Continuing in my miniseries on arguments that support calling obesity a disease, is the simple fact that, once established, it behaves like a chronic disease.
Thus, once people have accumulated excess or abnormal adipose tissue that affects their health, there is no known way of reversing the process to the point that this condition would be considered “cured”.
By “cured”, I mean that there is a treatment for obesity, which can be stopped without the problem reappearing. For e.g. we can cure an ear infection – a short course of antibiotics and the infection will resolve to perhaps never reappear. We can also cure many forms of cancer, where surgery or a bout of chemotherapy removes the tumour forever. Those conditions we can “cure” – obesity we cannot!
For all practical purposes, obesity behaves exactly like every other chronic disease – yes, we can modify the course or even ameliorate the condition with the help of behavioural, medical or surgical treatments to the point that it may no longer pose a health threat, but it is at best in “remission” – when the treatment stops, the weight comes back – sometimes with a vengeance.
And yes, behavioural treatments are treatments, because the behaviours we are talking about that lead to ‘remission’ are far more intense than the behaviours that non-obese people have to adopt to not gain weight in the first place.
This is how I explained this to someone, who recently told me that about five years ago he had lost a substantial amount of weight (over 50 pounds) simply by watching what he eats and maintaining a regular exercise program. He argued that he had “conquered” his obesity and would now consider himself “cured”.
I explained to him, that I would at best consider him in “remission”, because his biology is still that of someone living with obesity.
And this is how I would prove my point.
Imagine he and I tried to put on 50 pounds in the next 6 weeks – I would face a real upward battle and may not be able to put on that weight at all – he, in contrast, would have absolutely no problem putting the weight back on.
In fact, if he were to simply live the way I do, eating the amount of food I do, those 50 lbs would be back before he knows it.
His body is just waiting to put the weight back on whereas my biology will actually make it difficult for me simply put that weight on.
This is because his “set-point”, even 5 years after losing the weight, is still 50 lbs higher than my “set-point”, which is around my current weight (the heaviest I have ever been).
Whereas, he is currently working hard against his set-point, by doing what he is doing (watching what he eats, following a strict exercise routine), I would be working against my set-point by having to force myself to eat substantially more than my body needs or wants.
That is the difference! By virtue of having had 50 lb heavier, his biology has been permanently altered in that it now defends a weight that is substantially higher than mine.
His post-weight loss biology is very different from mine, although we are currently at about the same weight.
This is what I mean by saying he is in “remission”, thanks to his ongoing behavioural therapy.
Today, we understand much of this biology. We understand what happens when people try to lose weight and how hard the body fights to resist weight loss and to put the weight back on.
This is why, for all practical purposes, obesity behaves just like every other chronic disease and requires ongoing treatment to control – no one is ever “cured” of their obesity.
Not even people who have bariatric surgery – reverse the surgery and before you know it, the weight is back.
So, if for all practical purposes, obesity behaves like a chronic disease, why not just call a spade a spade?
For an illustration on why obesity acts like a chronic disease watch this short TEDx talk
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.
Are you an impulsive eater? Do you have a hard time meal planning or keeping a food journal? Do you find it hard to remember if you had breakfast or not (never mind what you actually ate)? Do you start every new diet or exercise program with super enthusiasm, only to lose interest a few days later? Does your day lack a routine (for no good reason)?
These are just some of the ways in which Attention Deficit Hypertactivity or just Attention Deficit Disorder (ADHD/ADD) can sabotage your efforts to control your weight.
Now, an article by Philip Asherson and colleagues from Kings College London, UK, published in The Lancet Psychiatry discuss important conceptual issues regarding the diagnosis and management of ADHD/ADD in adults.
Although ADHD/ADD is largely thought to be a problem in kids and youth, it remains a considerable and often undiagnosed issue in adults.
Thus, as the authors point out,
“…treatment of adult ADHD in Europe and many other regions of the world is not yet common practice, and diagnostic services are often unavailable or restricted to a few specialist centres.”
This is all the more surprising (and disappointing) given that adult patients respond similarly to current drug and psychosocial interventions, with the same benefits seen in children and adolescents.
With regard to diagnosis it is important to note that,
“Symptoms of ADHD cluster together into two key dimensions of inattention and hyperactivity-impulsivity, are reliably measured, and are strong predictors of functional impairments, but they reflect continuous traits rather than a categorical disorder.”
“Of particular relevance to adult ADHD is the relative persistence of inattention and improvements in hyperactive-impulsive symptoms during development, so that many patients who had the combined type presentation of ADHD as children present with predominantly inattentive symptoms as adults.”
“In clinical practice, the continuous nature of ADHD should not present diagnostic difficulties in moderate-to-severe cases, but might cause difficulties in mild cases with more subtle forms of impairment. Careful attention is needed to assess the effect of ADHD symptoms on impairment and quality of life, including an understanding of the broader range of problems linked to ADHD (eg, executive function [self-regulation] impairments, sleep problems, irritability, and internal restlessness), in addition to functional impairments such as traffic accidents and occupational underachievement. Therefore, some individuals, who seem to function well, might nevertheless suffer from a substantial mental health problem related to ADHD.”
