Every two years the Canadian Obesity Network holds its National Obesity Summit – the only national obesity meeting in Canada covering all aspects of obesity – from basic and population science to prevention and health promotion to clinical management and health policy.
Anyone who has been to one of the past four Summits has experienced the cross-disciplinary networking and breaking down of silos (the Network takes networking very seriously).
Of all the scientific meetings I go to around the world, none has quite the informal and personal feel of the Canadian Obesity Summit – despite all differences in interests and backgrounds, everyone who attends is part of the same community – working on different pieces of the puzzle that only makes sense when it all fits together in the end.
The 5th Canadian Obesity Summit will be held at the Banff Springs Hotel in Banff National Park, a UNESCO World Heritage Site, located in the heart of the Canadian Rockies (which in itself should make it worth attending the summit), April 25-29, 2017.
Yesterday, the call went out for abstracts and workshops – the latter an opportunity for a wide range of special interest groups to meet and discuss their findings (the last Summit featured over 20 separate workshops – perhaps a tad too many, which is why the program committee will be far more selective this time around).
So here is what the program committee is looking for:
- Basic science – cellular, molecular, physiological or neuronal related aspects of obesity
- Epidemiology – epidemiological techniques/methods to address obesity related questions in populations studies
- Prevention of obesity and health promotion interventions – research targeting different populations, settings, and intervention levels (e.g. community-based, school, workplace, health systems, and policy)
- Weight bias and weight-based discrimination – including prevalence studies as well as interventions to reduce weight bias and weight-based discrimination; both qualitative and quantitative studies
- Pregnancy and maternal health – studies across clinical, health services and population health themes
- Childhood and adolescent obesity – research conducted with children and or adolescents and reports on the correlates, causes and consequences of pediatric obesity as well as interventions for treatment and prevention.
- Obesity in adults and older adults – prevalence studies and interventions to address obesity in these populations
- Health services and policy research – reaserch addressing issues related to obesity management services which idenitfy the most effective ways to organize, manage, finance, and deliver high quality are, reduce medical errors or improve patient safety
- Bariatric surgery – issues that are relevant to metabolic or weight loss surgery
- Clinical management – clinical management of overweight and obesity across the life span (infants through to older adults) including interventions for prevention and treatment of obesity and weight-related comorbidities
- Rehabilitation – investigations that explore opportunities for engagement in meaningful and health-building occupations for people with obesity
- Diversity – studies that are relevant to diverse or underrepresented populations
- eHealth/mHealth – research that incorporates social media, internet and/or mobile devices in prevention and treatment
- Cancer – research relevant to obesity and cancer
…..and of course anything else related to obesity.
Deadline for submission is October 24, 2016
To submit an abstract or workshop – click here
For more information on the 5th Canadian Obesity Summit – click here
For sponsorship opportunities – click here
Looking forward to seeing you in Banff next year!
Now a study by Peter Nordström and colleagues, published in JAMA Internal Medicine, reports that a higher BMI in identical twins is associated with a greater risk for type 2 diabetes but not myocardial infarction or death.
The researchers looked at data from 4,046 monzygous twin pairs with discordant BMIs (difference >0.01 units) from the nationwide Swedish twin registry.
During a mean follow-up of 12 years, the rate of myocardial infarcts and deaths were similar in the twins with lower BMI compared to their higher BMI co-twin (5.0% vs. 5.2% and 13.6% vs. 15.6%, respectively).
This lack of difference remained true even when the researchers compared the extremes of BMI discordance and only considered twins with BMI greater than 30.
In contrast, both higher BMI and greater increase in BMI since 30 years before baseline was associated with greater risk of incident diabetes.
Given that diabetes is such a powerful risk factor for cardiovascular disease, one can only wonder why this did not translate into a higher cardiovascular risk in the higher weight twins.
One possible explanation, offered by the authors is that cardiovascular risk may have been well managed in these individuals thus minimizing any increased risk due to diabetes (or other BMI associated risk factors such as dyslipidemia or hypertension).
Indeed, it would probably have required a far larger group of twins (or much longer follow-up) to fully rule out higher cardiovascular risk in these twins.
Let us also not forget that BMI is a rather lousy measure of overall cardiovascular risk.
