Although “weight-loss” is a booming global multi-billion dollar business, we desperately lack effective long-term treatments for this chronic disease – the vast majority of people who fall prey to the natural supplement, diet, and fitness industry will on occasion manage to lose weight – but few will keep it off.
Thus, there is little evidence that the majority (or even just a significant proportion) of people trying to lose weight with help of the “commercial weight loss industry” will experience long-term health benefits.
When it comes to evidence-based treatments, there is ample evidence that behavioural interventions can help patients achieve and sustain important health benefits, but the magnitude of sustainable weight loss is modest (3-5% of initial weight at best).
Furthermore, although one may think that “behavioural” or “lifestyle” interventions are cost-effective, this is by no means the case. Successful behaviour change requires significant intervention by trained health professionals, a limited and expensive resource to which most patients will never have access. Moreover, there is ample evidence showing maintenance of long-term behaviour change requires significant on-going resources in terms of follow-up visits – thus adding to the cost.
This severely limits the scalability of behavioural treatments for obesity.
If for example, every Canadian with obesity (around 7,000,000) met with a registered dietitian just twice a year on an ongoing basis (which is probably far less than required to sustain ongoing behaviour change), the Canadian Health Care system would need to provide 14,000,000 dietitian consultations for obesity alone.
Given that there are currently fewer than 10,000 registered dietitians in Canada, each dietitian would need to do 14,000 consultations for obesity annually (~ 70 consultations per day) or look after approximately 7,000 clients living with obesity each year. Even if some of these consultations were not done by dietitians but by less-qualified health professionals, it is easy to see how this approach is simply not scalable to the size of the problem.
A similar calculation can be easily made for clinical psychologists or exercise physiologists.
Thus, behavioural interventions for obesity, delivered by trained and licensed healthcare professionals are simply not a scalable (or cost-effective) option.
At the other extreme, we now have considerable long-term data supporting the morbidity, mortality, and quality of life benefits of bariatric surgery. However, bariatric surgery is also not scalable to the magnitude of the problem
There are currently well over 1,500,000 Canadians living with obesity that is severe enough to warrant the costs and risks of surgery. However, at the current pace of 10,000 surgeries a year (a number that is unlikely to dramatically increase in the near future), it would take over 150 years to operate every Canadian with severe obesity alive today.
This is where we have to look at how Canada has made significant strides in managing the millions of Canadians living with other chronic diseases?
How are we managing the over 5,000,000 Canadians living with hypertension?
How are we managing the over 2.5 million Canadians living with diabetes?
How are we managing the over 1.5 million Canadians living with heart disease?
The answer to all is – with the help of prescription medications.
There are now millions of Canadians who benefit from their daily dose of blood pressure-, glucose-, and cholesterol-lowering medications. The lives saved by the use of these medications in Canada alone is in the 10s of thousands each year.
So, if millions of Canadians take medications for other chronic diseases (clearly a scalable approach), where are the medications for obesity?
Sadly, there are currently only two prescription medications available to Canadians (neither scalable, one due to cost the other due to unacceptable side effects).
So what would it take to find treatments for obesity that are scalable to the magnitude of the problem?
More on that in tomorrow’s post.
Unfortunately, all current treatments fail to “cure” obesity, as they fail to reset the set point to what would be considered “normal weight”. This makes ongoing treatment (be it behavioural, medical, or surgical) inevitable.
For all we know, any attempt at creating and sustaining weight loss regularly activates complex neurohormonal responses that serve to promote weight regain.
The only treatment, which may prove to be an exception is bariatric surgery (although this also only works as long as the surgery is in place – reverse the surgery, and the weight comes back).
Now, a paper by Hans Rudi Berthoud and colleagues, published in the International Journal of Obesity takes an in depth look at if and how gastric bypass surgery changes the body weight set point.
The paper reviews the data in support of the notion that surgery physiologically reprograms the body weight defense mechanism.
Thus, behavioural studies in animal models have shown that the defended body weight is indeed lowered after RYGB and sleeve gastrectomy.
For example, after surgeries, rodents return to their preferred lower body weight if over- or underfed for a period of time, and the ability to drastically increase food intake during the anabolic phase strongly argues against the physical restriction hypothesis.
Furthermore, these authors have also demonstrated that the defense of fat mass is less efficient (whereas defense of lean mass remains intact) after surgery.
However, as they point out,
“…the underlying mechanisms remain obscure. Although the mechanism involves central leptin and melanocortin signaling pathways, other peripheral signals such as gut hormones and their neural effector pathways likely contribute.”
Trying to elucidate the exact underlying mechanisms will hopefully not just improve our understanding of how bariatric surgery works, but also hopefully ultimately lead to the development of novel medical treatments that specifically target the body weight set point and its defence.
Now, a paper by Ari Schechter and colleagues from Columbia University, NY, published in Physiology and Behaviour, publish data from a small ‘pilot study’ suggesting that treating obesity with CPAP may reduce calorie intake, at least in some individuals.
