’ll explain what I mean by that in a second. This is the World Health Organization definition of obesity, and here you can see that it says, overweight and obesity are defined as abnormal, their word, not mine, or excessive fat accumulation that presents a risk to health.

Now this is the opening bit of their definition, that there’s more to come. There’s a few things in this that are very positive, and there’s a few things in this that are not so positive. The fact that it identifies fat or adipose tissue accumulation as being central, rather than body mass index, is a real strength of this opening definition, and I’ll explain why that is in a moment.

And the association with a risk to health is important, although I don’t find the word abnormal to be that helpful, and obviously defining excessive is extremely difficult as well. And that’s why the WHO’s definition goes on, perhaps predictably, to talk about body mass index. And it says that it’s a crude population measure of obesity, it’s the body mass index, and as we all know, that’s a person’s weight in kilograms divided by their height in metres squared.

And they say that a person with a BMI of 30 or more is generally considered obese, and obviously that should really change now to have obesity, but I guess this is a slightly out of date definition, I’m sure that will be revised by the WHO. And a person with a BMI or equal to more than 25 is considered to have overweight. Now there are clearly ethnicity differences in BMI classification, and to be fair to the WHO, they accept that body mass index is a crude population tool, and it clearly doesn’t apply to every individual, and we’ll see why that might be shortly.

So when we think about body mass index, it is useful at the population level, and I’ll show you some convincing data about why that is, but it doesn’t necessarily tell you a lot about the person that you are, or that you’re talking to in clinic, it tells you about a big group of people and the risk of certain things happening at a whole population level. And this is some data, a few years old now, done in America, and it compares percentage body fat to body mass index. And all the data that I’m going to show you today is going to be about adults, unless I explicitly say this is about children.

So everything you’re going to hear is mostly about adults, because that’s my particular expertise. And you can see that BMI is along the bottom, and body fat percentage is along the top, and it’s separated by gender and age. And there does look to be what we call a correlation, so this line is fairly straight, and that tells us that as BMI goes up mostly, percentage body fat goes up.

Well, that’s kind of fair enough, that’s what we would hope to see if BMI is perhaps useful. And then once we just start to overlay some lines, and there’s two red lines here, one is at that magical BMI of 30, and the other is overlaid at a body fat percentage of 25. And look at all of these people that you can all of a sudden misclassify, and each of these little blue dots represents a person.

So all of the people down here, by BMI, have been told that they have obesity, but actually look, lots of them have got a very low percentage body fat, so what’s actually that person’s real metabolic risk, whereas the people up in the top left, who’ve got a normal body mass index, have actually got a significantly elevated percentage body fat. So there’s an enormous amount of misclassification at an individual level with BMI. That said, I’ve said it’s not great at an individual level, there is important data at a population level, and this is an enormous, what we call a registry study, so it’s kind of population numbers.

So in the top panels, this is 3.6 million adults, bottom panel is 2 million adults who have never smoked, and these are mortality risks, and the red lines represent a body mass index of 30. And you can see here that at a population level, there is an increased risk of mortality beyond the body mass index of 30 at a population level. So it doesn’t necessarily tell you about the person in front of you, but as an entire country, or Europe, or the world, that’s kind of inconformative data, and it’s separated by different causes of mortality.

We’ll see that slide again soon. But actually, how relevant is that to people? And I would suggest not very. So some of you will already be familiar with the Edmonton Obesity Staging System or Scoring System, and I’m going to explain that in more detail shortly.

But you can see here, this is the historical classification of obesity by the WHO, by BMI criteria. Class 1 obesity, historically, termed the body mass index of 30 to 35. Class 2, 35 to 40.

Class 3, body mass index of more than 40. And this is a survival graph. So if everybody in this study, I haven’t put the numbers on here, but big, big, big numbers for a massive American study, prospectively followed up.

If everybody survived in this study, that line at the top would just go straight across along the number 1. So unfortunately, as this line falls, that actually represents people dying. And you can see here that different classes of obesity, there’s no separation whatsoever of the data, is there? And this is the BMI data over here. So this is complete overlap.

So actually, the BMI classification on this population had no impact, really. And you can see that thing fairly clearly there. On the other hand, on the Edmonton school, and I’m going to come back to exactly what that is soon, when we look to think more about the person in front of us, and the… Yes, please.

For the white hand graph, do you have the survival data for normal weight people? Yeah. That obviously is available, but not within that paper. So that was just separated out.

That was a study of people living with obesity. So that would be really important, because actually what we’d like to see is, is there a separation at all on this? No, that isn’t in that paper. It’s a really important question, actually.

And then on the Edmonton obesity staging system, so black line is 0, and I’ll explain what that is in a minute. Red line is 1, green is 2, blue is 3. That will all become clear what that means shortly. You can see that there’s a big separation about survival.

So there’s a big, big difference. That’s far more… I would argue that that’s far more informative than body mass index. Yes, please.

Again, the left slide only includes people with BMI over 25. It only includes people with a BMI of more than… I think slightly higher than 25, actually. Yeah.

So no people with normal BMI. Correct. It would be very interesting to have… It would be nice to have that on that graph to see the differences, although we know from some of the very large studies, one of which I briefly mentioned, some more are going to come shortly, that there is a separation based on body mass index, which are going to come up.

And we know of the separation from body mass index, and I’ve told you that the EOSS score separates even further. So it’s a fairly powerful tool. Yeah, but I would love to see how the EOS state zero compares with… Yes, absolutely.

..with normal BMI. And I think that’s a crucial question when we’re thinking about obesity as a disease. And we’re going to come on to some data around metabolically healthy obesity in a second, which I think will in part answer some of your thoughts and queries.

Thank you. And why is BMI more common and more used than EOSS? Because it’s extremely easy and cheap to do, and it requires no time at all. I don’t agree.

Because it’s a thing from insurance companies. Yeah. So the origin, as you say, Garth, is the origin of body mass index was a Belgian mathematician many, many years ago who was looking to design a population tool for an insurance company.

No, no. Sorry, I’m from Belgium. I’m a statistician.

I know this was designed for nothing to do with insurance companies at all. The Cordelet Index? Cordelet Index was designed on young soldiers in the army. Yeah.

Had nothing to do with insurance companies. So what was the origin then? Where’s that myth come from? Huh? Where’s the myth come from? The classification was made in the United States using the Kitteler Index. So the Kitteler Index was actually made as something to describe how fat the recruits were.

In one number? Yeah. But nothing to do with survival. Yes, yeah.

There clearly must be a lot of myths and counter-information out there. I think that’s probably something we’ve all heard many times before. It sounds like a couple of us have certainly read about it.

So that’s part of being here today, isn’t it? To dispel some of the myths on both sides. It was made in the early 19th century. There was nothing going on with overweight and obesity then.

I don’t even know whether there were insurance companies then. Okay. Take care of your mom.

Can I ask a question? Because maybe we use BMI because it’s known since really a very long time. It’s very easy. EOSS is really far more recent and it’s more difficult because you have to stage the psychological aspects, physical aspects, everything before making the stage.

So it’s maybe more complicated. You’re absolutely right. And after all, for BMI, all you need is a height and weight.

And for EOSS, we actually need to have a proper detailed assessment and a conversation about that person living with obesity. And I’m hopefully going to argue that that’s crucial to treatment strategies and aims. So one of the criticisms of BMI are that it is a useful population tool.

I’ve said that it might be less applicable to an individual’s risk. There obviously doesn’t take into account body fat distribution or differences in muscle versus adipose. There’s no correction for lean mass rather than adipose tissue mass.

But actually, many centers, it’s all we have potentially. There are other ways to assess adiposity or obesity. For example, measures of body composition like DEXA.

