As this year’s Congress President, together with World Obesity Federation President Dr. Walmir Coutinho, it will be our pleasure to welcome delegates from around the world to what I am certain will be a most exciting and memorable event in one of the world’s most beautiful and livable cities.
The program committee, under the excellent leadership of Dr. Paul Trayhurn, has assembled a broad and stimulating program featuring the latest in obesity research ranging from basic science to prevention and management.
I can also attest to the fact that the committed staff both at the World Obesity Federation and the Canadian Obesity Network have put in countless hours to ensure that delegates have a smooth and stimulating conference.
The scientific program is divided into six tracks:
Track 1: From genes to cells
- For example: genetics, metagenomics, epigenetics, regulation of mRNA and non–coding RNA, inflammation, lipids, mitochondria and cellular organelles, stem cells, signal transduction, white, brite and brown adipocytes
Track 2: From cells to integrative biology
- For example: neurobiology, appetite and feeding, energy balance, thermogenesis, inflammation and immunity, adipokines, hormones, circadian rhythms, crosstalk, nutrient sensing, signal transduction, tissue plasticity, fetal programming, metabolism, gut microbiome
Track 3: Determinants, assessments and consequences
- For example: assessment and measurement issues, nutrition, physical activity, modifiable risk behaviours, sleep, DoHAD, gut microbiome, Healthy obese, gender differences, biomarkers, body composition, fat distribution, diabetes, cancer, NAFLD, OSA, cardiovascular disease, osteoarthritis, mental health, stigma
Track 4: Clinical management
- For example: diet, exercise, behaviour therapies, psychology, sleep, VLEDs, pharmacotherapy, multidisciplinary therapy, bariatric surgery, new devices, e-technology, biomarkers, cost effectiveness, health services delivery, equity, personalised medicine
Track 5: Populations and population health
- For example: equity, pre natal and early nutrition, epidemiology, inequalities, marketing, workplace, school, role of industry, social determinants, population assessments, regional and ethnic differences, built environment, food environment, economics
Track 6: Actions, interventions and policies
- For example: health promotion, primary prevention, interventions in different settings, health systems and services, e-technology, marketing, economics (pricing, taxation, distribution, subsidy), environmental issues, government actions, stakeholder and industry issues, ethical issues
I look forward to welcoming my friends and colleagues from around the world to what will be a very busy couple of days.
For more information on the International Congress on Obesity click here
For more information on the World Obesity Federation click here
For more information on the Canadian Obesity Network click here
Much of the research on the contribution of screen time, sedentariness, food consumption and other factors comes from cross-sectional or longitudinal studies, where researchers essentially describe correlations and statistical “effect sizes”.
To be at all meaningful, analyses in such studies need to be adjusted for known (or at least likely) confounders (or at least the confounders that happen to available).
No matter how you turn and wind the data, such studies by definition cannot prove causality or (even less likely) predict the outcome of actual intervention studies.
Nevertheless, such studies can be helpful in generating hypotheses.
Thus, for example, I read with interest the recent paper by Lei Shang and colleagues from the University of Laval, Quebec, Canada, published in Preventive Medicine Reports.
The researchers looked at cross-sectional data on 630 Canadian children aged 8-10 years with at least one obese biological parent.
While the overall median daily screen time was about 2.2 hours, longer screen time was associated with higher intake of energy (74 kcal) and lower intake of vegetables & fruit (- 0.3 serving/1000 kcal).
This unhealthy “effect” of screen time on diet appeared even stronger among children with overweight.
Thus, there is no doubt that the study shows that,
“Screen time is associated with less desirable food choices, particularly in overweight children.”
The question of course remains whether or not this relationship is actual causal or in other words, does watching more television lead to an unhealthier diet (I am guessing no one assumes that eating an unhealthier diet leads to more TV watching).
Unfortunately, this is not a question that can be answered by this type of research.
Nor, is this type of research likely to predict whether or not reducing screen time will get the kids to eat better.
Indeed, it doesn’t take a lot of imagination to come up with other explanations for these findings that would not require any assumption of a causal link between eating behaviours and television watching.
For one, TV watching could simply be a surrogate measure for parenting style – perhaps parents that let their kids watch a lot of TV are also less concerned about the food they eat.
And, for all we know, reducing TV time may (e.g. by cutting the kids off from TV – or cutting the parents off from a convenient babysitter) in the end make the kids eating behaviours even worse.
Who knows – that’s exactly the point – who knows?
To be fair, the authors are entirely aware of the limitations of such studies:
“This study was cross-sectional, so no causal inference could be made and the possible mechanism is not clear. Although our data collection strictly followed the detailed manual procedure to guarantee the quality control (QUALITY Cohort Technical Documents, 2011), potential bias and errors may still exist in those self-reported questionnaires. A number of potential confounding factors have been adjusted in the regression models, but the results may still be confounded by other known and unknown factors.”
