If you are planning to attend the 4th Canadian Obesity Summit in Toronto next week (and anyone else, who is interested), you can now download the program app on your mobile, tablet, laptop, desktop, eReader, or anywhere else – the app works on all major platforms and operating systems, even works offline.
You can access and download the app here.
(To watch a brief video on how to install this app on your device click here)
You can then create an individual profile (including photo) and a personalised day-by-day schedule.
Obviously, you can also search by speakers, topics, categories, and other criteria.
Hoping to see you at the Summit next week – have a great weekend!
The recently released Canadian Practice Guidelines on the prevention and management of overweight and obesity in children and youth released by the Canadian Task Force on Preventive Health Care (CMAJ 2015), rightly recommended that surgery not be routinely offered to children or youth who are overweight or obese.
Nevertheless, there is increasing evidence that some of these kids, especially those with severe obesity, may well require rather drastic treatments that go well beyond the current clinical practice of doing almost nothing.
Just how ill kids can be before they are generally considered potential candidates for bariatric surgery is evident from a study by Marc Michalsky and colleagues, who just published the baseline characteristics of participants in the Teen Longitudinal Assessment of Bariatric Surgery (Teen-LABS) Study, a prospective cohort study following patients undergoing bariatric surgery at five adolescent weight-loss surgery centers in the United States (JAMA Pediatrics).
While the mean age of participants was 17 with a median body mass index of 50, the prevalence of cardiovascular risk factors was remarkable: fasting hyperinsulinemia (74%), elevated hsCRP (75%), dyslipidemia (50%), elevated blood pressure (49%), impaired fasting glucose levels (26%), and diabetes mellitus (14%).
Not reported in this paper are the many non-cardiovascular problems raging from psychiatric issues to sleep apnea and muskuloskeletal problems, that often dramatically affect the life of these kids.
While surgery certainly appears rather drastic, the fact that these kids are undergoing surgery is merely an indicator of the fact that we don’t have effective medical treatments for this patient population, which would likely require a combination of behavioural interventions and polypharmacy to achieve anything close to the current weight-loss success of bariatric surgery.
That this cannot be the ultimate answer to obesity management (whether for kids or adults), is evident from the rising number of kids and adults presenting with ever-higher BMI’s and related comorbidity – not all of these can or will want surgery.
Thus, while current anti-obesity medications cannot compete with the magnitude of weight-loss generally seen with surgery, medications together with behavioural interventions may well play a role in helping prevent progressive weight gain in earlier stages of the disease.
Unfortunately, I am not aware of any studies that have explored the use of medications in kids to stabilize weight in order to avoid surgery. This would, in my opinion, be a very worthwhile use of such medications.
Given that virtually every risk-factor guideline (from hypertension to diabetes) recommends “weight-loss” as “first-line” treatment, to many this may seem a rather stupid question, but in reality, there is in fact almost no high-qulaity evidence to show that intentional (non-surgical) weight loss actually reduces mortality.
This may well be simply because randomised controlled studies on intentional weight loss have either never been long enough, big enough, or able to sustain large enough differences in body weight between the interventions arms.
Nevertheless, now a meta-analysis by Stephen Kritchevsky and colleagues from the Wake Forest School of Medicine, published in PLOS one, suggests that being randomised to the intervention arm in a weight-loss study may reduce mortality by 15%.
The researchers identified 15 randomised controlled trials of behavioural interventions for weight loss of at least 18 months duration, of which 12 reported at least one death in either of the intervention arms.
These studies included 17,186 participants (53% female, mean age 52 years, mean BMI range 30–46 kg/m2 ) with follow-up times ranging from 18 months to 12.6 years (mean: 27 months), and an average weight loss of 5.5±4.0 kg.
Based on a total of 264 deaths in weight loss groups compared to 310 in non-weight loss groups, the authors calculated a 15% lower all-cause mortality risk (RR = 0.85; 95% CI: 0.73–1.00) in the weight-loss group.
Thus, the authors conclude that being randomized to the weight-loss arm in a behavioural weight-loss study may indeed reduce mortality risk.
