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.
Given that untreated sleep apnea negatively affects restorative sleep, which in turn affects both metabolism and appetite, it may well be that sleep apnea is an important barrier to weight loss.
This is exactly what is suggested in a recent study by Whited and colleagues, published in Health Psychology.
The researchers conducted a secondary analysis of a 12 month randomized trial comparing 2 weight loss interventions consisting of dietary counseling for adults with obesity and metabolic syndrome.
Subjects who screened positive for high risk of sleep apnea using the STOP questionnaire (about 50% of the 175 participants), lost less weight (1.2% vs. 4.2%) and were less likely to lose 5% or greater (24% vs. 75%) than participants without risk for sleep apnea.
Thus, the authors conclude that,
“…an OSA screening indicating high risk identifies individuals who will struggle to lose weight when participating in a weight loss intervention, despite equal attendance at treatment sessions and study assessments. Findings of this study suggest that OSA is a significant barrier to weight loss.”
Whether or not treating sleep apnea makes weight loss any easier, the authors have this to offer:
“Although we found that participants reporting current OSA treatment had greater weight loss (6.5% vs. 0.6%), the small sample of individuals receiving OSA treatment (n = 24) precluded statistical comparison.”
“OSA screening as a standard component of weight loss interventions has a high potential for usefulness, as identified individuals can be targeted for more intense or comprehensive treatment. The benefits of OSA treatment as a standard part of weight loss interventions among individuals with obesity and metabolic syndrome has yet to be determined, and future research must include examination of adherence to both OSA and weight loss intervention components.”
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.
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.