Before you respond “of course” – you may wish to take a look at the systematic review by Laura Cobb and colleagues from Johns Hopkins University, published in OBESITY.
The authors looked at 71 Canadian and US studies that examined the relationship between obesity and retail food environments and concluded that,
“Despite the large number of studies, we found limited evidence for associations between local food environments and obesity. “
To be fair, the researchers also concluded that much of the research in this area lacks high-quality studies, that would lead to a more robust understanding of this issue.
In fact, the authors had to slice and dice the data to tease out “positive” findings that included a possible relationship between fast food outlets and obesity in low-income children or an inverse trend for obesity with the availability of supermarkets (a supposed surrogate measure for availability of fresh produce).
Of course, not finding a robust relationship between the food environment and obesity should not be all that surprising, given the many factors that can potentially play a role in obesity rates.
(Readers may recall that there used to be similar enthusiasm between the role of the built environment (e.g. walkability) for rising obesity rates, till the research on this issue turned out to be rather inconclusive. )
None of this should be interpreted to mean that the food or built environments have nothing to do with obesity – however, we must remember that these type of studies virtually never prove causality and that the factors that determine food and built environments are in fact almost as complicated as the factors that determine individual body weights, so finding a robust relationship between the two would be rather surprising.
Allow me to predict that with the increasing trend of fast food outlets offering healthier (or rather less-unhealthy) choices and supermarkets offering ample amounts of “fast food” and a vast array of unhealthy packaged foods, any relationship between retail food environments and obesity (even if it does exist), will be even harder to prove that ever before (outliers are no better than anecdotal evidence and should generally be ignored).
Changing food environments to provide better access to affordable healthier foods should be a “no-brainer” for policy makers, irrespective of whether or not the current environment has anything to do with obesity or not (the same could be said for walkability of neighbourhoods and the prevention of urban sprawl).
As part of the 4th Canadian Obesity Summit, EPODE Canada presents its first Canadian Regional Forum. This one-day workshop is designed for program managers, local community coordinators or program advisors of childhood obesity prevention programs, and to share knowledge and practical advice between EPODE and Canadian programs.
Senior members of the EPODE global team including program managers from programs in Belgium and the Netherlands will share their practical experience on program design, social marketing actions, private public partnerships and program evaluation. Canadian program managers will report on their experience and learnings and discuss barriers and levers to working in the Canadian context. A special workshop on program evaluation, chaired by Dr. Emile Levy of Hospital St. Justine in Montreal will discuss practical approaches to evaluating process and outcomes. A special luncheon presentation on kids and nutrition will be given by the founders of Real Foods for Real Kids. A networking event will be held afterwards for more informal discussion or questions. By attending this landmark event you will find ideas that can help you improve the efficiency and effectiveness of your childhood obesity prevention program.
The cost of the full day workshop includes lunch and the networking event. Attendees can choose to attend only the EPODE Canada workshop or to continue on with the full Summit program and presentations. Program members of the EPODE International Network may attend at a significantly reduced rate.
Through these presentations and workshops, participants will learn to improve the efficiency and effectiveness of a community-based childhood obesity prevention program by learning:
- The 23 year evolution of the EPODE methodology and its critical success factors. e.g. the four pillars.
- Best practices from community-based programs around the world in program design, social marketing actions, private public partnershipsand program evaluation methodologies.
- Valuable insights into barriers and opportunities in the Canadian context via experts in the field presenting their findings and experience.
- Participants will share knowledge with other similar programs, and become part of a Canada-wide network of childhood obesity prevention programs.
Who should attend:
Anyone interested in improving the efficiency and effectiveness of implementing a childhood obesity prevention programs. This includes:
- program managers
- local community coordinators
- program advisors (academics, health care professionals) of childhood obesity prevention programs
See a full list of topics in our schedule (as of January 19th 2015).
Registration (ends April 28, 2015)
General – $350
EPODE Network members- $225
Registration is now open!
Regular readers are well aware of the considerable evidence now supporting the notion that inter-generational transmission of obesity risk through epigenetic modification may well be a key factor in the recent global rise in obesity rates (over the past 100 years or so).
Now a brief review article by Susan Ozanne from the University of Cambridge, UK, published in the New England Journal of Medicine, describes how researchers have now identified a clear and conserved epigenetic signature that is associated with obesity across species (from the fruit fly all the way to humans).