But the downside of that is it incorporates a small exposure to radiation, which is obviously something best avoided if it’s not necessary. But there is some data about waist-hip ratio and I’m going to come on to that in a moment and as to why that might be relevant, particularly when we start to unpick metabolically healthy obesity. So this is from the same American cohort, around about 15,000 adults.

And actually this is quite interesting because this is the beginning of what I’m going to talk to you about with the metabolically healthy obesity paradox and what that means. And I’m going to explain that clearly in a second. But you can see here, this is some mathematical modeling.

But if you can imagine a person with a body mass index of 33, but a comparatively lower waist-hip ratio. And then up here in that red circle, there’s somebody with a body mass index of 22, but a higher waist-to-hip ratio. And then if you compare the mortality risk of these two groups, very interestingly, the mortality risk was greater for the person up here.

This is a model, but for the example person up here, with a normal body mass index, but increased waist-hip ratio. So that starts to speak to me about the distribution of adipose tissue and metabolic risk. When I speak to people in clinic, who’s more at risk of subsequent complications, assuming there aren’t any to begin with? Somebody who has a body mass index of 40, who’s perhaps very active, very muscular, their adipose tissue is distributed evenly.

Somebody with a body mass index of the same 40, but actually they’re less muscular, and their adipose tissue is all accumulated central abdominally, what we know increased risk is. So in this study at least, normal weight central obesity, defined here by waist-to-hip ratio, was actually associated with a bigger mortality risk than BMI-defined obesity. So we really do need to look a little bit beyond BMI, and think about people at an individual level.

And that’s really part of the key message of this data. We do need to talk about metabolically healthy obesity, and whether that exists. And that’s a very contentious area.

And actually at ECO this year, I guess some of us were there, and there were some fairly heated debates from the audience. There were some fairly strong believers in metabolically healthy obesity, I think it’s fair to say. And there are some fairly strong deniers as well.

And I don’t think I’m going to necessarily be able to solve that today, but I am going to tell you what underlies what I think, and my interpretation of the data. And I invite you to think about what it might mean to you, or perhaps to people you know, and come to your own conclusions. And really this is designed to answer the question that people pose, which is, well some people with obesity are really fit.

And that’s obviously true, there’s no discussion about that. So how can it be a disease? And that’s the question that underlies what I’m going to talk about in a moment. And the central theme to this is what’s known as the obesity paradox, and whether or not this is true.

And for people that aren’t familiar with the obesity paradox, and it is a bit strange, I’ve just crept a definition from a paper. And what it says is that it appears that some people with a body mass index in the obesity or overweight range have got better short and long term health outcomes than those with a normal body mass index. And that might relate to some of the data I just showed you about where we perhaps carry our adipose tissue perhaps.

Research suggests that the obesity paradox might be in part due to physical fitness, and there’s quite a lot of debate about that, and physical activity. Now, in my opinion, I think when we think about metabolically healthy obesity as a paradox, I think the key to this paradox is how we define obesity. Because lots of the studies that examine metabolically healthy obesity are so BMI reliant, and I’ve told you that that might not necessarily be the best measure of adiposity in an individual.

I personally question the idea of metabolically healthy obesity, and I’m going to show you some data in a second that you can also think about. So this is what we call a systematic review, so some of you might be familiar with systematic reviews. It’s where the researchers analyse data from lots of other well, in this case not actually that many, but from other research studies and analyse them together.

And this is a comparison of people with metabolically healthy obesity, just over 4,000 people in the total pooled analysis, and people who were metabolically healthy but defined as having a normal weight. And this is a comparison with more than 10 years of follow-up of these two different groups. And I think it’s important to see here, and this is all-cause mortality, including cardiovascular events.

And you can see here so the dotted line represents no change at all. As we move this way, this is the summary statistic here. Some of you might be familiar with that, but because it separates this way it shows us that there’s an increased risk in these people who were defined as having metabolically healthy obesity.

And actually, clearly that’s been studied a lot. Here’s another study, this is a UK GP registry database study and I think the average follow-up in this study was between 4 and 7 years, that kind of time frame. More than 120,000 people defined as having metabolically healthy obesity.

So that was defined in the study as a raised body mass index, but without any complications present in terms of diabetes, blood pressure, dyslipidemia. I think sleep apnea was included in this study too. And this graph, if the line just went straight across, that would mean that everybody was staying healthy.

So this isn’t about survival or mortality, this is about if it just goes straight across the green line that would be about staying healthy, if it goes down that’s about becoming unhealthy. And you can see that lots of these people who were defined as having metabolically healthy obesity at the onset of this study developed metabolically unhealthy obesity with follow-up. And another study, this time an even bigger cohort of people, again a registry study, and this time it’s 3.5 million adults in total, so this is a pretty large study of people defined as having metabolically healthy obesity.

The figure I’ve circled shows the 96% increased risk of heart failure across the follow-up interval of this kind of patient group. So what lots of us believe from our interpretation of the data, and feel free to disagree with me, is that metabolically healthy obesity is a risk factor for all-cause mortality and for cardiovascular disease. And I think at least in some it might only be a temporary state of health.

And I do firmly believe that that’s what the data shows. There are always people that will disagree with me about that and there will be individuals who live with obesity who obviously do not develop any consequences or complications and obviously we very much want that to happen. But I think on the large data sets and the data that we have available, I do think that’s what the data shows.

So the next question I’d like to answer is how common is obesity? And this is really to answer the question well look, 650 million people in the world surely don’t have a disease. And that’s obviously something that people say. My kind of immediate thought to that was this 2015 study which showed that 422 million people in the world have got cardiovascular disease.

It’s important to note though in that study that cardiovascular disease was classified as a composition of various cardiovascular diseases and it does slightly artificially inflate that figure. But whatever we think, the status quo of saying obesity isn’t a disease isn’t working. So something fundamentally has to change.

And how common is obesity globally? This is reasonably recent data from the WHO and dark blue means that obesity is more common in those countries. And you can see that obesity is common throughout the world. Obviously there is some protection for areas in the world of significant and extreme poverty.

Although some of the data that I haven’t, I’m not going to show today, actually shows that some of the increased prevalence in obesity that we’re seeing, so obesity being more common is actually being driven by rises in rates of rural obesity rather than in urban obesity. And that’s quite interesting data but I’m not going to touch on that today. This is data from fairly developed countries from the OECD data and some of you in the room might be from some of you might be from some of the countries listed here.

On the left hand panel, the light colours are that self-reported data. So that’s perhaps less reliable than some of the darker bars where we’ve got direct measurement data. And on the right it’s divided by gender.

No big separations in these very developed countries by gender of male and female differences. But actually in the world at large there’s some very significant separations. In some countries obesity will be far more common in men.

In other countries it will be more common in women. And some of these countries are actually in very close geographical proximity which is very interesting and not at all understood. That’s why I’m going to stay away from it today.

And when we think about obesity and obesity prevalence we’ve got to think about what’s happening over time. This panel is from 1975 and it’s not ideal because it actually shows the average BMI of the underlying areas rather than the prevalence of obesity which is perhaps not a great assessment but this is the data that was available. And on the right it’s the 2014 average BMI.

And this is data from 20 million, well near enough, 20 million adults in 186 countries of the 200 countries that they tried to get the data from. So this is fairly significant and shows that the situation is clearly changing. So the current status, yes please.

So my big question and the struggle that I have and one of the big struggles that we’re having, which I’ve actually outlined in the ARB session at the World Service for Public Health a few weeks ago, is that there’s a big difference between saying obesity is a disease but what sort of disease? So a chronic relapsing disease which is what ECPO is absolutely advocating as is ARZO and others in the community. So all that you’re saying, lovely, absolutely fantastic and I’m going to go into that tomorrow in my session with the jury. Sorry, too fast.

