Continuing in my miniseries on why obesity (defined here, as excess or abnormal body fat that affects your health) should be considered a disease, is the simple observation that obesity responds less to lifestyle treatments than most people think.
Yes, the internet abounds with before and after pictures of people who have “conquered” obesity with diet, exercise, or both, but in reality, long-term success in “lifestyle” management of obesity is rare and far between.
Indeed, if the findings from the National Weight Control Registry have taught us anything, it is just how difficult and how much work it takes to lose weight and keep it off.
Even in the context of clinical trials conducted in highly motivated volunteers receiving more support than you would ever be able to reasonably provide in clinical practice, average weight loss at 12 – 24 months is often a modest 3-5%.
Thus, for the vast majority of people living with obesity, “lifestyle” treatment is simply not effective enough – at least not as a sustainable long-term strategy in real life.
While this may seem disappointing to many (especially, to those in the field, who have dedicated their lives to promoting “healthy” lifestyles as the solution to obesity), in reality, this is not very different from the real-life success of “lifestyle” interventions for other “lifestyle” diseases.
Thus, while there is no doubt that diet and exercise are important cornerstones for the management of diabetes or hypertension, most practitioners (and patients) will agree, that very few people with these conditions can be managed by lifestyle interventions alone.
Indeed, I would put to you that without medications, only a tiny proportion of people living with diabetes, hypertension, or dyslipidemia would be able to “control” these conditions simply by changing their lifestyles.
Not because diet and exercise are not effective for these conditions, but because diet and exercise are simply not enough.
The same is true for obesity. It is not that diet and exercise are useless – they absolutely remain a cornerstone of treatment. But, by themselves, they are simply not effective enough to control obesity in the vast majority of people who have it.
This is because, diet and exercise do not alter the biology that drives and sustains obesity. If anything, diet and exercise work against the body’s biology, which is working hard to defend body weight at all costs.
Thus, it is time we accept this reality and recognise that without pharmacological and/or surgical treatments that interfere with this innate biology, we will not be able to control obesity in the majority of patients.
Whether we like it or not, I predict that within a decade, clinical management of obesity will look no different than current management of any other chronic disease. Most patients will require both “lifestyle” and probably a combination of anti-obesity medications to control their obesity.
This does not take away from the importance of diet and exercise – as important as they are, they are simply not enough.
Despite what “lifestyle” enthusiasts will have us believe, diet and exercise are no more important (or effective) for the treatment of obesity, than they are for the treatment of hypertension, diabetes, dyslipidemia, depression, or any other condition that responds to “lifestyle” interventions.
In the end, most patients will require more effective treatments to manage their obesity and all of the comorbidities that come with it. The sooner we develop and make accessible such treatments, the sooner we can really help our patients.
Continuing in my miniseries on reasons why obesity should be considered a disease, I turn to the idea that obesity is largely driven by biology (in which I include psychology, which is also ultimately biology).
This is something people dealing with mental illness discovered a long time ago – depression is “molecules in your brain” – well, so is obesity!
Let me explain.
Humans throughout evolutionary history, like all living creatures, were faced with a dilemma, namely to deal with wide variations in food availability over time (feast vs. famine).
Biologically, this means that they were driven in times of plenty to take up and store as many calories as they could in preparation for bad times – this is how our ancestors survived to this day.
While finding and eating food during times of plenty does not require much work or motivation, finding food during times of famine requires us to go to almost any length and risks to find food. This risk-taking behaviour is biologically ensured by tightly linking food intake to the hedonic reward system, which provides the strong intrinsic motivator to put in the work required to find foods and consume them beyond our immediate needs.
Indeed, it is this link between food and pleasure that explains why we would go to such lengths to further enhance the reward from food by converting raw ingredients into often complex dishes involving hours of toiling in the kitchen. Human culinary creativity knows no limits – all in the service of enhancing pleasure.
Thus, our bodies are perfectly geared towards these activities. When we don’t eat, a complex and powerful neurohormonal response takes over (aka hunger), till the urge becomes overwhelming and forces us to still our appetites by seeking, preparing and consuming foods – the hungrier we get, the more we seek and prepare foods to deliver even greater hedonic reward (fat, sugar, salt, spices).
