While much has been written on how the current obesity epidemic is not limited to humans but also includes house hold pets and zoo animals, some species appear to be more obesity prone than others.
Among dogs, which for centuries have been selectively bred to transform the wild type into all shapes, sizes and temperaments, some breeds likewise appear more prone to weight gain than others – these include labrador retrievers.
Now, a study by Eleanor Raffan and colleagues from Cambridge University, UK, in a paper published in Cell Metabolism, have identified a common deletion within the POMC gene that enhances appetite and feeding behaviour.
The 14 bp deletion in pro-opiomelanocortin (POMC) with an allele frequency of 12% disrupts the β-MSH and β-endorphin coding sequences and is associated with body weight (mean effect size 1.90 kg per deletion allele, equivalent to 0.33 SDs), adiposity, and greater food motivation.
Among another 39 dog breeds, the deletion was only found in the closely related flat-coat retriever (FCR), where it is similarly associated with body weight and food motivation.
The influence of this mutation on feeding behaviour is likely complex:
“It has been reported that owners of more highly food-motivated dogs make greater efforts to limit their dogs’ access to food. However, there is evidence to suggest dogs are able to influence both the type and quantity of food offered to them by their owners. It is possible that behavior changes related to the mutation are sufficient to lead to increased food intake (either by scavenging or soliciting owner-provided food).”
Interestingly, the mutation was found to be significantly more common in Labrador retrievers that had been selected to become assistance dogs than pets suggesting that there may be something about this deletion that positively influences temperament, making them best suited for this kind of work.
“Temperament and “trainability” are the main drivers for selection of assistance dogs, and “positive reinforcement” with food reward is a mainstay of puppy training. We therefore hypothesize that dogs carrying the POMC deletion may be more likely to be selected as assistance dogs.”
Overall, and this should come as no surprise, these findings show that mutations in the same system that regulates human weight and appetite (and perhaps temperament?) is found in obesity prone canines.
Which, incidentally, brings up the issue of selective breeding in humans – but that’s another story.
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.
Given the highly rewarding nature of food, picking a favourite food over. almost anything else appears the natural choice. Thus food reinforcement is generally established at an early age and tends to continue throughout life.
Now, Kai Ling Kong and colleagues, in a paper published in OBESITY, test the hypothesis that conditioning infants as young as 9-16 months to an cognitively stimulating alternative reinforcer may reduce the appeal of food as the default goto reward.
The researchers studied 27 infants, who were found to have rather high food reinforcing ratios at baseline, half of who were randomised to 6 weeks of a program that provided them with a rich variety of music and playful activities, which encouraged infants and parents to participate at their own level in singing, moving, listening, or exploring musical instruments. Participating parents and infants attended weekly, 45-min classes as a group for 6 weeks and parents were encouraged to listen and sing together with their infants at home during everyday home activities such as bath time, meal time, and bed time using the CD and instructional song book provided by the program.
“Our findings provide initial evidence that alternatives to food may be cultivated at a young age to alter the reinforcing value of food in children who are strongly motivated to eat…..Interventions targeting non-food behavior may be a new and promising avenue for the prevention of obesity in infants.“
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.