But my big question is how do you translate scientifically all of the data and evidence explanation into saying up front this is a chronic relapsing disease because that is the big issue that we’re facing certainly on a policy level. I’m going to come to the relapsing component shortly. Don’t worry.

I think I’ll be answering that question subsequently but if I don’t then just tell me again. Or at least trying to because I don’t think there is actually a clear answer. So when we think about obesity and I’ve told you that obesity prevalence is rising, let’s just have a quick look at bariatric surgery and this is surgery registry data from 2015 The dots the black dots represent the number of bariatric surgeries performed per million of the population and the shaded columns represent the number of surgeries in total performed at annual.

So you’ll see that some countries with a slightly smaller population are actually doing a lot of bariatric surgery per 1 million population. For example 2015 data identified Belgium as a country that does a lot of surgery relative to the size of the population and unfortunately the slide that’s disappeared is about prevalence of obesity in each country because you can see here in the UK, well actually in England this data here, there’s actually not much bariatric surgery per million of the population but the prevalence of obesity is higher in England than it is certainly in Belgium and it is in France as well. So it looks to me that there’s a bit of a mismatch between areas where obesity prevalence is high and the delivery of perhaps the most effective treatment for obesity.

The statistics, the numbers are important because we have a health system that allows this to. For example in France it works because in France we can use a system to treat ourselves whenever which is not the case in other countries. So it’s about basically access because in France and Belgium you can just go straight whereas in other systems like the UK for instance it can take up to 3 or 4 years to actually get a referral so that will reflect on So this is direct access what you’re telling me to the health care system to different parts of it so say I know the Belgian system really well I’m a GQ level I know the Belgian system very well and basically once people have made that decision to be treated we don’t need to do all of the prevention stuff it’s a different budget, different part of the system we can go straight to surgery.