The tight biological link between eating and the reward system also explains why we so often eat in response to emotions – anxiety, depression, boredom, happiness, fear, loneliness, stress, can all make us eat.
But eating is also engrained into our social behaviour (again largely driven by biology) – as we bond to our mothers through food, we bond to others through eating. Thus, eating has been part of virtually every celebration and social gathering for as long as anyone can remember. Food is celebration, bonding, culture, and identity – all features, the capacity for which, is deeply engrained into our biology.
In fact, our own biology perfectly explains why we have gone to such lengths to create the very environment that we currently live in. Our biology (paired with our species’ limitless creativity and ingenuity) has driven us to conquer famine (at least in most parts of the world) by creating an environment awash in highly palatable foods, nutrient content (and health) be damned!
Thus, even without delving any deeper into the complex genetics, epigenetics, or neuroendocrine biology of eating behaviours, it is not hard to understand why much of today’s obesity epidemic is simply the result of our natural behaviours (biology) acting in an unnatural environment.
So if most of obesity is the result of “normal” biology, how does obesity become a disease?
Because, even “normal” biology becomes a disease, when it affects health.
There are many instances of this.
For example, in the same manner that the biological system responsible for our eating behaviour and energy balance responds to an “abnormal” food environment by promoting excessive weight gain to the point that it can negatively affect our health, other biological systems respond to abnormal environmental cues to affect their respective organ systems to produce illnesses.
Our immune systems designed to differentiate between “good” and “bad”, when underexposed to “good” at critical times in our development (thanks to our modern environments), treat it as “bad”, thereby creating debilitating and even fatal allergic responses to otherwise “harmless” substances like peanuts or strawberries.
Our “normal” glucose homeostasis system, when faced with insulin resistance (resulting from increasingly sedentary life circumstances), provoke hyperinsulinemia with ultimate failure of the beta-cell, resulting in diabetes.
Similarly, our “normal” biological responses to lack of sleep or constant stress, result in a wide range of mental and physical illnesses.
Our “normal” biological responses to drugs and alcohol can result in chronic drug and alcohol addiction.
Our “normal” biological response to cancerogenous substances (including sunlight) can result in cancers.
The list goes on.
Obviously, not everyone responds to the same environment in the same manner – thanks to biological variability (another important reason why our ancestors have made it through the ages).
But, you may argue, if obesity is largely the result of “normal” biology responding to an “abnormal” environment, then isn’t it really the environment that is causing the disease?
That may well be the case, but it doesn’t matter for the definition of disease. Many diseases are the result for the environment interacting with biology and yes, changing the environment could indeed be the best treatment (or even cure) for that disease.
Thus, even if pollution causes asthma and the ultimate “cure” for asthma is to rid the air of pollutants, asthma, while it exists, is still a disease for the person who has it.
All that counts is whether or not the biological condition at hand is affecting your health or not.
The only reason I bring up biology at all, is to counter the argument that obesity is simply stupid people making poor “choices” – one you consider the biology, nothing about obesity is “simple”.
Continuing in my mini series on the pros and cons of considering obesity a chronic disease, I would like to now discuss the perhaps most illogical argument against recognising obesity as a disease that I often hear, “Calling obesity a disease will reduce our efforts at prevention”.
This argument makes virtually no sense at all, as I cannot think of a single “preventable” disease, where calling it a “disease” would have reduced or thwarted prevention efforts.
Whether the aim is to prevent heart disease (dietary recommendations, fitness, smoking cessation), cancers (physical activity, healthy diets, smoking cessation, sunlight exposure), infectious diseases (vaccinations, food safety, hand washing, condom use), road accidents (helmets, seat belts, speed limits), in no instance has calling something a “disease” ever stopped us from doing the utmost for prevention (although more can always be done).
Rather, if you truly embrace the concept that obesity, once established, becomes a life-long problem for which we have no cure (the very definition of “chronic disease”), we should be doubling or even quadrupling our efforts at prevention.