Key criteria according to DSM-5 include:
- Mind seems elsewhere, even in the absence of any obvious distraction
- Starts tasks, but quickly loses focus and is easily side-tracked
- Fails to finish tasks in the workplace
- Reporting unrelated thoughts
- Problems returning calls, paying bills, keeping appointments
- Difficulty in managing sequential tasks; difficulty in keeping materials and belongings in order; messy, disorganised work
- Poor time management
- Tends to fail to meet deadlines
- Feeling restless
- Unable or uncomfortable being still for an extended time, such as in restaurants or meetings
- Might be perceived by others as being restless and difficult to keep up with
- Butts into conversations or activities, might start using other people’s belongings without permission, might intrude into or take over what others are doing
Other common features, that do not quite rise to level of diagnostic criteria include include poor concentration, distractibility, restlessness, over-talkativeness, sleep problems, irritability, impulsiveness, and low self-esteem.
It is important to note that other mental or physical disorders can mimic some of the symptoms of ADHD. These include anxiety, depression, bipolar disorder, hyperthyroidism and sleep apnea.
While the paper does not mention obesity or difficulties managing weight as a possible “complication” of ADHD, in my experience, identifying and treating ADHD in bariatric patients can often make all the difference.
Thus, I concur with the authors’ conclusions that,
“…ADHD should be recognised in the same way as other common adult mental health disorders, and that failure to recognise and treat ADHD is detrimental to the wellbeing of many patients seeking help for common mental health problems.”
While much has been written on how the current obesity epidemic is not limited to humans but also includes house hold pets and zoo animals, some species appear to be more obesity prone than others.
Among dogs, which for centuries have been selectively bred to transform the wild type into all shapes, sizes and temperaments, some breeds likewise appear more prone to weight gain than others – these include labrador retrievers.
Now, a study by Eleanor Raffan and colleagues from Cambridge University, UK, in a paper published in Cell Metabolism, have identified a common deletion within the POMC gene that enhances appetite and feeding behaviour.
The 14 bp deletion in pro-opiomelanocortin (POMC) with an allele frequency of 12% disrupts the β-MSH and β-endorphin coding sequences and is associated with body weight (mean effect size 1.90 kg per deletion allele, equivalent to 0.33 SDs), adiposity, and greater food motivation.
Among another 39 dog breeds, the deletion was only found in the closely related flat-coat retriever (FCR), where it is similarly associated with body weight and food motivation.
The influence of this mutation on feeding behaviour is likely complex:
“It has been reported that owners of more highly food-motivated dogs make greater efforts to limit their dogs’ access to food. However, there is evidence to suggest dogs are able to influence both the type and quantity of food offered to them by their owners. It is possible that behavior changes related to the mutation are sufficient to lead to increased food intake (either by scavenging or soliciting owner-provided food).”
Interestingly, the mutation was found to be significantly more common in Labrador retrievers that had been selected to become assistance dogs than pets suggesting that there may be something about this deletion that positively influences temperament, making them best suited for this kind of work.
“Temperament and “trainability” are the main drivers for selection of assistance dogs, and “positive reinforcement” with food reward is a mainstay of puppy training. We therefore hypothesize that dogs carrying the POMC deletion may be more likely to be selected as assistance dogs.”
Overall, and this should come as no surprise, these findings show that mutations in the same system that regulates human weight and appetite (and perhaps temperament?) is found in obesity prone canines.
Which, incidentally, brings up the issue of selective breeding in humans – but that’s another story.
As this year’s Congress President, together with World Obesity Federation President Dr. Walmir Coutinho, it will be our pleasure to welcome delegates from around the world to what I am certain will be a most exciting and memorable event in one of the world’s most beautiful and livable cities.
The program committee, under the excellent leadership of Dr. Paul Trayhurn, has assembled a broad and stimulating program featuring the latest in obesity research ranging from basic science to prevention and management.
I can also attest to the fact that the committed staff both at the World Obesity Federation and the Canadian Obesity Network have put in countless hours to ensure that delegates have a smooth and stimulating conference.
The scientific program is divided into six tracks:
Track 1: From genes to cells
- For example: genetics, metagenomics, epigenetics, regulation of mRNA and non–coding RNA, inflammation, lipids, mitochondria and cellular organelles, stem cells, signal transduction, white, brite and brown adipocytes
Track 2: From cells to integrative biology
- For example: neurobiology, appetite and feeding, energy balance, thermogenesis, inflammation and immunity, adipokines, hormones, circadian rhythms, crosstalk, nutrient sensing, signal transduction, tissue plasticity, fetal programming, metabolism, gut microbiome
Track 3: Determinants, assessments and consequences
- For example: assessment and measurement issues, nutrition, physical activity, modifiable risk behaviours, sleep, DoHAD, gut microbiome, Healthy obese, gender differences, biomarkers, body composition, fat distribution, diabetes, cancer, NAFLD, OSA, cardiovascular disease, osteoarthritis, mental health, stigma
Track 4: Clinical management
- For example: diet, exercise, behaviour therapies, psychology, sleep, VLEDs, pharmacotherapy, multidisciplinary therapy, bariatric surgery, new devices, e-technology, biomarkers, cost effectiveness, health services delivery, equity, personalised medicine
Track 5: Populations and population health
- For example: equity, pre natal and early nutrition, epidemiology, inequalities, marketing, workplace, school, role of industry, social determinants, population assessments, regional and ethnic differences, built environment, food environment, economics
Track 6: Actions, interventions and policies
- For example: health promotion, primary prevention, interventions in different settings, health systems and services, e-technology, marketing, economics (pricing, taxation, distribution, subsidy), environmental issues, government actions, stakeholder and industry issues, ethical issues
I look forward to welcoming my friends and colleagues from around the world to what will be a very busy couple of days.
For more information on the International Congress on Obesity click here
For more information on the World Obesity Federation click here
For more information on the Canadian Obesity Network click here