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
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.
This, however, does not mean that genetic risk is not modifiable.
Thus, a paper by Carlos Celis-Morales and colleagues, published in OBESITY, suggests that physical activity may attenuate some of the weight gain attributable to the FTO gene, one of the more common obesity risk alleles.
Their study includes data from 1,280 participants in the European Food4Me trial.
Overall, the FTO (rs9939609) genotype was associated with a higher body weight of about 1 Kg per risk allele, 0.5 Kg/m2 higher BMI, and 1.1 cm greater waist circumference.
While these “effects” were higher among inactive individuals (BMI by 1.06 kg/m2 per allele and waist circumference by 2.7 cm per allele), they were lower in individuals with moderate to high physical activity (BMI by 0.16 kg/me and Waist circumference by 0.5 cm).
Thus, it appears that increased physical activity may attenuate (but not fully prevent) the effect of FTO genotype on BMI and WC.
Exactly how clinically relevant these findings are and whether they would have any effect at all on public health messages or individual counselling, where increased physical activity is likely to be recommended irrespective of any “genetic markers” (or at least should be) is pretty doubtful.
Currently, we have yet to await any practical consequences of genotyping individuals for obesity “risk” alleles.
A recent issue of The Lancet features a short review article on obesity management by George Bray and colleagues.
The paper summarizes the general approach including behavioural (lifestyle), medical and surgical treatments.
While the section on behavioural interventions focuses much on the experience of the Look AHEAD trial (of which several of the authors were co-investigators), it adds little to what is already known on this. As I often say, “lifestyle” treatments for obesity are no more important or effective in real life than “lifestyle” treatments for other chronic conditions including diabetes, hypertension or dyslipidemia – without medications, the vast majority of patients with these issues will be “uncontrolled”.
Thus, the only real new change in obesity management is the increasing number of anti-obesity drugs available in the US (and hopefully soon elsewhere). The paper gives a nice review over the various medications that have been approved as well as several that are in development.
As for obesity treatment with medication, the authors note,
“Several guiding principles should be followed when prescribing drugs for weight loss.First, effective lifestyle support for weight loss should be provided during their use. These medications work to reinforce the patient’s attempts to change eating behaviours and produce an energy deficit. Second, the prescriber and patient should be familiar with the drug and its potential side-effects. Third, unless clinically meaningful weight loss occurs after 3 to 4 months, (generally defined as loss of more than 4–5% of total bodyweight in patients without diabetes; in patients with obesity and diabetes, loss of more than 3% of total bodyweight can be considered satisfactory) a new treatment plan should be implemented. No one medication is effective in every patient just as not every patient is appropriate for every medication.”
All of the above is correct and could be said about using medications for any other chronic condition – medications for hypertension, diabetes, or dyslipidemia work best when combined with “lifestyle” interventions, both prescribers and patients need to be familiar with the drugs for these conditions and their potential side effects. Obviously, when patients do not respond to or tolerate these drugs, they should be discontinued. Also, for these indications, no one medication is effective for every patient and not every patient is appropriate for every medication.
Thus, in summary, medical management of obesity is beginning to look pretty much the same as management of other chronic medical diseases – the only difference is that it is still far less accepted and access to such treatments are still limited by lack of professional education and barriers to access including coverage for these treatments.
Fortunately, I expect this to change in the coming years.
One of the coming features of the Canadian Obesity Network’s patient engagement strategy is a new series of public webinars on topics relevant to obesity by Canadian experts.
I will have the honour of giving the inaugural talk in this series on Tuesday, Feb 23, 2016, 12.00 pm (Eastern) on the topic of “why obesity is a chronic disease”.
The webinar is free but seats are limited, so registration for this event is recommended.
You can also join the discussion on Facebook.
In case you miss it, the talk will be posted on the CON website after the event.
Join me in looking forward to this and forthcoming webinars in this series.