And how long does that pathway pre-surgery take from someone that’s perhaps seeking surgery or wants surgery? In my particular case I could have had surgery within 2 weeks I chose to make it take 6 months and did my research but it could have taken me it could have taken me 2 months It’s very interesting because in the UK we obviously have this tier 3 medical weight management system prior to bariatric surgery and there’s no data that our tier 3 weight management system is effective or helpful or predicts outcomes in people undergoing bariatric surgery and I’m very happy to say that because I’ve looked at our own data in the UK we have a slightly artificial barrier that applies to most of the people seeking treatment where people have to go through this period of time pathway assessment intervention prior to surgery that’s not always a very good idea and sometimes it’s fairly bad in certain centres in Scotland and in London there are Scottish representatives present who might tell me differently but I know from some of the Scottish data that some people in Scotland who are seeking bariatric surgery are expected to lose a certain percentage of their body weight before they actually have surgery and there’s no data whatsoever that that’s useful helpful or predicts outcomes so we don’t have that in England currently in the overwhelming number of centres but we don’t have that access sooner I am going to talk about bariatric surgery shortly but I do think some sort of pre-assessment process before such a significant thing as bariatric surgery is important and I’m sure that does happen in France and Belgium but it sounds like it’s a shorter time pathway and that’s got to be a good thing actually it’s not on paper it can be long but the reality is in Belgium depending on where you live it’s the Belgian way of let’s find a solution so you can run through depending on where you are and what your relationship is how well you can walk through the system so it should really take 6 months but in my case I could have done 2 weeks because of where I happen to live you can get back from some local situations to the chart itself the chart tells us something about the difference between the health system but nothing about the risk prevalence so that might be the missing part if you look at the total number of severely obese people and compare to those numbers that’s actually the slide that somehow disappeared because you’re quite right and unfortunately what that slide shows is that the more common obesity in that country the less surgery that happens and I hope no more of my other slides disappear but you’re quite right because that’s the crucial point and I’m really heartened to hear some examples from other European countries and partners with shorter pre-op intervention pathways and in our own centre in Harlan Hospital in Birmingham we are now going to be in a new 3 month pathway but that’s particularly aimed at people with established type 2 diabetes so it won’t necessarily be for everybody but we are trying to improve our own pathways and speed for patients where we can because it’s extremely important but when we think about what causes obesity there’s obviously lots of genetic determinants and this is an answer to the question that I don’t believe and I probably would rather people didn’t take photos of this question because I don’t believe it surely it’s just caused by eating too much and we’ve all heard that and actually I have patients in my own clinic who tell me that which is interesting in itself and some people here will be involved in I’m not and I’ll hopefully have time to show some of that data although it may be being talked about later in the weekend So I’m also going to talk about genetics and biology and a few other things as well and this is that diagram that always gets shown in all of these talks from the Foresight report in 2007 where the speaker speaks to bamboozled people as far as I can tell and I think this is quite bamboozling actually even when it’s subgrouped like this and what this is is a systems mapping approach generated by 300 experts from different organisations including some people living with obesity and experts across different fields that are related to obesity to try and think about some of the causes and contributors to obesity so when people show you this, that’s the origin of it so people can put that in a bit more of a context and you’ll note that nowhere on that slide does it say lack of willpower anywhere on that, clearly that’s not relevant How big do you need to print that to be able to wait? Exactly and that’s why I said from the outset that I think this slide is sometimes used to confuse and bamboozle so that’s why I’ve included it today to try and demystify the origin of that because it’s kind of a waste I actually want to know If I want to read the individual things how big do I need to print it? A1 A1 you’d be able to read it and at the centre of that process although you can’t see is appetite regulation within the brain and I’m going to talk about why that’s overgrown and re-genetically driven and within that panel that I’ve shown you before this time classified slightly differently grouped differently but ostensibly the same diagram there’s lots of different drivers to dietary habits and energy intake and lots of different contributors as well to energy expenditure So we also need to think about genetics as a major driver to obesity and this is a study of 340,000 adults most of those of European origin and this is what we call a genome-wide association study so this is a study that looks for lots of very tiny changes within the genetic material and it doesn’t necessarily tell us about the gene involved but it tells us about the location of that change, that’s what these kind of studies tell us when we talk about gene loss or genome-wide association studies and all I really want you to see is that of the signals that are associated in this study with obesity defined by body mass index the overwhelming signal when these locations were grouped by genes that were expressed in different tissues that the signal was clearly within the central nervous system it’s within the brain and that’s really the key regulator of obesity in my opinion it’s the genetic regulator of appetite lots of other things as well that I’m going to talk about but I think that’s a really important thing that we’re going to come back to now you always see about these twin studies they’re quite easy to criticise and they’re very old as well this is the first of the twin studies I’m going to talk about today this was a study of 101 twins 40 were identical and 61 were non-identical and these are children who were studied at age 7 and I don’t really like this image and I don’t use it in every presentation but I thought I would share it with today’s audience I think some of these images are fairly out of date in modern society we all know that identical twins are more similar to each other than non-identical twins we obviously all know that and that applies to all sorts of characteristics but it also applies to obesity and adiposity as well the most striking data though I think in regards to the twin studies is this Swedish twin registry study and this is now of twins who were studied actually as adults so not age 7 but studied as adults and it’s self-reported values of body mass index but with a significant attempt at validation of that self-reported data as well and it’s looking at some twins, so identical and non-identical who grew up together, so in the same house same mum and dad etc and also some groups of twins who for whatever reason were separated and grew up in adopted environments or in foster care and grew up apart and the average age of separation of twins that grew up apart was less than 3 years old so separated quite early in their life and then their body mass index is studied as adults and what I just want to show you is that in these monozygotic, so exactly the same genetic material twins the twins that were reared apart so I don’t know if they weren’t reared but grew up separately the correlation of the body mass index was 0.7 so you can imagine their BMI was 70% similar as a way to perhaps think about that and then breed together but those twins that were the dizygotic, so the non-identical twins that were reared together, grew up together the similarity in BMI is only 33% so that really speaks to me about the genetic signature underlying obesity so these are people growing up with essentially near enough the same well identical twins in different environments ones growing up perhaps even in this country or in this city and yet actually the body mass index more closely matches well I’m a statistician if I look at the women I see different… yes exactly there’s a separation isn’t there but also I see that for the women the identical twins, it’s exactly the same yeah I mean I think that is probably a so this is monozygotic twins that grew up apart and obviously grew up together and there was no difference whatsoever so I guess one way to look at this is actually the female data is almost even more convincing because actually here you can see that the only clear difference is where they grew up and the data is exactly the same some of that of course will be a feature of the numbers and the statistical size but I think it’s reasonably interesting data and I think it does show that most of the body mass index is determined I think by genes at least in these kind of studies I can give one more thing to add to that women have one more thing in common they definitely have the the the microchondrial they come from the mother so microchondrial DNA is identical for women always so what we’re talking about here is we have our chromosomal DNA half from mum and half from dad and our microchondrial DNA as well and that’s the point you kind of which is all just from mum and that could easily be a potential explanation of some of this particularly the role of mitochondria in energy expenditure and this is again some data from systematic reviews grouping together some of the available studies and this is just data from some of the non-twin studies and this shows what happens in terms of heritability so the genetic influence on heritability on body mass index and it shows here that across age development there’s an extremely high near enough if we skew the data slightly around about 75% in these kind of studies looks to be from genetic causes but ok why do we always talk about these twin studies from well over 20 years ago and how relevant are they to the non-twin population these slides always get trotted out and I’m sure some of you have seen them before and I think this is actually a really important study this is a study that was only published this year and I think it’s actually fundamental in how we classify and think about the causes of obesity and I’m slightly surprised it didn’t get more coverage and traction it’s a study of 2 million genetic changes that was looked at in more than 300,000 people from birth to when they were malnourished and from that 2.1 million common genetic changes the authors derived what we call a polygenic risk score so it was a score based on the number of accumulated genes that they thought were relevant to being of higher weight and the number 1 is you’ve got a fairly low score and the number 10 is you’ve got a high score so they were deciles of score and what you can see at birth there’s not much difference in scores but by the time you’re 18 this is people over here with a high score and people on the left with a low score and look at the separation in weight by age 18 just from a study looking at a genetic score and actually when you look at I’ll just flash this up when you look at data on middle aged adults or people at a higher risk and a lower genetic risk the weight difference here is actually 13kg that’s obviously a significant amount of weight and I think this study is really important when we think about the genetic causes of obesity lots of the previous genome wide association studies they only usually explain a very small percentage of variance in body mass index but I think this study is actually quite crucial to how we think about the genetics of obesity and