2014 CDC Obesity Maps
For readers, who like showing images that demonstrate just how increasingly prevalent obesity is across the US, here are the 2014 obesity maps released by the US Centre for Disease Control this week. Not that much new (unless you want to quibble about a couple of percent points here or there) – the situation is bad, with no sign of getting any better (no surprise here). Here are the basic facts: No state had a prevalence of obesity less than 20%. 5 states and the District of Columbia had a prevalence of obesity between 20% and <25%. 23 states, Guam and Puerto Rico had a prevalence of obesity between 25% and <30%. 19 states had a prevalence of obesity between 30% and <35%. 3 states (Arkansas, Mississippi and West Virginia) had a prevalence of obesity of 35% or greater. The Midwest had the highest prevalence of obesity (30.7%), followed by the South (30.6%), the Northeast (27.3%), and the West (25.7%). What else can one say? @DrSharma Kelwona, BC
Are Cost-Saving Arguments For Treating Obesity Another Form of Discrimination?
Yes, health care costs consume an increasing proportion of taxes (in countries with public healthcare systems) or personal income. Yes, there is also considerable waste in healthcare systems and not every dollar spent is necessary or provides any meaningful benefit. Indeed, even where health benefits are achieved, these may perhaps be had at a lower cost than in our current systems. Thus, there is no argument against reducing waste and improving cost-effectiveness of treatments (or for that matter, prevention). However, arguing in favour of cost-effectiveness should not be confused with arguments for cost-savings, as is often put forward in discussions about obesity treatment. Indeed, authors often bend over backwards to demonstrate the potential cost-savings that may come from treating obesity. Case in point is a study by Oleg Borisenko and colleagues, who in a paper published in Obesity Surgery, suggest that (based on the Scandinavian Bariatric Surgery Registry), surgical treatment of severe obesity led to savings of €8408 per patient, which translates into lifetime savings savings of €66 million for the cohort, operated in 2012. Be that as it may, I feel that savings cannot be the sole argument in favour of providing treatments for a disease. Given the tremendous impact that obesity has on the health and lives of people living with obesity, I would argue for treatments even if they increase healthcare costs. Let us remind ourselves that we do not argue about whether or not treating people with heart attacks, osteoarthritis, kidney failure or cancer saves money for the health care system – it rarely does, and is besides the point. The reason we spend money treating these conditions is because the people presenting with these conditions deserve treatment – period! Thus, I would argue that the primary reason that health care systems should be spending money on treating obesity is because people with obesity deserve treatment – not because it saves money for the system. Thus, even if there was a net cost to treating obesity, people with obesity deserve treatment as much as people with diabetes, heart disease or chronic kidney disease. If this means a greater cost to the health care system, so be it – raise taxes or increase payers contributions – don’t try to save money by simply refusing to pay for obesity treatment (or rationing it by making it difficult for patients to access). Using cost-savings as the prime argument for treating obesity… Read More »
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
Transgenerational Transmission of Metabolic Disease
If anyone ever tells you that the current obesity epidemic can have nothing to do with genetics because “genes don’t change in a couple of generations”, it is completely fair to let them know that they probably do not know what they are talking about. Indeed, there is now overwhelming evidence showing that a variety of health problems, particularly related to metabolic diseases including obesity, can well be transmitted from generation to generation as a result of epigenetic modifications that persist in subsequent generations, even if these are no longer exposed to the “trigger” environment. Anyone who is interested in learning about how much we know about these intergenerational mechanisms, will probably want to read a recent review article on this subject by Rachel Stegemann and David Buchner, published in Seminars in Cell & Developmental Biology. In this papers the authors review examples of transgenerational inheritance of metabolic disease in both humans and model organisms and how these can be triggered by both genetic and environmental stimuli.ors As the authors note, “A diverse assortment of initial triggers can induce transgenerational inheritance including high-fat or high-sugar diets, low-protein diets, various toxins, and ancestral genetic variants. Although the mechanistic basis underlying the transgenerational inheritance of disease risk remains largely unknown, putative molecules mediating transmission include small RNAs, histone modifications, and DNA methylation.” They also discuss example of therapeutically targeting the epigenome (e.g. through dietary modification or exercise) to prevent the transgenerational transmission of metabolic disease. These findings have substantial implications for our attempts to prevent or even reverse the development of obesity in future generations. @DrSharma Vancouver, BC
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