Yesterday, I discussed the desperate need for scalable obesity treatments.
I pointed out that neither behavioural nor surgical interventions are readily scalable to provide long-term obesity treatments to the over 7,000,000 Canadians currently considered to have obesity.
I also noted that, like for other chronic diseases, only medical treatments with anti-obesity medications have the potential for scalability in the millions – we do this regularly for the millions of people living with diabetes, hypertension, heart disease, or any of the other common chronic diseases affecting Canadians.
Nevertheless, before we discuss what it would take to scale up medical treatments, let us take a look at whether all 7,000,000 affected Canadians really need obesity treatment.
Let us first note that the number 7,000,000 refers to Canadians with a BMI over 30. This may well overestimate the problem – as not everyone will actually need or likely benefit from anti-obesity treatments (BMI measures size – not health!).
In fact, if we apply the actual WHO definition of obesity, namely the presence of abnormal or excess body fat that impairs health, we can perhaps readily reduce this number by about 5-10% (anyone with Edmonton Obesity Stage 0) obesity, as these individuals are pretty healthy despite their excess weight. As there is no evidence that these rather healthy individuals would experience any long-term benefits from anti-obesity treatments, it would be entirely reasonable to take a “watch and wait” approach.
The 7,000,000 also includes an additional 15-20% of people, who would have rather mild impairments in health (Edmonton Obesity Stage 1), associated with a very low long-term risk – for these there is also no proven long-term benefit of obesity treatment.
Thus, we can readily exclude about 20 to 30% of individuals for whom the risk-benefit ratio (and thus, the cost-benefit relationship) would hardly justify the use of prescription medications.
This would reduce the number needed to treat by as many as 2 million – leaving us with about 5,000,000 left to treat.
Of these (by definition), all would have Edmonton Obesity Stage 2 or higher, meaning that they will all have some obesity related health impairments.
However, many of these individuals will have obesity related health risks (e.g. hypertension, diabetes, sleep apnea) that are currently well managed with other available treatments (e.g. anti-hypertensive or anti-diabetic medications, CPAP, etc.). For these well-managed patients, it is not clear what additional value anti-obesity medications would offer.
Let us assume that this number of well managed patients is about 50% of the remaining 5,000,000 – this leaves us with only 2,500,000 individuals with obesity related health problems that are not well managed with the available treatments for their comorbidities. It is probably only in these individuals that medical obesity treatment would make sense – both in terms of cost and benefit.
Let us further assume that for another 50% of the remaining for various reasons (e.g. too sick, too old, no ready access to medically supervised care, not interested in obesity treatment, etc.) medical treatment for obesity is not feasible.
This would leave us with only about 1,250,000 patients where medical treatment with prescription drugs would be both practical and likely cost-effective.
This is now a much more manageable problem. In fact, this is only about half the number of Canadians currently living with diabetes, a problem that is routinely managed with medical treatments.
So where are the anti-obesity treatments for these patients?
That will be the topic of tomorrow’s post.
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.
Yesterday, I posted on a study suggesting that people at high risk of obstructive sleep apnea may have a harder time losing weight that people without sleep apnea.
This prompted a reader to send me a link to a study by Luciano Drager and colleagues, published in Thorax, that presents a meta-analysis of randomised controlled trials on the effect of CPAP treatment on body weight.
The authors found 25 randomised controlled trials (RCTs) enrolling over 3000 patients with OSA ranging from 1 to 48 months in duration.
Paradoxically, they report that overall CPAP is associated with a 0.5 kg weight gain compared with control therapy.
Whether this weight gain is clinically relevant or not, the key finding is that (perhaps contrary to popular belief – including my own), the data does not support the idea that commencement of CPAP treatment for sleep apnea leads to weight loss.
As for the reasons for weight gain, an accompanying editorial by Sanjay Patel has this to offer,
“The reduction in leptin levels associated with CPAP therapy may result in increased hunger if the degree of leptin resistance does not change. Another explanation is that CPAP leads to reduced energy expenditure during sleep, as work of breathing is reduced due both to a patent upper airway as well as lung volumes rising to a more efficient point on the pressure–volume curve. Removal of the anorectic effects of hypoxia also may play an important role.”
It is also not exactly clear where the additional weight goes.
“A number of trials have demonstrated no substantial impact of CPAP on visceral fat volume, although the imaging methods used may not be sensitive enough to exclude the small magnitude of weight gain observed. Improvements in growth hormone and insulin-like growth factor 1 signalling with CPAP might result in increased muscle mass.13 Further studies are clearly needed to determine whether CPAP-induced weight gain represents increases in fat, lean body or water compartments.”
As for the potential health effects of the weight gain,
“The impact of 0.5 kg weight gain on health outcomes is fairly minimal and so should not change decision making regarding the use of CPAP in symptomatic OSA. However, it does give one pause regarding the use of CPAP in asymptomatic OSA where a cardiovascular benefit of CPAP has yet to be definitively established and makes more urgent the need for RCTs adequately powered to assess meaningful outcomes in this population.”
Clearly, the relationship between sleep apnea and body weight is a fair bit more complex than I would have thought.
Also, whether or not treating sleep apnea actually makes it easier for patients to lose weight (if they get adequate obesity treatment) remains to be seen.
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.”