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.”
One of the most pervasive problems with quitting cigarettes, is the accompanying weight gain – in fact, post-cessation weight gain is reportedly the number one reason why smokers, especially women, fail to stop smoking or relapse after stopping.
But what exactly happens when you stop smoking?
This is the topic of a comprehensive review article by Kindred Harris and colleagues published in Nature Reviews Endocrinology.
The paper begins by examining the magnitude of weight gain generally experienced after smoking cessation – an amount that can vary considerably between individuals.
As for mechanisms, the authors note that,
“Several theories have been proposed to explain increased food intake after smoking cessation. One theory is that the ability of nicotine to suppress appetite is reversed. Substitution reinforcement, which replaces the rewards of food with the rewards of cigarettes could occur. Nicotine absence increases the rewarding value of food. Reward circuitries in the brain, similar to those activated by smoking, are activated by increased intake of food high in sugar and fat. Furthermore, nicotine withdrawal leads to an elevated reward threshold, which might cause individuals to eat more snacks that are high in carbohydrates and sugars.”
There are also known effects of smoking on impulsive overeating and individuals with binge eating disorder are at risk of even greater weight gain with cessation.
Smoking cessation also has metabolic effects including a drop in metabolic rate that may promote weight gain and new evidence shows that smoking cessation can even change your gut microbiota.
The authors provide evidence that behavioural interventions can prevent much of the cessation weight gain and argue that such programs should be offered with cessation programs.
Finally, it is important to always remember that the health benefits of smoking cessation by far outweigh any health risks from weight gain, which is why fear of weight gain should never stop anyone from quitting.
This is once again demonstrated in a fascinating series of experiments by Stefano Guidotti and colleagues from the University of Groningen, The Netherlands, in a paper published in Physiology and Behaviour.
The researchers performed their experiments in mice that were selectively bred over 50 generations to voluntarily spend hours in running wheels. Interestingly, the female “runner” mice remain resistant to becoming obese as adults when exposed to a high-fat diet even when they don’t have access to a running wheel.
Thus, these mice are resistant to developing obesity whether they run or just sit around.
What the researchers now show is that this “resistance” to gaining excess weight (bred over generations) can be fully cancelled out simply by exposing the mice to a high-fat diet for a couple of days shortly after birth.
With this exposure, these mice (and even their offspring) are suddenly no longer resistant to weight gain later in life and in fact gain as much weight on high-calories diets as normal mice.
Even more interestingly, the short term perinatal exposure to the high-energy diet does not cancel out their love for running. When given a wheel, they continue running just as much as before but even this no longer prevents them from gaining weight.
Thus it appears that exposure to a high-energy diet during the perinatal period can have profound effects on the risk of developing adult obesity even in animals bred to be obesity resistant – and, the love for running, does not appear to protect against weight gain.
Or, as the authors put it,
“..resistance to high-energy diet-induce obesity in adult female mice from lines selectively bred over ~ 50 generations for increased wheel running behavior was blocked by additional perinatal high-energy diet exposure in only one cycle of breeding. An explanation for this effect is that potential allelic variants underlying the trait of diet-induced obesity proneness were not eliminated but rather silenced by the selection protocol, and switched on again by perinatal high-energy diet exposure by epigenetic mechanisms”
Moreover, this effect of perinatal high-energy diet exposure and its “reversal effect” on obesity resistance can be passed on to the next generation.
Reason enough to wonder just how much the rather dramatic changes in perinatal feeding of infants over the last few decades may be contributing to the obesity epidemic.
Thus, a study by Claire Chevalier and colleagues from Geneva, Switzerland, published in CELL, not only shows that cold exposure (of mice) changes their gut microbes but also that, when transplanted into sterile mice, these “cold” microbes stimulate the formation of thermogenic brown fat.
All of this makes evolutionary sense, as the increase in heat-generating (and calorie-burning) brown fat with cold exposure would protect the organism against cold exposure – however, that gut bacteria would be involved in this process is indeed rather surprising.
Unfortunately, at least for those thinking that “cold bacteria” may be the panacea for stimulating brown fat and thus weight loss are likely to be disappointed.
The researchers also show that with prolonged exposure to cold, these “cold bacteria” induce changes to the structure and function of the gut that enable more glucose to be absorbed.
While in the short-term, this extra fuel can be used by the brown fat to generate heat, in the long-term, some of these extra calories probably go towards building more white fat and thus weight gain.
Again, this makes evolutionary sense. After all, it is ecologically a far better strategy to insulate the house than to waste extra calories heating it.
This is why, the naive notion that simply lowering ambient temperature as a means to generate more brown fat and thus, burn more calories, may not be all that effective.
Indeed, these experiments suggest rather that chronic cold exposure would ultimately stimulate extra insulation, i.e. more subcutaneous fat and weight gain.
Funnily enough, these findings turn the hypothesis that reducing room temperature would promote weight loss into exactly the opposite. Perhaps it is the excessive use of air-conditioning to generate freezing indoor temperatures (as any European visitor to the US will readily attest to), is part of the problem.
Fascinating stuff for sure.