After all, who would want to be stuck with a chronic disease, if it can indeed be prevented?
Governments, NGOs and individuals should be even more enthusiastic about preventing a “real” disease than simply modifying a “risk factor” (which sounds a lot less threatening).
Indeed, if I was working in population health, I’d be all for emphasizing just how terrible and devastating the disease of obesity actually is – all the more reason to double down on efforts to do what it takes to prevent it.
In fact, considering obesity a “real disease” would put all the folks working hard to prevent obesity right up there on par with those working to prevent “real” diseases like cancer, HIV/AIDS, or Alzheimer’s disease.
Thus, the argument that calling obesity a “disease” would somehow distract from efforts to prevent it makes absolutely no sense at all.
New Orleans, LA
Yesterday, in my brief series on the pros and cons of calling obesity a chronic disease, I addressed the issue of BMI as a poor definition of obesity (understood here as “abnormal or excess body fat that affects health”).
Another common argument I hear from those who do not support the notion of obesity as a chronic disease, is that there is an inconsistent relationship between body fat and health.
This is no doubt the case.
Indeed, whether or not your body fat affects your health depends on a range of factors – from your genetic predisposition to certain “complications” to the “nature” of your body fat, factors that cannot be captured or assessed by simply stepping on a scale.
Often, this variability in the relationship between excess body fat and its impact on health, is used to argue against a “causal relationship” between the two. This argument is often presented along the lines of, “If obesity is a disease, how come I don’t have diabetes?”.
Where the direct impact of excess body fat on health should be evident, is when the amount of excess fat poses a direct “mechanical” problem that impedes physical functioning. This impact, however, is likely to vary from one person to the next.
A good example of this, is obstructive sleep apnea, where an increase in pharyngeal fat deposition is directly and causally related to the airway obstruction. The causal relationship of pharyngeal fat and the symptoms is directly evident by improvement in symptoms following surgical removal of the excess fat (an operation that is seldom undertaken due to possible complications and redeposition of fat). There is also substantial evidence that significant weight loss (such as induced by bariatric surgery) results in a dramatic improvement in apnea/hypopnea index and sometimes even in complete resolution of the problem.
Yet, not everyone with excess weight develops obstructive sleep apnea. One of the factors that explains this variation, is the anatomical dimension of the pharyngeal space, which varies significantly from one person to the next. So, just how much excess fat in the neck region results in symptoms (if any) will necessarily be highly variable. This is not an argument against the relationship between excess body fat and obstructive sleep apnea, it is just the expected variation between individuals that is evident in many diseases.
Likewise, when the amount of excess fat impairs the body’s capacity to perform essential functions (from mobility to performing simple tasks of personal hygiene), it is not a matter of “opinion” whether obesity is the cause of the problem. There is however variation in how people perceive these “limitations” as limitations, which explains why there may well be considerable variation and inconsistncy in the objective vs. subjective impact of excess body fat on physical functioning.
The relationship between excess or abnormal body fat and metabolic problems is perhaps less easy to understand but biologically as evident. Thus, there is an almost linear relationship between the presence of visceral fat and the risk for diabetes. This risk is greatly amplified in individuals with a family history of diabetes. Thus, the amount of visceral fat necessary to impair glucose homeostasis varies from one person to the next and depends on other factors including beta-cell capacity to produce insulin.
Note that I said “visceral” fat rather than body fat. This is because subcutaneous fat appears to have little (if any) effect on diabetes risk and may even be protective. Thus, it is not the total amount of body fat but rather its location and biological function that determines its effect on metabolic disease. Therefor, it is easy to see why there would be an inconsistent relationship between body fat (or even cruder measures such as BMI) and risk for diabetes.
There is also considerable evidence that the metabolic effects of excess body fat can be substantially modified by cardiorespiratory fitness (“fat but fit” vs. “lean but unfit”). This is in part because although exercise does not necessarily reduce overall body fat, it appears to have a very specific effect on visceral fat. Moreover, increased muscle mass appears to neutralise some of the metabolic consequences of excess body fat. While all of this is true, it does not negate the fact that visceral fat remains one of the key drivers of metabolic risk, even if there remains substantial variations in how much this risk translates into severe health problems for a given individual.
