Next in my miniseries on the pros and cons of calling obesity a ‘disease’, I turn to the issue of medical education.
From the first day in medical school, I learnt about diseases – their signs and symptoms, their definitions and classifications, their biochemistry and physiology, their prognosis and treatments.
Any medical graduate will happily recite the role and function of ADH, ATP, ANP, TSH, ACTH, AST, ALT, MCV and a host of other combinations of alphabet soup related to even the most obscure physiology and function – everything, except the alphabet soup related to ingestive behaviour, energy regulation, and caloric expenditure.
Most medical students and doctors will never have heard of POMC, α-MSH, PYY, AgRP, CART, MC4R, or any of the well studied and long-known key molecules involved in appetite regulation. Many will have at best a vague understanding of RMR, TEE, TEF, or NEAT.
The point is, that even today, we are graduating medical doctors, who have at best a layman’s understanding of the complex biology of appetite and energy regulation, let alone a solid grasp of the clinical management of obesity.
Imagine a medical doctor, who has never heard of β-cells or insulin or glucagon or GLUT4-transporters trying to manage a patient with diabetes.
Or a medical doctor, who has never heard of renin or aldosterone or angiotensinogen or angiotensin 2 trying to manage your blood pressure.
How about a medical doctor, who has never heard of T3 or T4 or TSH managing your thyroid disease?
Elevating obesity to a ‘disease’ means that medical schools will no longer have an excuse to not teach students about the complex sociopsychobiology of obesity, its complications, prognosis, and treatments.
As I mentioned in a previous post, suddenly, managing obesity has become their job.
No longer will it be acceptable for doctors to simply tell their patients to control their weight, with no stake in if and how they actually did it.
Thus, if there is just one thing that calling obesity a ‘disease’ can change, it is expecting all health professionals to have as much understanding of obesity as they are currently expected to have of diabetes, heart disease, lung disease, and any other common disease they are likely to encounter in their medical practice.
Apparently, simply treating obesity as a ‘lifestyle’ problem or ‘risk factor’ was not enough – hopefully, recognising obesity as a ‘disease’ in its own right, will change the attention given to this issue in medical training across all disciplines.
Next in my miniseries on arguments for calling obesity a disease is the issue of empathy.
Our normal response to people who happen to be affected by a disease – including lung cancer and STDs – is at least some measure of empathy (even if residual stigma continues to exist).
Even if the disease was entirely preventable and you did your lot to hasten its development, once you declare yourself as having diabetes, or heart disease, or stroke, or cancer, the expected social response is empathy – and not just from family, friends, and colleagues.
Thus, diseases demand empathy – that’s the normal, ethical, humane response.
But apparently not towards people affected by obesity.
Here the response is blame, shame, disgust, jokes, name calling, and even physical attacks (spitting, pushing, shoving, beating – you name it).
No empathy, so sympathy, no understanding, no compassion – i.e perhaps until we call obesity a “disease”.
Then, suddenly, everything changes – because diseases demand empathy.
Perhaps this is the real reason that some folks are so vehemently against calling obesity a disease – to fully accept that obesity is a disease, they would have to show empathy – not something they feel people living with obesity quite deserve.
After all, how can you still make jokes and poke fun at people living with a disease?
How can you still shame and blame people living with obesity, if we call it a disease?
How can you still wage a “war” on obesity – take no prisoners?
That’s definitely a spoiler!
Think about it!
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”.
In my miniseries on arguments that I often hear against calling obesity a chronic disease, I now turn to the objection that declaring obesity a disease would reduce or even abolish personal responsibility.
The argument being, that the term “disease” carries the connotation of being inevitable and will thus reduce motivation in patients to do anything about it.
This is complete nonsense!
When has calling something a disease ever taken away an individuals “responsibility” to do what they can to avoid or ameliorate it?
Take for example type 2 diabetes – a very avoidable and modifiable condition. Calling diabetes a disease does not mean that the individual can do nothing to prevent it or that, once it occurs, the patient can do nothing to change the course of the disease – of course they can and should and often do!
Or take people with a high risk of heart disease or lung disease or bone and joint disease or even cancer – in no instance do we expect less of patients to do their part in helping manage these conditions just because we call them “diseases”.
There is even a term for this – it is called “self-management” – a key principle of chronic disease management.
The course of almost every chronic disease can be changed by whether or not patients change their diet, follow their exercise program, monitor their symptoms, take their medications, come in for their visits – all a matter of “responsibility” if you so wish.
So just how exactly would calling obesity a disease take away from any of this?
Frankly, I cannot help but sense that people who use this argument most often, are erring on the side of “shame and blame” and probably still see obesity largely as a matter of personal “choice” rather than the complex multifactorial problem that it actually is.
Indeed, the opponents often appear “morally” opposed to the very notion of accepting obesity as a disease, as it now gives people the “excuse” to not do anything about it. Sorry, but this whole line of arguing reeks of nothing less than weight bias and discrimination.
As far as I can tell, calling something a disease often leads to exactly the opposite response – when obesity happens (and it can happen to anyone), it places a tremendous mental, physical and social burden on the people who get it – no matter what you call it.
People living with obesity have no greater or lesser “responsibility” of contributing to the self-management of their disease, than people living with hypertension, diabetes, depression, heart disease, or cancer – people living with any disease should be doing what they can – why would obesity be any different?
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.