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5th Canadian Obesity Summit – Four More Days To Submit Your Abstracts!

banff-springs-hotelEvery 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!

Edmonton, AB


How Strong Is The Physiological Drive To Regain Lost Weight?

Yo-Yo Rubber Band Feb 2014It is now well established that the almost non-existant rates of long-term weight loss are not because of lack of will power or lack of motivation. Rather, they are firmly embedded in human (and animal) physiology, that is designed to defend body weight at all costs through complex neuroendocrine homeostatic mechanisms that will eventually wear out even the staunchest dieter.

But just how strong is the physiological drive to defend and regain lost body weight? Or even more specifically, how much does an increase in appetite counteract weight loss?

This is the topic of a paper by David Polidori and colleagues, prepublished on bioRxiv*.

The researchers use data from a 52-week trial of canagliflozin, a sodium glucose co-transporter (SGLT2) inhibitor leads to a urinary glucose loss of approximately 90 g/day throughout the duration of treatment.

This amounts to a net daily energy loss of ~360 kcal/day that occurs without directly altering central pathways controlling energy intake and without the patients being directly aware of the energy deficit.

Based on the observed changes in body weight over time, the researchers used a validated mathematical method to calculate changes in daily energy intake using principles from engineering control theory.

The complex mathematical formula takes into account a wide range of parameters including changes in the energy expenditure rate and density of fat and fat-free mass, energy cost of fat and protein turnover, dietary and adaptive thermogenesis as well as changes in physical activity (no change in physical activity was assumed in this study).

Subjects in the treatment arm showed the typical initial weight loss (of about 5 Kg) followed by the maintenance of a weight-loss plateau throughout the remainder of the study, a pattern which, in light of a continuing daily energy loss of about 360 kcal is consistent with a proportional feedback control system that serves to limit the amount of weight loss and creates a drive towards weight regain (think of this as the tension that counteracts a steady pull  on a rubber band).

Based on their calculations, the amount of daily increase in caloric intake required to maintain the weight loss plateau (rather than continuing to lose weight), was in the order of about 100 Kg/day per Kg weight loss. This is substantially more than the reduction in metabolic rate generally seen with weight loss (of about 10-20% of body weight) is only about 30 kcal/day per Kg weight loss).

When applying these finding to the typical weight-loss curve seen in the usual commercial weight loss programs (an initial weight loss followed by gradual weight regain), the researchers show that the difference between the homeostatic drive to eat and the actual energy intake, a quantitative index of the ongoing effort to sustain the intervention in the face of the continuing biological signals to overeat, requires that subjects have to demonstrate a persistent effort to avoid overeating above baseline during the intervention even when the average energy intake returns to near baseline levels.

Despite the elegant use of real data, the authors caution about limitations of their study, which include the fact that all subjects had type 2 diabetes and the overall degree of weight loss was rather modest. Thus, the model may well look different in subjects without diabetes or more extreme weight loss.
Nevertheless, as the authors discuss,
“…homeostatic feedback control of energy intake is likely a primary reason why it is so difficult to achieve large sustained weight losses in patients with obesity. Rather, weight regain is typical in the absence of heroic and vigilant efforts to maintain behavior changes in the face of an omnipresent obesogenic environment. Unfortunately, there is no evidence that the energy intake feedback control system resets or relaxes with prolonged maintenance of lost weight – an effect similar to the long-term persistent suppression of energy expenditure in weight-reduced humans. Therefore, the effort associated with a weight loss intervention persists until either body weight is fully regained or energy intake increases above baseline to match the homeostatic drive to eat.”
Thus, the key to finding long-term obesity treatments that work, will be to find means of permanently subverting or countering this feedback control system (which is exactly how medications or surgery theoretically work).
No wonder, that will power alone will rarely result in sustainable weight loss and will always require on-going (heroic?) effort in the cases where it does.
Edmonton, AB
*Papers published on bioRxiv are “preprints” before peer review, thus allowing other scientists to see, discuss, and comment on the findings immediately. Readers should therefore be aware that articles on bioRxiv have not been finalized by authors, might contain errors, and report information that has not yet been accepted or endorsed in any way by the scientific or medical community.



When The Risk of Treating Exceeds The Risk of Not Treating, Then Don’t

sharma-obesity-risk1To conclude my miniseries on the recent “Clinical Discussion” on obesity, published in the New England Journal of Medicine, I now turn to the final question – does this relatively healthy 29 year-old woman with a BMI of 32 warrant treatment?

And if yes, what treatment would you recommend.

This question cannot be answered without considering the following:

Often, we tend to focus on potential benefits of treatment, and so most of us would probably approach this question by comparing the potential benefits of treatment vs. the potential risks of not treating this patient – this is often referred to as the benefit-risk ratio.

When this ratio exceeds 1 (i.e. the potential benefits of treatment outweigh the potential risks of treatment), we would recommend treatment.

One could, however, also turn this into a risk-risk ratio.

Both, the decision to treat and the decision to not-treat bear risks.