Thus, which the study is certainly compatible with the (genetics-independant?) role of higher BMI in the risk for diabetes, it certainly should not be interpreted as demonstrating that this increased risk in benign in terms of cardiovascular disease.
Yesterday, I posted about the “Clinical Discussion” of obesity management, presented to us by the venerable New England Journal of Medicine.
I wrote about how the ignorant and moralizing “opinion” of one of the discussants, devoid of even the smallest insight in to the complex sociopsychobiology of this chronic disease, is exactly the kind of “thinking” that is holding back the field (and has been for decades).
But these are not the only problems with the “Clinical Discussion”.
Rather, the problems start with the very choice and description of the “case”.
Indeed, the case warrants a careful line-by-line analysis, to reveal just how the use of the “stereotypical” depiction paints a picture of what (as we will see in a later post), could well turn out to be a much more complicated case than either of the discussants acknowledge.
As we are told,
Ms. Chatham is a 29-year-old woman who recently joined your practice; this is her second visit to your clinic.
In other words, this is a young woman, whose life you know virtually nothing about, not that this should ever stop you from stating your sound medical opinion.
She made today’s appointment to discuss how she can lose weight and whether there are medications that she can take to aid in weight loss.
In other words, a typical “fat” patient looking for a “quick fix” via “diet pills”?
She is relatively healthy, except for a history of childhood asthma.
Did the asthma play any role in her weight gain? Did it limit her physical activity as a kid? Was she on anti-allergic drugs or even systemic steroids that may have led to weight gain? Your guess is as good as mine.
She says that she has been told indirectly, by her friends and family, that she is “overweight.”
Because, obviously, she does not own a mirror, never shops for clothes, and has probably never given her shape or size a second thought, and therefore, needs to be “told” by the good people around her (and perhaps on occasion by perfect strangers she may just happen to meet on the street), that she has a serious health problem and needs to urgently see a doctor.
She has tried several popular diets without success; each time, she has lost 4.5 to 6.8 kg (10 to 15 lb) but has been unable to maintain the weight loss for more than a few months.
Which, I’m guessing, simply goes to prove her lack of motivation and effort. Obviously, like most “fat” people, she is just too weak-willed to maintain weight loss and apparently always gives up far too soon. Never mind, that this is exactly what happens to 95% of people (skinny or fat) who lose weight and never mind, that (as some of us now realise) there is in fact a complex neurohormonal physiology, which tightly regulates body weight and is there solely for the purpose of effectively “defending” against weight loss.
She does not have a history of coronary artery disease or diabetes.
Which would in fact be surprising, given that she is a 29 year-old woman!
She has a regular menstrual cycle.
Which means what exactly? Are we supposed to rule out PCOS or fertility issues based on this clinical “pearl”?
She does not take any medications or nonprescription supplements.
So at least we know that she cannot simply blame her weight gain on any current medications.
She does not smoke but does drink alcohol, occasionally as many as 4 or 5 drinks in a week, when she is out with friends.
Which you could also say about millions of other people (including myself), irrespective of their BMI or health status – it’s what people do!
She tells you that she “watches what she puts in her mouth”…
Which, of course we should have a hard time believing, because as we all know, “fat” people are habitual liars when it comes to what they “tell” us about their diets.
…and reads the nutritional labels on food packaging.
or, at least that’s what she “tells” us – you’re welcome to believe her or not.
However, she enjoys eating out and orders take-out meals 8 to 12 times a week.
Wow! Here we have a “fat” person who actually “enjoys” eating out – as many times as (hold your breath) once or twice a day – and that, despite claiming to read food labels! Never mind that this is exactly how 99.9% of the US population happens to eat (no matter what their size or health status) – clearly, this irresponsible behaviour must change if there is to be any hope for her!
She works as a computer programmer and spends most of her day sitting in an office.
There we have it – typical “sedentariness” a well-known “cause” of obesity (or so we are told), because (as should be obvious to anyone who understands the complexity of energy homeostasis), all people who sit in offices (not to mention the now immortalised 400 lb “hacker”), struggle with their weight.
She belongs to a fitness club and tries to go there about once a week but notes that her attendance is inconsistent.
Because, of course, it’s typically the fat people with gym memberships, who never show up for training. Also relevant, because most of us continue to believe that exercise is the best way to lose weight.