The researchers examined ad libitum energy intake in four adult males with overweight or obesity, who had been diagnosed with sleep apnea but had not yet initiated CPAP.
After participants began using CPAP at their titrated setting (active) at home each night for 2 mo, they were invited to participate in this study for two days in an in patient setting.
On the first inpatient day, participants were fed a controlled weight maintenance diet with fixed meal times and participants were asked to use CPAP at their prescribed setting during the scheduled in-lab sleep episode (23:00–7:00).
Ad libitum energy intake was measured throughout the waking period on laboratory day 2, whereby all meals were presented in excess. Participants were instructed to eat until they felt comfortably full.
After a 1-mo washout, participants crossed over into the sham phase. Participants were provided with the sham CPAP devices, and instructed to use the CPAP at the titrated level for 2 mo. This was followed by the second laboratory period (repeat of first phase). After the second phase, participants were debriefed and instructed to return to active CPAP.
Mean total ad libitum EI including fixed meals and free snacks was 3744 ± 511 kcal in the active and 4030 ± 228 kcal in the sham CPAP setting. Three of the four participants increased their total daily EI during sham vs. active, whereas one participant showed a decrease.
While these findings are far from conclusive, they do point to the possibility that ongoing treatment of sleep apnea may influence appetite in a way that serves to reduce energy intake.
This is perhaps not all that surprising given that there is increasing recognition of the importance of restorative sleep on appetite and food intake.
I look forward to seeing more definitive studies exploring this interesting issue.
I would also be interested in hearing is anyone else has experience changes in appetite with starting CPAP treatment for sleep apnea.
Behavioural interventions (generally aimed at reducing caloric intake and/or increasing expenditure) are notoriously unsuccessful as a strategy for sustainable weight loss in the vast majority of people (at any weight).
For the few, who do succeed (and the word “succeed” is used here rather loosely), it takes nothing short of constant (daily) diligence and ongoing determination to make it work – any reduction in effort is immediately “punished” by weight regain – even after years of successful weight-loss maintenance.
Yet, the scientific literature abounds with study after study after study with one behavioural strategy (diets are behaviours!) after the next to try and achieve the almost impossible – sustainable weight loss.
The simple reason why behavioural measures fail is because they are up against a powerful array of neuroendocrine defences that our bodies can harness to effectively sabotage our efforts.
Any time we try to wander off into negative energy balance, our bodies instantly respond with opposing increases in appetite and reduction in energy expenditure to defend and restore energy stores.
That is simply the reality of human (=animal) physiology.
However, this does not mean that behavioural interventions in obesity management are useless.
Indeed, if behaviours are causing weight gain, then changing those behaviours is in fact the first step in addressing ongoing weight gain.
So, if drinking two litres of sugary pop a day or eating most of your food out of boxes is contributing to your weight gain, then changing your diet can stop the gain.
If sitting at your desk (or on your couch) all day is contributing to your weight gain, then increasing your activity levels can stop the gain.
The critical part of the preceding two sentences is “stop the gain”.
When you identify and address the cause of weight gain, you do not automatically get weight loss – you do, however, stop the gain.
If not having breakfast contributes to your overeating (as it may well do in some individuals), then having breakfast may help you stop the gain – it does not necessarily mean that having breakfast will get you weight loss.
Thus, while I expect to see better weight control with regular breakfasts in someone who is actively gaining weight, I do not expect to see weight loss in someone who is weight stable (even if they just eat once a day).
Similarly, if binge eating disorder is contributing to ongoing weight gain, then successful treatment of that disorder should prevent further weight gain – it does not automatically reverse the process and lower your body weight.
Yes, there are behaviours that can make maintenance of weight loss more manageable – like regular weighing, keeping a food diary, managing hunger, mindfulness, etc. but by themselves, these behaviours will rarely result in significant sustainable weight loss in most people.
Can healthy behaviours improve health at any weight – of course they can!
Can healthy behaviours limit further weight gain – of course they can!
Can healthy behaviours result in significant sustainable weight loss – in some people perhaps?
Let us stop overselling behavioural interventions as a “treatment” for obesity, when in real-life, they are supportive at best.
That doesn’t make behavioural interventions any less valuable – patients can sure use all the support they can get.
Much of dietary research relies on people self-reporting what they may or may not eat and drink – this method is fraught with uncertainty with wide gaps between what people self-report and what they actually consume.
Now, a systematic review of the literature suggests that self-reported appetite ratings, another often used method to study effects of food or other interventions on appetite, do not reliably predict actual food intake.
The study by Guy Holt and colleagues, published in Critical Reviews in Food Science and Nutrition, identified 462 relevant papers, only half of which found any relationship between appetite scores and actual energy intake.
This leads the researchers to conclude that self-reported appetite ratings of appetite should be treated with caution, at least when it comes to predicting energy intake.
Clinically, these findings would imply that people are generally poor judges of their own appetite or that their perceived levels of appetite have little influence on their actual energy consumption.
Clearly, more robust study designs involving measurement of actual food intake should be included in any studies on the impact of interventions on appetite.