The article discusses how the transmission of susceptibility to obesity can occur as a consequence of “developmental programming,” whereby environmental factors (e.g. a high-fat diet) encountered at the point of conception and during fetal and neonatal life can permanently influences the structure, function, and metabolism of key organs in the offsprin, thus leading to an increased risk of diseases such as obesity later in life.
There is now evidence that such intergenerational transmission of disease can occur through environmental manipulation of both the maternal and paternal lines – thus, this is not something that is just a matter of maternal environment.
Thus, as Ozanne points out,
“Epigenetic mechanisms that influence gene expression have been proposed to mediate the effects of both maternal and paternal dietary manipulation on disease susceptibility in the offspring (these mechanisms include alterations in DNA methylation, histone modifications, and the expression of microRNAs).”
Work in the fruit fly has linked the effect of paternal sugar-feeding on the chromatin structure at a specific region of the X chromosome and transcriptome analysis of embryos generated from fathers fed a high-sugar diet, revealed dysregulation of transcripts encoding two proteins (one of them is called Su(var)) known to change chromatin structure and gene regulation.
Subsequent analyses of microarray data sets from humans and mice likewise revealed a depletion of the Su(var) proteins in three data sets from humans and in two data sets from mice.
“This finding is consistent with the possibility that the depletion of the Su(var) pathway may be brought about by an environmental insult to the genome that is associated with obesity.”
Not only do these studies provide important insights into just how generational transmission of obesity may work but it may also lead to the development of early tests to determine the susceptibility of individuals to the future development of conditions like obesity or diabetes based on epigenetic signatures.
All of this may be far more relevant for clinical practice than most readers may think – indeed, a focus on maternal (and now paternal?) health as a target to reduce the risk of childhood (and adult) obesity is already underway.
This issue will certainly be a “hot topic” at the Canadian Obesity Summit in Toronto later this month.
Now a study by Jennifer Fenn and colleagues from the University of Vermont report significant weight gain with methadone treatment for opioid addiction in a paper published in the Journal of Substance Abuse Treatment.
The retrospective chart review included 96 patients enrolled in an outpatient methadone clinic for ≥ 6 months.
Overall mean BMIs increased by about 3 units (from 27.2 to 30.1), which corresponds roughly to an 18 lb or 10% increase in body weight.
Interestingly, the weight gain was predominantly seen in women, who gained about 28 lbs or 17.5% body weight compared to men, who only increased their weight by about 12 lbs or 6.4%.
As the study did not have access to food records, one can only speculate as to the causes. While better nutrition may well play a role, one could also speculate that there may be some addiction transfer from opioids to calorie-dense foods.
Whatever the cause, clinicians should probably be aware of this potential impact of methadone treatment on body weight, as prevention of excess weight gain may be easier than treating obesity once it is established.
Now a study by Benoit Chassaing and colleagues published in NATURE, suggests that dietary emulsifiers may promote weight gain and the metabolic syndrome by altering the composition of intestinal microbes.
The researchers hypothesized that emulsifiers may increase bacterial translocation across intestinal mucosa, thereby promoting local and systemic inflammation as well as affecting the composition of gut bacteria.
Their study in mice show that relatively low concentrations of two commonly used emulsifiers (carboxymethylcellulose and polysorbate-80) can induce low-grade systemic inflammation, weight gain and features of the metabolic syndrome, as well as promote intestinal inflammation in mice susceptible to inflammatory bowel disease.
Importantly, they used germ-free mice and faecal transplants to show that these changes can be induced simply by transferring the gut microbes from emulsifier-treated animals to controls.
As the authors note,
“These results support the emerging concept that perturbed host-microbiota interactions resulting in low-grade inflammation can promote adiposity and its associated metabolic effects. Moreover, they suggest that the broad use of emulsifying agents might be contributing to an increased societal incidence of obesity/metabolic syndrome and other chronic inflammatory diseases.”
While these findings (if replicated in humans) certainly point to the industrial use of food emulsifiers as a potential cause of the global increase in obesity and inflammatory bowel disease, given that these compounds are present in virtually all processed foods, they may well be difficult to avoid.
Guess it’s back to home cooking with raw ingredients.