obviously we all perhaps have seen some slides around monogenic causes of obesity so now I’ve just shown you lots of different genes adding together and perhaps contributing to obesity and now just one or two slides on problems with a single gene contributing to obesity and all of these genes are implicated in how the brain responds to various chemicals and regulates appetite and the column on the right it’s not a complete list but that’s just a list of some of the genes known to have monogenic changes that can drive obesity but of course everybody says when you hear about monogenic obesity you may have heard or seen some slides of families perhaps with monogenic leptin deficiency and then people receiving recombinant leptin and have an incredible change in body mass index and weight but these are very rare and overwhelmingly these are rare conditions but I am going to come on to perhaps why they might not be quite so rare in just a minute and I’m not going to talk about monogenic obesity today because I think that is something all of itself but these causes are very rare and surely people say well when someone has got a problem with one gene causing obesity isn’t it very obvious? and people say that to me and I used to do clinics in a condition called Barley-Weedle syndrome and also Alstrom syndrome which are syndromic conditions that include obesity and patients with those conditions have a group of symptoms and signs and findings on examination and results that make it clear enough at least to me that that’s the diagnosis but actually what about people living with obesity who seem just like you and I and perhaps don’t have anything to make it obvious that somebody has got a particularly rare condition or a syndrome or anything like that and this is a study that I think came out from France looking at more than 2,500 people with obesity and more than 2,500 controlled people and it was looking at mutations in the MC4R receptor which I just flipped back is a central receptor for lots of the processes regulating appetite and what they found I’ll just go straight to the conclusion very interestingly was that in the controlled population so people without obesity the prevalence of the mutation was 0.15% so very very rare but in people with obesity the prevalence of that mutation was 1.7% that’s a very high prevalence of a genetic mutation in an unselected cohort an unselected group of people with obesity and what they also showed was that the chance of if you had that mutation whether you were not obese or whether you did have obesity the chance of you having obesity was 60% so that was the penetrance of the mutation so there’s going to be a lot of people in the world who have this genetic mutation and there are some drugs being designed to treat people with this particular mutation and actually bariatric surgery can still apply and be effective in people with an MCR4 receptor mutation but actually it’s a hard thing to diagnose because we don’t have access to genetic testing apart from certain fairly rare circumstances in my own service it’s very difficult to do genetic testing for obesity and there’s lots of arms I have to twist and people I have to convince to get that to happen so what people say is you’ve said genes are really important but look the genes aren’t changing genes aren’t changing are they but obesity is becoming more common and I showed you this slide earlier on this is the average BMI in 1975 and 2014 yes the prevalence of obesity is increasing the genes haven’t changed in that interval but the environment has and I’ll ask you to talk about that and also some biology as well I’m going to talk to you now a little bit about the biological determinants of obesity and this is to answer well look if the genes are so important and our genes haven’t changed why is prevalence increasing and that’s partly biological partly environmental because this has been a bit death by powerpoint so far I’m just going to share some experiences of people I look after obviously there will be nothing identifiable in any way about some of these relevant conditions I’ll actually start right to left because I’m an endocrinologist I need to start in the green endocrine box Cushing’s syndrome a patient around 6 months ago a lady who had lived with obesity for most of her adult life and had type 2 diabetes but her weight had been stable for many years actually no real change and in over a period of about 3 months she put on 20kg of weight in just 3 months and her HbA1c her overall measure of diabetes control had gone from being in target to being significantly elevated and she was referred to our general diabetes clinic please can you help this lady who’s diabetes control is getting worse I suppose we could say but obviously I had a detailed conversation around her weight trajectory and what was happening and her diet it became very clear that there was something else happening and because of the way her adipose tissue was distributed she struck me as somebody who may well have this very rare condition that we call Cushing’s and then we obviously did the biochemical testing and sure enough she did have Cushing’s and she had a fairly large adrenal tumor of about 4.5cm which has now been removed and we’re now anticipating significant improvement in her diabetes control and potentially her weight as well and we’ve got a number of patients who’ve had that condition who’ve had an experience of quite significant weight gain and then weight loss post surgery but it is a very very rare condition and we mustn’t test for it indiscriminately outside of certain circumstances and one of that is the change in weight and weight trajectory if we think as well perhaps about perhaps this box over here, hypothalamic obesity so part of hypothalamic obesity and I’ve told you that appetite is mostly regulated within the brain there are a few patients at the moment who’ve had brain tumors called craniopharyngiomas which directly invade the hypothalamus the area of the brain responsible for lots of things but in particular appetite regulation being what so this is a patient who’s had her tumor removed she’s now deficient in various hormones that come from the pituitary gland because that’s been damaged and partly removed as part of this surgery and these two ladies I’m thinking of have now got profound hypothagia so they’re really driven tippies and they’re both working very hard because they know it’s because of the tumor and the surgery and the radiotherapy and they’re working incredibly hard to try and overcome an enormous biological signal and it’s very, very, very difficult indeed and they’ve got other complications that make things tricky so for example they’re both on steroids and I’ll talk about steroids in a second so we’ve now got both of those ladies on a GLP-1 agonist I won’t name which one because they both have type 2 diabetes as well so they meet our criteria locally I don’t know how significantly that will be effective in those two patients and they may well undergo bariatric surgery but these are just some biological examples of people we meet and look after who perhaps have got something slightly different driving their obesity you say that’s surgery, is that any surgery or just surgery on the hand? where are we looking, which column? third column on the top it really is brain surgery brain surgery just being the devil’s advocate for a minute you started off the talk with how that chart reached adult patients with obesity from a well-developed standpoint to saying different diseases a lot of different diseases have just one common effect which manifests in having more weight I completely agree with you I think if I’ve heard you correctly what you’re saying is that obesity is set for different diseases as defined by its different causes and I couldn’t agree with that statement anymore I think that will become clear when we revisit some of the conclusions because actually obesity is clearly multifactorial as I’m increasingly showing you and treatments and responses have to be bespoke to the person but they’ve also got to be fairly bespoke to the cause as well and in every other type of medicine we would identify that as a slightly different disease a related but perhaps different disease so I think that’s a completely fair point and there’s other things as well I mentioned steroids just a moment ago lots of medications that people are on are clearly very obesogenic lots of people in the world need to take steroids around about 2% of the adult population in Europe will be prescribed steroids either inhalers, tablets or creams creams less so but inhalers and tablets have a weight gain effect and of course insulin lots of people with type 2 diabetes or type 1 diabetes as well rely on insulin and as we know as diabetes control changes and the overall control perhaps sometimes gets worse I don’t really like that word but I’m not sure what else to say the dose of insulin often goes up and that has an effect on people’s weight and then the weight goes up, people become more insulin resistant and then the insulin goes up and then the weight goes up and perhaps some of you in this room might have experienced that kind of biological phenomenon and it’s very difficult to break that cycle there are some drugs that we try and use but it’s a very difficult cycle whilst the patient is experiencing that conflict between controlling their diabetes with ever increasing doses of insulin appreciating that that ever increasing dose of insulin is also going to have a significant effect on weight as well but what about the environment and how it interacts with our genetic risk and this is really to answer the question a little bit that if genes are so important and our genes haven’t changed why is obesity prevalence increasing because of course a few of the things I’ve told you in the kind of biology section the rates of some of those conditions is increasing but overwhelmingly it’s not so there’s clearly something else that’s a significant driver and I think everyone in this room would agree it’s the world in which we live and the lives that we sometimes have to live so the real godfather academically speaking of the term obesogenic environment is this academic who’s based between Australia and New Zealand who previously coined the term, I think in the 80s when he’d been studying the Pima Indian population on a ranch, a reserve farm in Arizona and he’d seen the effect that adopting a so-called western lifestyle that we all hear about on this kind of indigenous population and that’s really the kind of origin, just the general interest of the obesogenic environment one of the things there’s a lot of data around now is the availability of takeaways and processed food and out of home eating I’m not sure if I really should nick this slide so if you wouldn’t mind not photographing it that would be great it’s quite a good site though it only applies to the UK unfortunately but those of you with a general interest might like to have a play with it because it’s very user friendly and it’s called the Food Environment Assessment Tool and this is just the number of takeaways in different counties within the United Kingdom so the darker red areas the more takeaways and when we drill in on a smaller level the blue arrow is our Heartland Hospital the kind of fiasco centre of obesity management that I mentioned earlier on in that red box around that blue arrow that’s only really a few streets and what you can see here in the few streets just around where I work we’ve got somewhere between 3 and 5 takeaways just across those few streets and we know from everywhere I live you live I’m sure as well unless you live somewhere very nice and rural in which case invite me to come and I’d love to come and visit everywhere we live the amount of takeaway food that we’re exposed to it’s constant isn’t it and I don’t know about you guys but certainly for me when I’m tired, I’ve been working hard etc etc and I’m frustrated it’s so easy to go and have a takeaway when everything is just there and it’s very very difficult to overcome that biological and environmental and genetic drive this is quite an interesting study looking at takeaway exposure in around about 5,000 adults in the