Even more difficult to understand is the relationship between excess body fat and its impact on mental health. This is particularly difficult because the emotional impact of excess weight also very much depends on the social context. Clearly, the impact of body shape and size on health and well-being will be different across societies that are more or less accepting of larger bodies.
Nevertheless, social context does not obviate the fact that excess body fat can significantly affect mental health in a given individual living in a given societal context. Indeed, there are numerous instances where the “environment” defines or amplifies the effect of biological variations on health. The most extreme example I can think of would be a peanut allergy. While this may have no impact whatsoever on the health of someone living in a nut-free environment, it can be fatal to someone living in a society where peanuts are found in almost every dish (e.g. Thailand).
Thus, despite variation in the relationship between body fat% or BMI and health, including the fact that this relationship may vary depending on societal or environmental context, is not really an argument against obesity as a disease.
All that matters for the definition of obesity as a chronic disease is whether or not a person’s physical, emotional or functional health is affected by excess or abnormal body fat – that this varies between individuals is only to be expected.
Indeed, the impact of many diseases on health can be substantially modified by environmental factors or social context (e.g. diabetes, heart disease, depression) – this does not prevent us from calling them diseases.
Similarly, the actual impact of many disease on an individual’s health can vary widely between individuals – this does not make them more or less of a disease.
In fact, I would claim that there is an “inconsistent” relationship between virtually every disease and morbidity and mortality at the level of the individual – from depression to cancer, from pneumonia to Alzheimer’s.
Thus, inconsistencies in the relationship between body fat and its impact on health across a population, does not speak against the notion that when excess or abnormal body fat negatively affects a given individual’s health, it should be considered a chronic disease.
It must have been a pretty cheap rubber band, because every few months it would wear out and lose its stretch, so it had to be replaced it with a new band.
Unfortunately, this is not what can be said about the rubber band that I used in my recent TEDx talk to demonstrate what happens when you try to lose weight.
Unlike the cheap band in my pyjamas, the rubber band I used to represent our physiology trying to gain the weight back, never seems to lose its stretch.
No matter how hard or how long we pull, the rubber band keeps wanting to bring our weight back to where we started.
Yes, perhaps for some people, eventually the rubber band may relax (these would certainly be the exceptions) or may be the “muscles” that we use to pull on the band just grow stronger, which makes it seem easier to keep up the pull – but for all we know, in most people, this “rubber band” is of pretty good quality and seems to last forever.
So, how do we take the tension out of the rubber band ?
Well, we do know that people who have bariatric surgery have a much better chance of keeping the weight off in the long-term and we now understand that this has little to do with the “restriction” or the “malabsorbtion” resulting from these procedures but rather from the profound effect that this surgery has on the physiology of weight regain.
Thus, we know that many of the hormonal and neurological changes that happen with bariatric surgery, seem to inhibit the body’s ability to defend its weight and perhaps even appears to trick the body into thinking that its weight is higher than it actually is.
In other words, bariatric surgery helps maintain long-term weight loss by reducing the tension in the rubber band, thus making it far easier for patients to maintain the “pull”.
And that is exactly how we think some of the anti-obesity medications may be working.
For example, daily injections of liraglutide, a GLP-1 analogue approved for obesity treatment, appears to decrease the body’s ability to counteract weight loss by reducing hunger and increasing satiety, thus taking some of the tension out of that band.
Think of it as sprinkling “magic dust” on that rubber band to reduce the tension, which makes it easier for patients to maintain that pull thereby helping them keep the weight off.
Of course, both surgery and liraglutide only reduce the tension as long as you continue using them.
Undo the surgery or come off your anti-obesity meds and the tension in that band comes back as strong as ever.
For readers, who have no idea what I’m talking about, hopefully things will become clearer after you watch my talk by clicking here.