However, as readers may realise, this study certainly does not “prove” that it is the actual weight loss that mediates these effects. After all, to achieve and sustain weight-loss through behavioural interventions, participants would have had to change their diet and activity levels to a greater extent that those in the control group. Thus it is very possible that the difference in mortality between the groups could well have been due to changes in health behaviours rather than due to the actual weight loss.
Nevertheless, the findings are reassuring in that they at least do not show an increase in mortality, something that people have feared may happen with intentional weight loss, especially in older individuals.
I guess the most we can conclude from this study is that being lucky enough to be randomised into the “weight-loss arm” of a behavioural weight-loss RCT may just help reduce your mortality risk.
Warning – this is not an April Fool’s post! Rather, it is a follow up to yesterday’s post warning that even “lifestyle” or behavioural interventions can have adverse effects – at least for some people.
Point in case, is this paper by Claude Bouchard and colleagues, published in PLOS one back in 2008, clearly documenting clinically significant harmful metabolic effects of exercise in some individuals (about 1 in 10).
I would probably have disregarded this paper, except for the fact that the authors include a who-is-who of exercise experts, Steven Blair, Timothy Church, Nathan Jenkins, just to name a few. These are all enthusiastic supporters of increasing physical activity with rock-solid expertise in exercise physiology.
Their findings are based on completers from six exercise studies involving a total of 1,687 men and women.
Although metabolic parameters in general improved (as expected) in most participants, 8.4% had an adverse change in fasting insulin, 12.2% has a clinically significant increase in resting systolic blood pressure, 10.4% had a relevant increase in fasting triglycerides, and 13.3% had a reduction in HDL-Cholesterol. About 7% of participants experienced adverse responses in two or more risk factors.
While the authors note that the explanation for these findings remain unclear,
“…the adverse response traits are not explained by prior health status of subjects, age, amount of exercise imposed by the program, or lack of improvement in cardiorespiratory fitness. No evidence could be found for the hypothesis that adverse responses were the result of drug-exercise interactions.”
Which brings me back to yesterday’s post, that even the best meant behavioural recommendation (in this case “move more”) can carry risks for some individuals and may require personalised and ongoing monitoring.
Funnily enough, I would imagine that if you packed exercise into a pill with these types of “adverse effects”, I wonder if the FDA would actually let you sell it.
Incidentally, Claude Bouchard will be one of the key note speakers at the upcoming 4th Canadian Obesity Summit in Toronto, April 28-May 2. I’m sure he will be presenting some of these data and the fascinating genetic studies that have since been done on this issue.
Hat tip to Morgan Downey for reminding me of this study.
To preregister for the Canadian Obesity Summit click here
On the last day of the 8th Annual Obesity Symposium here in Norderstedt, Germany, Marco Bueter from the University of Zurich presented a fascinating series of studies (just published in Circulation), demonstrating the “weight-independent” benefits of gastric bypass surgery on endothelial function (using an animal model).
Besides showing that 8 days after bypass surgery rats with diet-induced obesity had higher plasma levels of bile acids and GLP-1, that were associated with improved endothelium-dependent relaxation, not seen in sham-operated weight matched controls, but also that these effects could be prevented by blocking GLP-1 receptors with exendin 9-39.
In contrast, similar effects to those seen on vascular function in bypass rats were seen in sham-operated rats treated for 8 days with the GLP-1 analogue, liraglutide, or as the authors describe it,
“liraglutide restored NO bioavailability and improved endothelium-dependent relaxations and HDL endothelium-protective properties, mimicking the effects of RYGB”
Together these studies suggest that GLP-1 may well play an important causal role in the improved vascular function seen in patients undergoing gastric bypass surgery.
These findings are all the more interesting as liraglutide has now been approved for obesity treatment in the USA, Canada and Europe.
While these data are certainly not enough to describe liraglutide as “surgery in a pen”, they are indeed promising in terms of potential benefits of this treatment that may well be weight independent.
All the more reason to anticipate the outcome of the ongoing LEADER trial, which is currently evaluating the effect of liraglutide treatment on cardiovascular outcomes in patients with type 2 diabetes.
Disclaimer: I have served as a paid consultant and speaker for Novo Nordisk, the maker of liraglutide.