Cambridge area and what they looked at was the effect that being exposed to takeaways had whether it was around the home whether it was near work whether it was when they were commuting for work or a combination of all of the above and what the data showed was that the more exposure you had to takeaways you had an increased body mass index I don’t think that will surprise perhaps anybody but I do think it is useful to actually prove some of these things when you might be thinking about implications for policy so for example Birmingham City Council now has a restriction on new takeaway restaurants and it has actually stopped a few being developed because it has a rule around no one particular given area and I think this is a really nice study really carefully done by Kevin Hall in America looking at the effect of ultra-processed against unprocessed food and it is only a small study but I do think it speaks to me a lot about the biology of what’s going on in response to exposure to the food that we are exposed to and this is a study of 20 adults who were defined as being weight-stained and they were housed in a research unit so it’s not the real world, everybody is asked to come and live essentially in a research centre for about a month so it doesn’t sound like a lot of fun to me and they are randomised in a random order to one particular diet or the other diet some people will get this diet first and then that diet some people will get that diet first and then the other diet completely kind of random design and the meals that they are offered are matched for what we call presented calories so that doesn’t mean the calories that people eat but it’s the calories that are available within that meal so they are matched for presented calories that include energy density macronutrients, sugar, salt and fibre and the people within this study I’ve cropped that word subject from the paper the people that were instructed to consume as much or as little as they wanted so there was no you’ve got to finish it all you’ve got to eat half it was here’s your meals, eat as much or as little as you want that was the advice in this carefully chosen design study between a processed diet with a very well matched unprocessed diet and the top line shows how much energy was consumed across the day and in the very processed diet there’s a significant increase in the amount of energy that people consume compared to the unprocessed diet and the bottom panel shows the body weight change in measured in kilograms so this is only two weeks of being told you must always eat this processed food or you must always eat this unprocessed food very well designed, very carefully designed by only a very small number of people and it just shows the kind of food that we are surrounded by constantly the effect it can have on us and very interestingly in the unprocessed diet the healthier perhaps diet ghrelin, that important hunger hormone was lower and PYY satiety hormone was higher the study wasn’t powered to look at the causes of this difference, it was just to look at energy expenditure but it shows to me that we are surrounded by a lot of takeaways and the food that we are surrounded by is clearly obesogenic can we modify some of the obesogenic genetic signal that we have and this is a study looking at physical activity and it shows here the minor allele, the people who are at most genetic risk from this particular genetic change which I don’t need to explain and you can see that physical activity which is black and white is no physical activity physical activity which was self defined in this study had a differentiating effect on body mass index but look again, because actually by body mass index criteria the people who had the greatest genetic risk had a body mass index of more than 30 but how much more than 30 at least in this study seems to be at least in part controlled by physical activity and there’s a number of reasons why it’s important to take some of these studies with a slight pinch of salt so perhaps genetic risk might be to an extent modified by physical activity and some of the data is supported by fairly large systematic reviews with meta-analysis but I can’t show that here and what about the interaction of sedentary behaviours for example watching television and exercise and this is a study of around 10,000 people and it’s an effect of genetic risk score on changing body mass index and what it shows is if you start off if you start off over here on this side here perhaps not doing much exercise and progress this way to doing more exercise the effect that the genes had on BMI was perhaps and here if you watch lots of television compared to watching less television and that was clarified by hours per day but I can’t remember the numbers it looked to have a small modifying effect in that particular study using that particular genetic risk score so here by the scores that they used here it looks like there was a potential modifying effect of physical activity and TV watching or body mass index in this study and in fact much can be said and I’ll whisper a couple of slides now in the interest of time in sugar sweetened beverages as well so people with a higher genetic risk seem to be more susceptible to the effect of sugar sweetened beverages just once a day on markers of obesity so all this genetic risk people say to me, it’s so small most of the studies they only explain 1-3% of the variance in BMI and you’ve just shown that it can be partially modified by exercise and changing sensory behaviours or exposure to the food environment so how important is the genetic signal really? and that’s not my question but that’s the kind of thing that people are going to say when you start talking about some of that data and I refer you back to this study once again which I think is so important which I think very convincingly shows us that the more genes there is the more risk and this is a really powerful study looking at lots of different gene locations and a big number of people and the people with the most genes as middle aged adults have a 13kg difference between the high and the low school people so this is a really clear to me study showing that there is a major effect not a statistical effect not a the grass does this type of effect but a real effect that affects real people by genes in an unselected population so I think there is a clear genetic basis for obesity risk and what about the in utero environment because people say of course well look if the genes are so important don’t some people just need to make better choices when they are adults so we use the word choices and that’s the kind of thing that people say but how can that be possibly true when I’m about to show you that the effects of things that happened before we were even born have a very significant effect on us as an adult and I hope some of this is kind of convincing now the top panel looks between the difference between women who had only had the one child so they weren’t previously pregnant is the black bars and the grey bars is women who had previous children as well so nulliparous, so they hadn’t been pregnant before or multiparous, which means they had been pregnant before and on the left it was about the mothers body mass index in early pregnancy and as was the right and here we’re looking at the percentage body fat in their offspring, importantly studied as adults so not as children, but studied as adults and you can see that there looks to be a separation in some of the data that’s shown and underneath those three different colours that’s about what happened to the mothers weight in early pregnancy so the white bars is the mother didn’t gain much weight and the grey shaded bar is she gained a little bit of weight and the black bar is she gained more than the recommended amount of weight which obviously weight gain in pregnancy is the sake of health and is normal but these women gained more weight than would be recommended and that showed here that the women who gained more weight their offspring were at an increased risk of gaining weight themselves, but you could say to me well that’s all genetic, the child’s got the same genes as the mum so what do you expect, and I’m going to come on to that obviously in a few moments and here this is looking at mum’s pre-pregnancy body mass index on the left and on the right her gestational weight gain, so how the weight changed and this is now studying the change in adults body mass index between the ages of 17 and the ages of 32 and I think what you can hopefully fairly convincingly show is that there’s a big difference and there’s a big change, even when you match it for the genetic signal and I think that data is fairly clear that what’s happening in utero is extremely important even as adults and if you don’t believe me here even when we correct the genetic risk every time it is important as adults as well well will you believe me when I show you Scottish data from 40,000 adults with available birth data and when we look at the classification of the mother based on her weight status as determined within the paper you will see that there was an increased risk of cardiovascular disease mortality in the adult offspring and what this classifies, what the numbers mean is that when the mother was classified as having obesity within the study there was a 40% increase in the chance of cardiovascular disease mortality in the adult child so it’s very important and there’s lots of studies going on it’s not my area but there’s lots of studies going on thinking about obesity preconception but also in pregnancy as well so I’m just going to try and very quickly link some of these causes together and I hope I’m still well okay for time because there’s still a bit more discussions to be had but trying to link some of the causes together I think I’ve shown that we’ve got some predisposed individuals whether that be genetic I haven’t talked about it in genetics today but maternal programming who are living in an obesogenic environment having adopted a westernised lifestyle I guess that term is still in fashion now because that’s just luxury to an extent we’re doing less and less home cooking we’ve got a significant availability of out of home eating with a high availability of calorie dense but also processed food actually just a comment that I didn’t mention that very carefully controlled study before with the processed food versus the unprocessed food study one of the very interesting things I think from that study is the speed at which the processed food was consumed in terms of calories against time compared to the unprocessed food we eat processed food far more quickly than we eat unprocessed food which is interesting when we think about biological changes in response to eating at the end of hunger and the beginning of satiety we’re also exposed to food marketing all the time I won’t name a particular company but there are fairly major fizzy drinks companies that seem to sponsor everything but we’re surrounded by advertising endocrine disrupting chemicals is probably a bit of an emerging field some chemicals are involved in stain resistance and they can have a direct effect on adipogenesis but I do think that’s a bit of an emerging area and actually there’s a big effect of socioeconomics on obesity that’s not consistent between different countries so in some countries you will see that people who live with more poverty live with more obesity and in other countries you will see the opposite pattern but in certain environments there does look to be a clear socioeconomic factor because of course typically when we think about diet and hopefully you’re all aware of the issue with diet is about what actually can people afford when we think about diet for those people who support low carb diets not everybody can afford to necessarily follow that very strict diet regimen and also reduce physical activity and that’s partly because of the built environment IT based leisure time, transportation work demands, perhaps it’s to do with safety in our neighbouring streets do we feel confident to go outside, are we safe to go outside there’s a huge amount of implications I’m not an expert in the obesogenic environment I’m coming at this from more of a biological