Given that the woman in this case has Edmonton Obesity Stage 1 at best (borderline hypertension?), her mortality risk over 20 years is rather low.

For one, this means that treating her obesity would likely also have rather modest benefits (if any). In fact, there is currently no proven health benefit of even just modest weight loss in a patient like her.

Thus, we would certainly want to rule out treatments that carry any potential risk.

Clearly, obesity surgery,would not even remotely enter the picture.

Even the risk of medication, although much safer than anything we may have had before, is probably too high. Although the statistical risk for severe side effects (ranging from teratogenicity to pancreatitis – depending on the chosen medication) is rather low, it may still be substantially higher than doing nothing.

This leaves us with behavioural modifications, which would pose the lowest treatment risk (although it is important to remember that the risk of behavioural treatments is not zero: exercise can result in injury, a too restrictive diet could result in nutritional problems or, as some folks fear, trigger an eating disorder).

The most conservative approach would be to reassure her that her mortality risk is indeed rather low (certainly not warranting the risk of medication).

However, treatment decisions are not only guided by mortality risk – we also need to consider quality of life.

Despite being at low medical risk, it may well be that our patient is unhappy with her weight (although we have no information in this regard other than that she has made previous attempts at weight loss).

Exploring this further would certainly require a much deeper dive into how she feels about herself – her weight may not even be the real problem here.

Can she eat better and be more active? Sure, most of us can!

Would I want to see her again, perhaps in a year or so to see how she is doing – sure, even if just to confirm that she still has EOSS 1.

Beyond that, I would be guided by the principle of “first-do-no-harm” and probably leave it at that (at least for now).

Edmonton, AB


In Analyzing A Case We Should Worry More About The Why Than The What

cause-effectContinuing in this miniseries on the rather stereotypical case presented to us in the New England Journal of Medicine “Clinical Discussion”, I would like to approach it in the same manner that I approach any case.

The first question I ask in any encounter with a patient (once the problem has been stated, in this case a BMI of 32), is to try and figure out WHY the patient may have this problem.

Unfortunately, in this case we are only told WHAT the patient is doing but are given no indication as to WHY this may be the case.

Thus, we are told that she drinks alcohol, occasionally as many as 4 or 5 drinks in a week and enjoys eating out and orders take-out meals 8 to 12 times a week.

We are also told that she spends most of her day sitting in an office and tries to go to her fitness club about once a week.

Let us assume for a minute, that her current caloric intake does in fact exceed her caloric expenditure (which we don’t really know, as we are not told whether or not she is currently weight stable or continuing to gain weight – an important detail in any weight history – as we will see in a later post), and knowing that in most cases, weight gain tends to be a “calories-in” rather than a “calories-out” problem, let us for a minute focus on her diet.

Let us further assume that the main source of “excess” calories is indeed from the many meals that she eats out or orders in (the quality of which we know nothing about).

Then, the real question here is WHY she does not eat more home-cooked meals (which, we will simply assume would be a “healthier” choice).

We know she works all day, so is this simply a matter of convenience or lack of time?

Or does she lack basic cooking skills or even hates cooking?

Or does she just not want to eat alone (does she have a partner? kids? room mate?)?

We don’t know!

Nor do we know anything about the many possible underlying drivers of her (supposed) “overeating”.

Does she habitually skip meals and only eats when she is starving?

Is she an emotional eater, who overeats in response to stress or loneliness?

Does she even have stress?

Is she even lonely?

Or unhappy?

Or depressed?

Or anxious?

Or frustrated?

Or an impulsive eater?

Or hungry all the time?

Or never feels full after a meal?

Or craves sweets or chocolate?

Or is sleep deprived?

I would certainly be interested in all of this information to try and figure out WHY this patient is doing WHAT she is doing (assuming, that WHAT she is doing is even the real problem here).

I call this performing a “root-cause analysis” – and it is what I teach my students and residents to do – try to understand the WHY, not just he WHAT.

So, if you asked me, if based on the information presented in the case, I fully understand WHY this patient has a BMI of 32 – I can only honestly answer, that I have no idea.

I also know nothing about her family history (are her parents and siblings overweight? genetics? epigenetics?)

Nor do I know anything about her weight trajectory (was she overweight as a child? gain excess weight during puberty? as an adult? aas there an adverse life-event that prompted the weight gain? does the problem still exist?)

Really, all we can do based on the information presented in this case, is to focus on the presumptive WHAT (eating out and not exercising), which is perhaps fine, if my generic approach to helping this patient is simply going to consist of advising her to, “eat at home and go to the gym”.

Sadly, that approach will prove to be about as effective as telling someone with depression to cheer up or telling someone with anxiety disorder to stop worrying and be happy.

Tomorrow, I will turn to the second question that I always ask myself, namely, does this patient even have a health problem that needs to be addressed?

Edmonton, AB






Stereotypical Stigmatizing Case Histories Are Not Useful For Teaching Doctors About Obesity

living-in-usa-spiral400bYesterday, 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.

Edmonton, AB