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!
It 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.
“…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.”
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.
To 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).
Continuing in my miniseries on the recent “Clinical Discussion” on obesity, published in the New England Journal of Medicine, I now turn to the second question that we need to answer before jumping into giving our patient any advice about managing her weight.
The first question, as discussed in yesterday’s post, is to understand the possible “root-causes” of her weight gain, as these may not only have to be targeted during treatment but can also pose important barriers to management (e.g. emotional eating, depression, lack of time, stress, etc.).
Unfortunately, as I noted yesterday, the case presentation did not provide much in terms of helping us understand, why this patient has a BMI of 32 in the first place.
Not only did we not get any information regarding her weight trajectory, we were also only told that she eats out often and is largely sedentary – not really much to go on, given that the same could be said about the vast majority of people living in the US (or in Canada), irrespective of their size or weight.
As for the second question that we now need to answer, before giving any advice, is whether or not she even has a health issue that needs to be addressed.
Thus, while we may be led to believe that her BMI of 32 in itself justifies the diagnosis of “obesity”, we must remember that BMI is a essentially a measure of body size, in fact, not much better than a dress size.
Although statistical risk for certain health problems (e.g. diabetes, hypertension, joint problems, sleep apnea, etc.) may rise with increasing BMI, this relationship is far weaker than most people think.
Indeed, as we have previously noted, as many as 25-30% of individuals in the BMI 30-35 range may have no clinically significant health impairments whatsoever. This is particularly true for younger individuals and for women – out patient just happens to be a 29 year-old female.
Thus, it is in fact not all that surprising, that the case report goes on to note that Ms Chatham has neither a history of coronary artery disease nor diabetes (which would indeed be rather unusual if did), and, apart from a marginally elevated blood-pressure, her health status is largely “unremarkable”. Although not mentioned in the case vignette, we can perhaps also assume that all her lab values are normal.
Thus, even if we assume that the blood pressure reading is reliable, this information would at best put her at an Edmonton Obesity Stage 1, a stage where her long-term mortality risk would be almost indistinguishable from “normal”.
And, if we apply the actual WHO definition of obesity (the presence of excess or abnormal body fat that impairs health), we may in fact have to bend over backwards to diagnose this woman as having obesity at all.
So if there is no relevant health impairment from her BMI of 32, why is she even concerned about her weight?
Because, as we learn from the case study, she has been told indirectly, by her friends and family, that she is “overweight.”
Which brings me back to our question at hand: does this woman even have a health problem that needs to be addressed?
My answer would be a rather enthusiastic, “not really”.
We could of course leave it at that, and simply reassure her that she is pretty healthy (although she may perhaps want to have her blood pressure rechecked in the near future).
If however, she does persist in her intention to lose weight, and continues to insist that we advise her on what she can do to improve her health (which are really two very different questions), we may need to have a much longer discussion with her.
This is something we will look at tomorrow, when we address the third question:
What would be the best management plan for this patient?