On physical examination, her vital signs are unremarkable except for a blood-pressure measurement of 144/81 mm Hg.
Which we must obviously assume to be reliable, as the docs have certainly ruled out the presence of “White-Coat” hypertension and bothered to ensure that they are indeed using an appropriate cuff size.
She is 1.7 m (5 ft 7 in.) tall and weighs 92 kg (203 lb), and her body-mass index (BMI; the weight in kilograms divided by the square of the height in meters) is 32.
Which contains about as much clinically valuable information as telling us that she is a size 16.
Her waist circumference is 94 cm (37 in.).
Another piece of useless information, especially in an otherwise healthy woman.
There is no peripheral edema.
Which, I guess, clearly tells us that she can forget about using “fluid retention” as an “excuse” for her weight.
The rest of the examination is unremarkable.
There you have it – with this information in hand, we are now clearly poised to give her meaningful clinical advice to help her better manage her weight.
What surprises me about this (apparently “typical”) case history, is that the editors of the New England Journal of Medicine, otherwise so concerned with brevity, did not simply decide to shorten the “case” to the following:
“Ms. Chatham is a pretty healthy 29-year-old working woman, who happens to live in the USA.”
That one line would in fact contain about all of the information we now have about Ms. Chatham, the difference being, that this statement is actually better, in that it is elegantly crafted to avoid the use of “stereotypical” fat-shaming language and imagery.
Furthermore, this sentence, quite like the “case”, is also void of any indication of the actual complexity that even “simple obesity” can present in clinical practice (which, I perhaps mistakenly, assumed would have been the whole point of the Clinical Discussion in the first place).
Is anyone curious as to the information that I would really liked to have about Ms. Chatham to come up with advice that would actual help her?
Then, please stay tuned for tomorrow’s post.
Anyone who follows these pages is aware of the fact that we desperately lack better medical treatments for obesity.
Last year, Health Canada approved the glucagon-like peptide 1 (GLP-1) analogue liraglutide (Saxenda(R)) for obesity treatment, which although effective and generally well-tolerated, has to be administered by daily injections.
Now, the results of the SUSTAIN-6 trial, published in the New England Journal of Medicine, show that the once weekly injection of the GLP-1 analogue semaglutide, not only decreases cardiovascular events, but also significantly lowers body weight, a promising finding for future obesity treatment with this drug.
The SUSTAIN 6 trial randomised 3297 patients with type 2 diabetes to once-weekly semaglutide (0.5 mg or 1.0 mg) or placebo for 104 weeks.
At baseline, 2735 of the patients (83.0%) had established cardiovascular disease, chronic kidney disease, or both.
The primary outcome (MACE) occurred in 108 of 1648 patients (6.6%) in the semaglutide group and in 146 of 1649 patients (8.9%) in the placebo group (hazard ratio, 0.74).
Nonfatal myocardial infarction occurred in 2.9% of the patients receiving semaglutide and in 3.9% of those receiving placebo (hazard ratio, 0.74); nonfatal stroke occurred in 1.6% and 2.7%, (hazard ratio, 0.61).
While average body weight at week 104 remained stable in the placebo group, it decreased by 3.6 kg in the semaglutide 0.5 mg group and and 4.9 kg in the semaglutide 1.0 mg group.
While this may not seem spectacular, it is important to remember that weight loss is notoriously difficult in patients with type 2 diabetes and that this was a diabetes and not an obesity trial, in which case participants would have also been counselled to change their diet and activity levels to achieve weight loss.
Thus, one can only speculate on what the differences in body weight would have been had the participants been actually trying to lose weight.
That said, it was perhaps surprising to note that fewer serious adverse events occurred in the semaglutide group, although more patients discontinued treatment because of adverse events, mainly gastrointestinal.
It will be interesting to see how well semaglutide fares in studies in which this treatment is assessed for the obesity indication, which will hopefully bring us closer to a once-weekly medication for obesity.
In the meantime, once-daily liraglutide 3.0 mg is certainly a welcome addition to medical management of obesity, but clearly there is more to come in terms of harnessing GLP-1 for obesity management.
Disclaimer: I have received consulting and speaking honoraria from Novo Nordisk, the makers of liraglutide and semaglutide
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