angle but I’m just trying to give you some of the key causes one of the things I do want to be really clear about is that I’m going to talk about some of the consequences of obesity in just a second obesity isn’t merely a risk factor for metabolic disorders it’s not a condition, it’s a disease in its own right and I think we’ve got to be really consistent as a community that it’s a disease in its own right not a condition, not a disorder and not a risk factor and I think it’s important, some of you might agree that’s fine, but I do think we have to be fundamentally on message about this kind of key area sorry John, actually I’m interrupting you making a message, but on the previous slide have you observed synergistic effects between the different causes so there’s a fair bit of data around that because obviously when we think about choice, again lots of choice is actually genetically mediated behaviour is largely genetically driven so there’s a fair bit of data about perhaps the food we consume or the activity we do, and how it ties into genetics so all of these signals interlink and that’s why your point is key that obesity is perhaps best classified as not one disease but very many diseases perhaps at the end defined by increased adiposity but of course we’re going to talk a little bit about some of the consequences of obesity and I’ve shown this slide before and this is just a trip back to VMI data but remember we spoke about the Edmonton Obesity Staging System earlier on, does that project? can you see that, can you see the words? just about, yes because remember earlier on I showed those graphs and the BMIs all look the same with all those different people but in the Edmonton Obesity Staging System they’ll do a difference and this really speaks to me that actually what the individual is experiencing is crucial in their assessment and you’ll notice when you look at some of the examples in the grey boxes I’ll give you a minute to look at them that actually Body Mass Index doesn’t really track so look at that green Body Mass Index from Green Stage 1 up there this is an example of someone with a 38 year old lady with a Body Mass Index of 59, broad eye hypertension, mild low back pain, knee pain and that patient has Stage 1 obesity by this letter of this law you’ll see here Stage 2 this is now a man who’s got a Body Mass Index of 36 obviously a lot lower than, that’s lower than 59 but he’s got primary hypertension and obstructed sleep apnea and that’s more informative than saying this person has a BMI of this or this person has a BMI of that and we know actually that the people most least at risk are those with a score of 0 but actually that’s not very common and I’ve shown you this separation already we’ve had lots of questions and I’m keen to talk a little bit about bariatric surgery data and we also have some room for some more questions so I’m going to deliberately whiz through a couple of slides I’m going to briefly mention cancer I’m going to briefly mention Cancer Research UK and this is just a graphic that I won’t go through that can link perhaps how obesity might be might be implicated in certain cancers they recently led a very stigmatising campaign some of you will have seen it the word obesity was put onto cigarette packets and various other elements of the campaign as well and it was in my opinion unhelpful and it was stigmatising but what I worry about at a people level is the risk of delayed presentation because of stigma particularly around cancer and the risk of misdiagnosis I hope no one here has heard this but people are often told who live with obesity that it’s all your weight it’s all your weight that’s causing these symptoms that’s causing your bad knee that’s causing your whatever it might be that’s somehow causing your postmenopausal vaginal bleeding I’m not quite sure how weight can do that and that’s really not appropriate and that is a major major concern and this is a registry database of 5 million or so people looking at the risk of 22 cancers and the effect on BMI and it’s important to know that increased BMI was associated with increased risk of cancer in 17 of the 22 cancer studies and in particular one of the clear signals that came out was the increased risk of uterine cancer and uterine cancer is comparatively rare, thanks goodness but the effect of a 5kg per metre squared increase in the body mass index has a 60% increase risk on somebody’s chance of having uterine cancer and lots of people are unable or don’t feel confident to access healthcare and I just wanted to reiterate that we must think about obesity as a disease and the answer is yes it more than meets the AMA criteria for a disease because it has an impairment of function and there can be characteristic signs of symptoms and there is significant harm and morbidity and lots of countries have recognised obesity as a disease which is fantastic but there is a long way to go and actually Portugal was one of the early initiators in recognising this this was the slide with some text in Portuguese I mentioned in the lift yesterday and this is childhood obesity surveillance data and in Portugal at least there looks to be a reduction in the prevalence of overweight and obesity within children which is a huge achievement and it’s not caused by just saying obesity is a disease, obviously it’s caused by so many of the policies that happen in Portugal and perhaps we’ll hear about some of them later but part of that and part of changing the dialogue and the dynamic is saying that obesity is a disease in my view and that’s why it’s important we have to improve our collaboration, government obesity professionals, healthcare services, authorities, the food industry and of course health and obesity has to be central to that and that’s why I think ECPO is so good and I actually think it’s a great organisation that should be a blueprint for other conditions and diseases that I also work in and external agents can be modified or are relevant because of course we do have to address the environment that we live in we can’t just treat people although we must treat people we also have to treat the environment as well both things need to happen and approaching them and addressing them is crucial it has to be both and we must improve our services and I am going to have to whiz through a couple of things because you’ve asked me so many questions and I thought just in case I don’t get any questions I’d better make a PowerPoint presentation but I just wanted to say that the chance of achieving a normal volumetric liposuction 25 in people with obesity is very very low in big numbers this is registry data, this isn’t people who are trying to do this necessarily but it’s people within this cohort who do do it and it’s extremely difficult and weight gain is extremely common and I will show this slide which is important this is an analysis of lots of different dietary studies the dark blue is what happened after the diet and the light blue is what happened after the follow up period and of course you can see that there’s significant weight regain hunger increases in response to weight loss some of us might have experienced that and that’s largely generated and changed not by fasting hormones, but hormones that change after we eat and even after weight loss those hormonal changes persist perhaps even after we’ve regained the weight and that’s why you’ll often see, or you may have experienced that some people who are able to lose weight but regain it can actually then regain more than their lost weight and that’s entirely biologically driven but I haven’t got time to go into that in great detail but I’m happy to talk about it later of course when I practice this presentation many times in a closed room it takes like an hour doesn’t it perhaps that’s me speaking too quickly I do want to just touch on bariatric surgery for perhaps 2 or 3 minutes lots of you will have heard of, and this is their term the Swedish Obese Subjects Trial obviously we don’t use that kind of language anymore but it’s ASWAS, and that’s the name of the study it’s multiple studies, it’s about 100 research papers that have come from this and it really is the fundamental basis to everything we know about bariatric surgery although there are a few criticisms of this study so it wasn’t a randomised controlled study because the ethics board wouldn’t let the authors randomise, but it was a matched study so they did as best as they could and I guess lots of you will have seen some of this data and this is just initially deployed lost data and it just shows you that bariatric surgery can be effective for a very long time indeed so this I guess is becoming increasingly historical now because the change in the numbers of different types of operations that we now do so I think you’ll hopefully now know that worldwide gastric sleeve is the most common type of bariatric surgery and this is just the data around survival on the left, and IBT for admission just to show you that bariatric surgery is clearly an effective treatment but it’s not for everybody it can’t be for everybody it is very difficult, there can be complications and there can be consequences some of you will ask me what’s the best type of bariatric surgery for me so people ask that question fishery, I don’t have an answer for that the bi-band sleeve study that Birmingham is a centre for has now finished recruiting, that’s a randomised controlled study of laparoscopically adjusted gastric crown, gastric sleeve and real online gastric bypass designed to answer some of those questions but it is data that we do have comparing sleeve and real online gastric bypass that doesn’t look to be a clear difference in percentage weight loss and that’s been echoed across 2 or 3 fairly well controlled, admittedly quite small studies and just before I skip through to my final conclusion there are lasting benefits, of course there are for weight loss surgery, and I think the quality of life which is quite a hard thing to put on a graph can be a key part of that as is obviously mortality and cardiovascular risk but there actually can be significant complications and consequences of bariatric surgery and risk so for example there are risks of long bone fracture risk of depression and risk of completed suicide as well as complications of the operation of the gastric anatomy so it shouldn’t be seen as a simple process and it’s extremely complicated living with bariatric surgery as some of you I’m sure will know and there’s lots of my patients tell me and as I see all the time I’ve got to have just a word on stigma as I finish and 80% of people, this is the UK survey the obesity all parliamentary group I think some people in the room contributed to that 80% of people with obesity are all the time being criticised stigmatised or abused as a direct result of their obesity I’ll just lap up and I can’t be in the room for a second a much bigger study a worldwide study with the support of Nova Nordisk Action IO, 5 continents, lots and lots of people has looked into this a bit further and there’s actually big discrepancies between what people living with obesity think and what healthcare practitioners think and you’re going to have to digest that in your own time I’m just going to end on this as I just come back to uterine cancer again and this is a qualitative study looking at experiences of people who’ve had obesity obviously that’s their words on that title not mine and end up being short cancer and there was a comment when this person initially went to be assessed when I was hemorrhaging it was hard to examine me because you know I was so big you have to understand being an obese woman you don’t want to get up on that table you don’t want anybody to see you with your clothes on and that’s quite a powerful way to end the talk because really this is all about prevention and treatment and a big part of treatment is access to care and a big part of that I think is addressing stigma as well so these are just the same conclusions that I started with so I’ll let them hang up so thanks very much indeed I’m sorry if I’ve talked too much but it’s because you’ve all asked me such good questions thank you very much indeed no you didn’t actually go over you’re still