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
To anyone following the “biological” literature on obesity, it should be pretty evident by now that environmental factors can epigenetically modify genes in ways that allow “information” on environmental exposures in parents to be directly transmitted to their offspring.
Now a paper by Peter Huypens and colleagues from the Helmholtz Zentrum München, Germany, published in Nature Genetics, shows that both maternal and paternal exposure to weight gain induced by a high-fat diet in mice can substantially increase the risk for obesity in their offspring.
The key novelty in this study was the fact that the researchers isolated egg and sperm from both male and female mice that had been exposed to high-fat diets (or not) and used these germ cells in various combinations using in-vitro fertilization to create the offspring that were then implanted into surrogate female mice.
In all cases, risk for obesity as well as signs of insulin resistant tracked with both the male and female exposures, pretty much confirming that diets eaten by mothers and fathers can directly influence “genetic” risk for obesity in the next generation.
If transferable to humans (and there is little reason to doubt that this is the case), these findings suggest that a large proportion of the “heritability” of obesity is due to epigenetic modification that transfers risk from one generation to the next.
This means that efforts to prevent childhood obesity need to focus on the parents rather than the kids – kids born to mothers and fathers who have obesity are already born with a substantial higher risk than those born to lean mothers and fathers.
Perhaps our best chances of tackling obesity in the next generation of kids is to focus efforts on younger adults of child-bearing age.
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.
Shortly after a meal, there is a spike in the cerebrospinal fluid concentration of nutrients with direct access to various nutrient-sensitive sites in the brain.
Now a paper by Olof Lagerlöf and colleagues, published in SCIENCE, shows that in mice, the glycosylation enzyme O-GlcNAc transferase (OGT), present in a wide range of neurons involved in energy regulation and feeding behaviours, may play an important role in the satiety response.
Genetic and molecular manipulation of this enzyme in adult mice resulted in marked effects on feeding and weight gain.
Reducing the activity of the enzyme resulted in animals eating much larger meals (but not more often) with substantial gain in fat (but not lean) mass.
In contrast, increasing the activity of this enzyme resulted in reduced food intake during eating episodes.
Not only does it make sense that a molecule known to play a role as a nutrient-sensor would play a role in the central regulation of food intake, but the authors are optimistic that this enzyme may be a target for finding new anti-obesity medications.
While this approach can be highly effective, it does require training, resources and ongoing (lifelong?) interventions (not unlike most other chronic diseases).
Now a rather comprehensive paper by Soleyman and colleagues from the University of Birmingham, Alabama, published in Obesity Reviews provides an overview of obesity management in primary care.
As readers are well aware, our body weight are tightly regulated by a complex neuroendocrine system and defends us agains weight loss through a multi-faceted physiological response to prevent further weight loss and restore body weight.
As the authors note,
“To maintain weightloss, individuals must adhere to behaviours that oppose these physiological adaptations and the other factorsfavouring weight regain. However, it is difﬁcult for peoplewith obesity to overcome physiology with behaviour over the long term. Common reasons for weight regain include decreased caloric expenditure, decreased self-weighing frequency, increased caloric intake, increased fat intake and eating disinhibition over time.”
The paper provides a succinct overview of the evidence supporting behavioural, medical and surgical obesity treatments.
It also reiterates the basic principles of obesity management as outlined in the various guidelines:
1. Obesity is a chronic disease that requires long-term management. It is important to approach patients with information regarding the health implications.
2. The goal of obesity treatment is to improve the health of the patient, and it is not intended for cosmetic purposes.
3. The cornerstone of therapy is comprehensive lifestyle intervention from informed PCPs or other healthcare professionals.
4. The initial goal of therapy is a weight loss of 5–10% in most patients, as this is sufﬁcient to ameliorate many weight-related complications. However, weight loss of ≥10% may be needed to improve certain weight-related complications, such as obstructive sleep apnoea.
5. Consideration should be given to the use of a weight-loss medication or possible bariatric surgery, as the addition of these treatment modalities to lifestyle therapy can promote greater weight loss and maintain the weight loss for a longer period of time.
6. It is important for clinicians to evaluate the patient for weight-related complications, that can be improved by weight loss, and to consider such patients for more aggressive treatment.
As for how to get more primary care clinics to actually implement these approaches, the authors note that,
“Primary care practitioners need to address the problem of obesity in their patients, just as they would with any other chronic condition such as hypertension or type 2 diabetes, and to ensure that their patients are aware of the health risks of obesity.”
Again something that the Canadian Obesity Network is working hard to promote in this country.