If there is one thing we know for sure about obesity management, it is the sad fact, that no diet, exercise, medication, not even bariatric surgery, will permanently reset the body’s tendency to defend and regain its body weight to its set point – this generally being the highest weight that has been achieved and maintained for a notable length of time.
Thus, any effective long-term treatment has to offset the complex neurobiology that will eventually doom every weight-loss attempt to “failure” (no, anecdotes don’t count!).
Just how complex and overpowering this biological system that regulates body weight is, is described in a comprehensive review by the undisputed leaders in this field (Michael Schwartz, Randy Seeley, Eric Ravussin, Rudolph Leibel and colleagues) published in Endocrine Reviews. Indeed the paper is nothing less than a “Scientific Statement” from the venerable Endocrine Society, or, in other words, these folks know what they’re talking about when it comes to the science of energy balance.
As the authors remind us,
“In its third year of existence, the Endocrine Society elected Sir Harvey Cushing as President. In his presidential address, he advocated strongly in favor of adopting the scientific method and abandoning empiricism to better inform the diagnosis and treatment of endocrine disease. In doing so, Cushing helped to usher in the modern era of endocrinology and with it, the end of organo-therapy. (In an interesting historical footnote, Cushing’s Energy Homeostasis and the Physiological Control of Body-Fat Stores presidential address was given in , the same year that insulin was discovered.)”
Over 30 pages, backed by almost 350 scientific citations, the authors outline in excruciating detail just how complex the biological system that regulates, defends, and restores body weight actually is. Moreover, this system is not static but rather, is strongly influenced and modulated by environmental and societal factors.
Indeed, after reading this article, it seems that the very notion, that average Jane or Joe could somehow learn to permanently overcome this intricately fine-tuned system (or the societal drivers) with will power alone is almost laughable (hats off to the very few brave and determined individuals, who can actually do this – you have climbed to the top of Mount Everest and decided to camp out there for the foreseeable future – I wish you all the best!).
Thus, the authors are confident that,
“The identification of neuromolecular mechanisms that integrate short-term and long-term control of feeding behavior, such that calorie intake precisely matches energy expenditure over long time intervals, will almost certainly enable better preventive and therapeutic approaches to obesity.”
Sadly, despite all we have learnt about this system, we are still far from fully understanding it. Thus, the canonical molecular/ cellular signaling pathway: LEP → LEPR → POMC, AgRP → PC → MC4R is just one pathway in a complex network of multiple interacting and sometimes redundant pathways that involve virtually every part of the brain.
Also, the effect of environmental factors appears to be far more complex than most people think. Thus,
“During sensitive periods of development, ontogenic processes in both brain and peripheral organs can be modified so as to match anticipated environmental conditions. Although many exposures during development could potentially predispose to obesity in adulthood, we focus here on two that some researchers think contribute to the secular trends in obesity: parental obesity and exposure to endocrine disrupting chemicals (EDCs).”
Throw in the role of gut bugs, infections, and societal factors, and it is easy to see why no simple solution to the obesity epidemic are in sight (let alone a range of effective long-term treatments like we have for most other common chronic diseases).
As for solutions,
“To be viable, theories of obesity pathogenesis must account not only for how excess body fat is acquired, but also for how excess body fat comes to be biologically defended. To date, the preponderance of research has focused on the former. However, we must consider the possibility that some (perhaps even most) mechanisms underlying weight gain are distinct from those responsible for the biological defense of excess fat mass. A key question, therefore, is how the energy homeostasis system comes to defend an elevated level of fat mass (analogous to the defense of elevated blood pressure in patients with hypertension). Answering this question requires an improved understanding of the neuro-molecular elements that underlie a “defended” level of body fat. What are the molecular/neuroanatomic predicates that help establish and defend a “set point” for adiposity? How do these elements regulate feeding behavior and/or energy expenditure, so as to achieve long-term energy balance? By what mechanisms is an apparently higher set point established and defended in individuals who are obese?” [sic]
“Given that recovery of lost weight (the normal, physiological response to weight loss irrespective of one’s starting weight) is the largest single obstacle to effective long-term weight loss, we cannot overstate the importance of a coherent understanding of obesity-associated alterations of the energy homeostasis system.”
There is much work to be done. Whether or not, in this climate of anti- and pseudo-science, funding for such fundamental work will actually be made available, is anyone’s guess.
Modelled on “Humans of New York”, WoL presents images and stories of Canadians living with obesity in all their diversity and variation.
After all, nothing is more effective in breaking down stereotypes and barriers than realizing that people living with obesity are no different from everyone else, in their hopes, their dreams, their challenges, their aspirations – doing their best to cope and overcome what life throws at them.
Rather than promoting a culture of fat-shaming and blaming, the Canadian Obesity Network seeks to destigmatise those living with obesity by encouraging them to share their real stories in their own words.
Thus, this project seeks to dismantle the stereotypes that surround the lives of people who live with obesity, including the notion that everyone who has overweight or obesity wants to lose weight because they are unhappy with themselves.
Many of the stories you will see in the upcoming weeks do not reflect this. The Canadian Obesity Network hopes that, by sharing these experiences, we all will realize that people who have overweight or obese have goals, dreams, and aspirations just like everyone else, and that their weight is not necessarily a barrier to achieving these, nor is it something that needs to be a source of fear and shame.
In contrast to many other “weight-loss” sites, the Canadian Obesity Network will not publish stories that glorify weight loss journeys, commercial programs or products, or extreme weight loss attempts.
“While we respect the importance and validity of each story we receive, publishing stories like these only serve to reinforce the idea that people who are overweight or obese are living unhappy, unfulfilling lives – and we know you are worth so much more than that.”
For more information on how to participate in this project click here or send an e-mail to email@example.com.
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”.