at number 10 but I wanted to make sure that we had time for questions I’ll ask you questions at any point, I’m here all day because I’m here to learn we have you for dinner as well so we can straddle up this item but what I wanted to do was I’m just going to open Mentimeter because I know we will have a lot of questions I think as well the importance of this session is that a lot of the time as patients we may not understand the complete science and it may not have been explained in the way in which we would understand it some people are quite new representatives some people have been around for quite a long time and have listened to the likes of John and Ad do a lot of these talks so what I want to do is code the code for Mentimeter so effectively this is your code if anybody wants to ask a question we can take a few questions now and we can keep the rest of the questions and make sure that John has time to have a look at them because I think it’s really important that we all understand so the code is 208654 so if you want to enter the code and the questions will come up on screen and while you’re doing that I actually have a question for John and I think it’s a really important one that we probably over the last couple of years are starting to dodge around really and patients who have had surgery or patients who may not have had bariatric surgery who have lost a lot of weight and then coming back and relapsing, regaining and people saying well eat less, move more does everybody get the code yet? yeah if you click the back arrow it will ask you for the code and the code is also up here so a lot of people they won’t regain weight so I’ll give you a perfect example myself 15 years post bariatric surgery, room wide and I’m half the weight I lost, I’ve regained and I know there’s a lot of studies such as back in 2009 there was a study that showed that the average person who has had a significant amount of weight loss needs to do three times the amount of physical activity than the average person and I don’t think that kind of gets out but when we talk about regain and we also talk about set point Ariel Sherman does a really good explanation and if you give a bit of the idea around the set point and the regain so as we lose weight from any intervention, including bariatric surgery our energy expenditure changes so as we lose weight we actually burn less energy so that’s the explanation is because we have a lower energy expenditure there have been lots of studies that I’ve shown you haven’t talked too much about that and that’s fairly well established but when we talk about defending the set point energy expenditure changes are only part of the story part of this is hormonal changes as well so bariatric surgery less so but certainly pharmacotherapy and lifestyle intervention studies, I mentioned very briefly so the hunger hormones go up with weight loss, the ghrelin goes up with weight loss of a non-bariatric surgery origin and some of the satiety hormones for example, QI, QII will go down but obviously leptin falls as well because as we lose adipose tissue, some of you in the room will know that leptin is a very important signal that comes directly from the adipose cells themselves and as we lose that signal and that’s a key satiety signal as we lose that signal, that has a direct effect on our brain regulation and appetite and that’s not willpower that’s biology actually and one of the things that happens a bit more in continental Europe in particular, I don’t know if there’s anyone here from Austria and I think from Switzerland as well some centres in Europe do a lot more revisional surgery than we do, and what I mean by revisional surgery is after somebody’s had an initial bariatric surgery but then has subsequent surgery, usually to change what we call limb lengths that can have an additive in its waste that’s what we call revisional surgery we do so little revisional surgery in parts of Europe like the UK and I suspect the Republic of Ireland as well, but some people might tell me differently because we can’t get funding for revisional surgery and the other thing that there’s data for is the use of GLP-1 analogues post bariatric surgery for patients who are experiencing regain, and again that is something that we very much struggle with and we do see this, whatever the weight loss intervention lifestyle, drug, or surgery we will always see an excellent initial weight loss for those people who are able to have that intervention and then a period of regain and that’s all biology but our response to that is so core and that’s why we have to recognise obesity is chronic and relapsing we don’t just do something and you were saying earlier on, we can’t just do something thank you very much, nice to meet you because that works for some people very nicely, fantastic all the best for those people but it doesn’t work for lots of people, our services have to be designed so that they can be accessed by people without jumping through lots of hoops that’s not the system I work in, we’ve got no hoops we are trying to change that, but it’s very very difficult but I do think that recognising obesity and disease and access is different I like this question because I was actually probably about 5 years out before I started to regain weight and I’m 15 years out so BMI was 25, bariatric surgery 3 years later, 20 do you still have the disease or has it gone into remission? this is a fascinating question some of us debate quite a lot actually my own personal take when we think about the definition of obesity I suspect that this person who has now got a BMI of 20 I suspect that this person doesn’t have significant adiposity and I suspect that their risk of fortunately the direct function change or impact of their obesity I suspect has probably changed in terms of perhaps maybe some restlessness or musculoskeletal problems and also of course this person’s cardiovascular risk and long term risk of lots of conditions has obviously reduced very remarkably so I would say at the moment that this person doesn’t have obesity actually because I think part of saying that obesity is a condition that’s chronic and relapsed we have to think of obesity as a disease that can be treated effectively and cured if something can relapse then it perhaps has to be able to be to be at least transiently temporarily put into cure is not a good word, remission is a better word remission is a better word so I’d like to come back to I want to get you on the mic so we can get you on video so I’d like to come back to the question, comment that I made during the presentation and also your comments just now excellent presentation but again when we look at the definition of chronic disease certainly within the European policy context it basically means that it never goes away and you may be having minimal symptoms, you may be having the particular disease under control but it’s still there so none of the hats that I will be wearing but I personally really struggle then with the comment that you just made in terms of if your BMI happens to be a particular level well I expounded on BMI didn’t I I talked about obesity and prostate function and consequences not just that, let’s just say you’re within a normal weight automatically you’re no longer there because actually when you start asking patients and I do say it on a personal level on various patient preferences when we start looking at things like that as well and when you ask the patients across different chronic diseases what they will talk about not just quality of life but the psychological and mental health elements of actually having to sustainably manage their disease so even if it’s hidden at any given point in time like a lot of people in this room doesn’t mean to say it’s not there doesn’t mean to say that they are actually managing in different ways which may be physical, which may be psychological which may be out and out mental health as well so I just wanted to say that because I’m really struggling on a personal level I agree with you having heard your comment of course everyone who’s had bariatric surgery who’s now then entered into that different situation by whatever the measure there is still an ongoing effect of treatment isn’t there so it’s a treated perhaps a better way to look at it it’s an ongoing, you’re not taking a tablet every day but you’ve still got an effect of a biological treatment every day so it’s an ongoing treatment for a disease that’s controlling things at the moment I think perhaps there’s a way to look at it many of you might agree with that and that can also apply to various diseases as well but obviously things may change they may not, we don’t know but it’s an ongoing, rather than taking a tablet every day to control the disease and there are things that are far more important than weight related outcomes and we didn’t talk today about non-scale goals because I didn’t have any time but my personal belief is that mental health is one of, if not the most important aspect particularly around the perioperative period but there was no time for the important and nuanced areas of that this question I have a very clear answer to that’s very easy to say but very hard to deliver should skin removal be accepted as part 2 if you get gastric surgery and look, I’ll tell you what my opinion is but at the moment it doesn’t change anything my opinion is yes, obviously what are people’s experiences in their own different countries have people managed to don’t feel you need to tell me about your own past personal experience but perhaps on an organisational level within the countries you’re from are people able to get excess skin surgery removed without pain so it does vary from country to country obviously we have a lot of best practice in certain countries I know the likes of Ireland particularly I think myself, there’s a few from the UK as well that would hands up say, it’s not a done deal unfortunately, Paul is probably a good person to answer we’re going to go to break in about 2 or 3 minutes so can we wrap up on this and then come back afterwards but we do have you for the day so we will hug you so in terms of when I went for my WLS in 2016 I was pretty much told straight away that the odds of me getting skin removal surgery on the NHS was literally none they said that you’ve got to get yourself down to under a BMI of 25 you’ve got to maintain your weight for 2 years and even then they’d only consider helping so I’ve been very fortunate in the fact that I found a company that helped me but in terms of the NHS help it’s even worse than the postcode lottery for a WLS in the first place it is literally 1 in thousands that get help couldn’t agree more Paul and as I said to you when we spoke about this really important area yesterday I’ve got a couple of people recently who had initially been interested in weight loss surgery and had done very well in our tier 3 programme and would have been all lined up and ready to go they would have jumped through our hoops that existed in the system and are now working very very well but their great fear was the effect of excess skin and when they asked me that specific question will I be able to definitely have skin surgery on the NHS afterwards I was duty bound to tell them the truth and the whole truth and nothing but the truth and no long conversation about the metabolic advantage or anything like that would dissuade these two people because that was what they were greatly concerned about and that’s kind of a failing of the system that I work in currently that lots of us have experienced I suspect I want to ask you for the question you put if someone needs to pay to the surgery to remove skin in Portugal this is part of the national package for the treatment of obesity so we have the preparation the surgery, the follow up and the surgery for removed skin and we don’t need to pay nothing I think as well that goes to show that in Portugal as we’ve seen as well the graphs are leading the way along France in various strides and this is why we actually have the ECPO so that we can all learn from best practice and we can all get to that level this is the whole reason that we are all here together so thank you John, thank you everybody big round of applause