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 miniseries on objections I have heard against calling obesity a disease, I now address the argument that, doing so “medicalizes a behaviour”.
This argument is of course based on the underlying assumption that the root cause of obesity is a behaviour.
This is perhaps true at the most superficial level of understanding of obesity – yes, there are behaviours that can promote weight gain like eating too much, sedentariness and working shifts.
Note however, that nowhere in the WHO definition of obesity as a “disease that results from excess or abnormal body fat that impairs health”, is there any mention of behaviour whatsoever.
This is because for many people, the relationship between behaviour and weight gain is not at all as straightforward as many think.
Take for example physical activity – although over 95% of Canadians do not meet even the minimum criteria for daily physical activity (a behaviour), only 20% of Canadians have obesity (using the BMI 30 cutoff for the sake of argument).
So if behaviour (not moving enough) is touted as one of the root causes of obesity, why does not 95% of the population have obesity?
The simple answer is that for any given level of physical activity (or rather lack of it), some people gain weight while others don’t.
Similarly, if you believe that eating a lot of junk food (a behaviour) is the root cause of obesity, you will have to explain why not everyone who eats a lot of junk food has obesity and why a lot of people have obesity despite never touching the stuff.
No matter what behaviour you pick, it will never explain all (or even most) of obesity and there will always be plenty of people with those exact same behaviours, who manage to maintain a “normal” weight with no additional effort.
As I have previously outlined in blog posts and articles. “behaviours” leading to obesity, if anything, are no more than a symptom of underlying root causes of energy imbalance that can be related to a wide range of psychological, social and/or biological factors, with the precise cause varying widely from one person to the next.
Thus, equating “behaviour” with “obesity” only happens in the minds of people who fail to see obesity for what it actually is – a complex heterogenous often multifactorial disease characterized by excess or abnormal fat tissue that impairs health.
Thus, all that declaring obesity to be a disease is really doing is “medicalising” obesity (which is of course exactly what medicine needs to do) – it is not “medicalising” a behaviour because obesity is not a “behaviour”.
That is not to say that some pathological behaviours (e.g. binge eating disorder) may lead to weight gain. But most of obesity is attributable to “normal” behaviours in an “abnormal” environment.
And so once again, I would like to remind readers that obesity is not a behaviour (unlike smoking or smoking cessation – which is!) – see here for an explanation of the difference.
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.
In March, I had the privilege of being invited by the organisers of TEDx UAlberta to present a talk on obesity.
This talk is now online – please take a look and join the discussion on facebook
If clicking on the image does not work for you, click on this link for YouTube
In the same week that we learned about the devastating metabolic effects of the weight loss induced by hours-long exhausting workouts in participants in the “Biggest Loser”, a paper byJenna Gillen and colleagues from McMaster University, Hamilton, Canada, published in PLOS One, shows that all it takes is one minute of vigorous all out exercise to significantly improve your health.
Unbelievable as it sounds, the rather rigorous randomised controlled 12-week trial in 27 sedentary men showed just that.
The researchers divided the participants into three groups: three weekly sessions of sprint interval training (SIT) involving a total of 1 minute of intense exercise within a 10-minute time commitment (n = 9), three weekly sessions of traditional moderate-intensity continuous training (MICT) involving 50 minutes of continuous exercise per session (n = 10) or no training controls (n = 6).
SIT involved 3×20-second ‘all-out’ cycle sprints (~500W) interspersed with 2 minutes of cycling at 50W, whereas MICT involved 45 minutes of continuous cycling at ~70% maximal heart rate (~110W). Both protocols involved a 2-minute warm-up and 3-minute cool-down at 50W.
Peak oxygen uptake increased by around 20% in both exercise groups as did insulin sensitivity as assessed by an intravenous glucose tolerance test.
Participants in both exercise groups also lost about 2% of body fat.
Furthermore, metabolic and mitochondrial function (as measured in muscle biopsies) improved similarly in both exercise groups.
Thus, the researchers conclude that
“12 weeks of brief intense interval exercise improved indices of cardiometabolic health to the same extent as traditional endurance training in sedentary men, despite a five-fold lower exercise volume and time commitment.”
This is not just news for people who find it hard to make the time for exercise (e.g. due to work or family commitments).
It is also of interest to anyone just trying to get fitter without wanting to invest hours in the gym.
The key however, is the term “all-out” – the 60 sec bout of exercise has to be at virtually maximum capacity, which may increase the risk of injury in some individuals and can hardly be described as “pleasant”.
As for the implications for my patients, who often present with considerable amount of excess weight and thus, every movement (e.g. just walking up a flight of stairs) often appears to happen at near maximum exercise capacity (no surprise given the tremendous weight that they are lifting and carrying), I can only speculate, of what these bouts of activity may have on their metabolic health.
Whatever the case, this study certainly corroborates the notion that one does not have to spend hours in the gym to improve one’s health.