Are Smaller Families Driving the Obesity Epidemic?
Readers may be aware of the “Resource Dilution Hypothesis”, which postulates that there is a dilution of familial resources available to children in large families, and a concentration of such resources in small ones. This “dilution” effect could not only affect material factors (including food, participation in organized sports, higher education, etc.) but also emotional factors (including parents undivided attention, time, interaction, etc.). While the importance of this “dilution” effect remains hotly debated, at face value, it sounds plausible. Indeed, there is no doubt that in most Western countries (with increasing standard of living), recent decades have seen a substantial reduction in the number of offspring per family, resulting in a significant increase in first and second-borns as part of the overall population. Now, a large longitudinal study by José Derraik and colleagues, published in the Journal of Epidemiology and Community Health, reports that first-born women (in Sweden) tend to be significantly heavier (and slightly taller) than second-born women, leading the authors to suggest that decreasing family size may have something to do with the increase in obesity seen over time in that country. Indeed, based on this study involving 13,406 pairs of sisters who were either first-born or second-born (n=26 812), the first-born were about 2.4% heavier than their second-born sisters with a 30-40% greater chance of having overweight or obesity. While this difference may seem rather subtle, at a population level, over generations, such effects can well result in substantial shifts in the population BMI, as a greater proportion of people are first-born. (if every family had 5 children, 20% of kids would be a first-born, If every family has 2 children, 50% of kids would be a first-born, if every family had only 1 kid, 100% of kids would be a first-born) As interesting as this idea may seem, there are several issues with this type of analysis, which may well be confounded by all kinds of issues and can hardly prove causality. Nevertheless, a similar finding has been reported in male first-borns and the hypothesis certainly has significant face value. Paradoxically, however, although overall family sizes have decreased, people in lower socioeconomic strata, who tend to have more kids, also tend to have the highest obesity rates. The obvious explanation for this would perhaps also implicate the “resource dilution hypothesis”, as more kids means less money for food, resulting in more (cheaper) caloric-dense processed foods and greater food insecurity. Accordingly, I would predict that there may well… Read More »
Does Cannabis Use Protect Against Obesity And Diabetes?
Anyone even remotely familiar with cannabis use and its potential to cause the “munchies” would immediately assume that regular cannabis use would likely promote weight gain and, in consequence, the risk forf type 2 diabetes. Thus, readers may well be as intrigued as I am by the work of Gerard Ngueta and colleagues from Québec, Canada, published in OBESITY, showing a rather strong inverse association between cannabis use and BMI in the Inuit. The researchers analyzed data from 786 Inuit adults from the Nunavik Inuit Health Survey (2004), which included self-reported use of cannabis as well as measured levels of fasting blood glucose and insulin. Not only was cannabis use highly prevalent in the study population (57%), but even after adjustment for a number of potential confounders, cannabis use was significantly associated with lower body mass index (BMI) (about 2 BMI points, P < 0.001), lower % fat mass (P < 0.001), lower fasting insulin (P = 0.04), and lower HOMA-IR (P = 0.01). In multivariate analysis, past-year cannabis use was associated with 0.56 lower likelihood of obesity (95% confidence interval 0.37-0.84), and it was this relationship that fully explained the seemingly positive effect of cannabis use on insulin resistance (as a surrogate for diabetes risk). It may also be worth noting that the association of cannabis use with lower BMI was only seen in past or non-smokers, but not in current tobacco smokers. Now normally, being highly sceptical of these types of association studies, which are generally hopelessly confounded and can never prove causality, I would have dismissed this as a chance finding of little significance. Imagine my surprise, however, when the authors go on to mention several previous studies, in a variety of populations, that have reported similar findings. Unfortunately, the authors have little to offer in terms of a plausible biological mechanism and can only speculate on possible genetic or functional factors involving the cannabinoid system or putative effects on energy expenditure associated with the pulmonary consequences of smoking. Thus, I can presently make little of this finding – but I will likely stay tuned. @DrSharma, Edmonton, AB
Does Food Availability Have Much To Do With Obesity?
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… Read More »
Epode’s Canada Obesity Forum
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. Learning objectives: 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 Topics include: See a full list of topics in our schedule (as of January 19th 2015). Registration (ends April 28, 2015) Members of EPODE Canada and the Canadian Obesity Summit receive discounts on registration! Become a member of the EPODE International Network today! General – $350 EPODE Network members- $225 Registration is now open! @DrSharma Edmonton, AB
Epigenetic Obesity In The Fruit Fly
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. Thus, “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… Read More »
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