So, while the findings may well fit into the “narrative” of sedentariness -> unhealthy diets -> obesity, we must remain cautious in not overinterpreting findings from these type of studies or jumping to conclusions regarding policies or other interventions.
Liraglutide, a GLP-1 analogue now available for the treatment of obesity (as Saxenda) in North America, works by reducing appetite and increasing satiety, thus making it easier to lose weight and keep it off (with continuing treatment).
Now, a study by Olivia Farr and colleagues, in a paper published in Diabetologia not only present data showing the presence of GLP-1 receptors in human cortex, hypothalamus and medulla, but also provide functional evidence for altered brain response to food cues.
After documenting the presence of GLP-1 receptor in human brains using immunohistochemistry, the researchers conducted a randomised controlled placebo-controlled, double-blind, crossover trial in 18 individuals with type 2 diabetes who were treated with placebo and liraglutide for a total of 17 days each (0.6 mg for 7 days, 1.2 mg for 7 days, and 1.8 mg for 3 days).
Using functional MRI neuroimaging studies, the researchers found that liraglutide remarkably decreased activation of the parietal cortex in response to highly desirable (vs less desirable) food images.
They also observed decreased activation in the insula and putamen, areas involved in the reward system.
Furthermore, using neurocognitive testing, the researchers showed that increased ratings of hunger and appetite correlated with increased brain activation in response to highly desirable food cues while on liraglutide.
In contrast, ratings of nausea (a well-known side effect of liraglutide) correlated with decreased brain activation.
As the authors note,
“Our data point to a central mechanism contributing to, or underlying, the effects of liraglutide on metabolism and weight loss.”
These findings no doubt match the reports from my own patients of experiencing less interest in highly palatable foods and finding it much easier to pass up on foods that they would have otherwise found hard to resist.
Clearly, as we learn more about brain function in eating behaviour, we are thankfully moving towards treatments that are clearly proving to be far more effective than just telling patients to “simply eat less” (which I have often likened to telling people with depression to “simply cheer up”).
Disclaimer: I have received honoraria for speaking and consulting from Novo Nordisk, the maker of liraglutide
While the often impressive benefits of bariatric surgery on health and quality of life in younger patients with severe obesity are well documented, the safety and benefits of bariatric surgery in older patients remains largely unclear.
Now, a systematic review by my colleague Alexandra Chow from the University of Alberta, Edmonton, Canada, published in Obesity Surgery looks at outcomes in patients older than 65 years of age.
The review includes data from 8 studies (1835 patients) of roux-en-Y gastric bypass surgery, all of which were case series.
Overall mean excess weight loss was about 70%, which is only marginally less than generally seen in younger patients with this procedure.
Mean 30-day mortality was 0.14 % with a post-operative complication rate of around 20%, with wound infections being the most common (8 %) followed by cardiorespiratory complications (3 %).
Thus, it appears that bariatric surgery is reasonably safe and produces meaningful clinical outcomes in patients beyond 65 years of age.
Obviously, I would assume that these numbers are better than expected as centres (including ours) are rather selective about patients as they get older. Thus, these outcomes may not be applicable to every patient above the age of 65.
Nevertheless, it appears that for selected elderly patients, bariatric surgery may well be considered an effective treatment for severe obesity despite a reasonable measure of risk.
Now, a study by Constantin Gasser and colleagues from Melbourne, Australia, in a paper published in the American Journal of Clinical Nutrition, present a systematic review and meta-analysis of confectionary consumption and overweight in kids.
The researchers identified 19 studies fort their systematic review, 11 of which (∼177,260 participants) were included in the meta-analysis.
Overall, odds of excess weight of kids in the highest category of sweets consumption was about 20% less than in the reference category.
This inverse association was true for both chocolate and nonchocolate confectioneries.
Furthermore, in the longitudinal studies and the randomised controlled trial included in the review, no associations were observed between confectionery consumption and overweight, obesity, or obesity-related outcomes.
Thus, based on data from well over 175,000 kids, there appears to be no relationship between sweets consumption and excess weight – if anything, the relationship is the opposite of what one may expect.
As so often, when data don’t fit the “accepted” hypothesis, the authors are also quick to point out that these findings could well be explained by reverse causality (overweight kids avoiding sweets) or underreporting by heavier kids (a polite way of saying that heavier kids may be less honest about their candy consumption).
On the other hand, it may also well be that regular (non-restrictive) sweet consumption actually does in fact make kids less vulnerable to overeating, simply by ruining their appetite (just as grandma always warned you it would – as in, “No sweets before supper!”).
Overall, the findings remind me of a previous study that failed to find any association between sugary pop consumption and body weight in Ontario and PEI kids (if anything skinny kids in PEI drank more pop than those with excess weight).
Whatever the true answer may be, these findings certainly do not support the notion that sweet or chocolate consumption is a key factor in childhood obesity.