As the latest HQCA report on obesity in Alberta released this week, the substantial population burden of overweight and obesity (now affecting 6 in 10 Albertans) is a significant driver of health care costs in the province. In the US, this increased health care cost for adult obesity is estimated at around $3,508 per individual with a BMI greater than 30 for a total of well over US$ 300 billion per year.
However, as highlighted in a recent article by John Cawley and colleagues in PharmacoEconomics, health care costs are not equally distributed across all people living with increased body weight – rather, obesity related health care costs rise exponentially with increasing BMI levels (i.e. at the extremes of BMI).
Thus, the greatest health care savings for individual patients can be expected in those living with severe obesity.
To illustrate this, the researchers used data from the US Medical Expenditure Panel Survey from 2000-2010 (n=41,435), to calculate the potential annual savings in health care costs (in US $ in the US health care system), for various reductions in body weight in individuals with BMI levels ranging from 30 kg/m2 to 45 kg/m2.
Thus, for e.g. the annual cost savings with a 5% reduction in body weight for someone with a BMI of 30 kg/m2 amounted to a mere $69 per year.
This figure, however, increased exponentially for people with higher BMIs, increasing to $528, $2,137, and $10,030 in an individual with a BMI of 35, 40, and 45 kg/m2, respectively (these figures were somewhat higher, when the individual also has diabetes).
Thus, while treating obesity to achieve a 5% reduction in body weight in someone with a BMI of 30 kg/m2 may never be “cost-effective”, the same amount of weight loss in someone with more extreme obesity, would likely pay for itself or even lead to significant savings.
Because the impact of obesity on mental and physical health, life-expectancy and quality of life is also greatest at higher levels of BMI, one could also make a strong ethical argument for singling out these individuals for priority treatment in the health care system.
Obviously, as readers should be aware, BMI is at best a crude measure for health – a more precise assessment would have used more sophisticated staging systems like the Edmonton Obesity Staging System to calculate individual risk and benefits. However, we should remember that at a population level BMI does function moderately well as an indicator of obesity related risk (although not in individual patients).
This analysis has important consequences both for population and individuals approaches to obesity.
Although the population burden of obesity lies in the middle of the BMI bell curve, and shifting this ever so slightly can move a substantial number of people living with overweight or obesity to a BMI that lies below the current cut-offs, such a change may have little influence on the overall health care costs of obesity, as these live in the extremes.
Thus, using the above numbers in a crude back-of-the-envelope calculation, to save $1,000,0000 per year in health care costs, one would have to lower BMI by 5% in about 14,500 people living with a BMI of 30 kg/m2 compared to only 100 people with a BMI of 45 kg/m2 – a much more manageable problem.
This is why it is harder to make a cost-savings argument for addressing obesity at a population level rather than focussing on those living with more severe obesity, unless such population measures can also substantially help lower the BMI of the latter.
Unfortunately, current population trends show that while rates of overweight and mild obesity appear to be levelling off (thank perhaps in part to population health measures), severe obesity continues to increase at alarming rates.
This is why a greater focus on finding and delivering better treatments to those living with severe obesity, including those that can only offer modest reductions in BMI, has to be the main priority of any health care system seeking to reduce obesity related health care costs.
A paper by Such and German, published in Veterinary Record, shows that a significant proportion of show dogs in the UK would be considered to have overweight or obesity.
The researchers did internet searches to identify 40 pictures per breed of 14 obese-prone dog breeds and 14 matched non-obese-probe breeds that had appeared at a major national UK show (Crufts). Of 1120 photographs initially identified, 960 were suitable for assessing body condition using a previously validated method, with all unsuitable images being from longhaired breeds.
None of the dogs (0%) were underweight, 708 (74%) were in ideal condition and 252 (26%) were overweight with pugs, basset hounds and Labrador retrievers were most likely to be in the latter category.
In contrast, standard poodles, Rhodesian ridgebacks, Hungarian vizslas and Dobermanns were least likely to be overweight.
In the discussion, the authors wonder whether or not breed standards should be redefined to be consistent with a dog in optimal body condition (read – body weight).
As someone, who could not really care less about breed standards and pedigrees (having shown dogs at dog shows myself as a kid), I find this paper of interest, as it reflects our thinking about appearances, that is by no means limited to animals.
The mental health and physical benefits of owning a dog are well-documented – whether they meet show standards or not, is probably not what determines their usefulness as (wo)man’s best friend.
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.
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).
Recent publications suggest that the increase in childhood obesity seen in the US over the past several decades may finally be leveling off – an observation happily interpreted as a sign that not all is lost and that preventive measures may be working.
However, as a paper by Ashlesha Datar and Paul Chung, just published in JAMA pediatrics, these findings may be misleading in that they hide the increasing disparities in the prevalence of childhood obesity across ethnic and social groups.
The authors analysed data from the Early Childhood Longitudinal Study kindergarten class (ECLS-K), consisting of two separate nationally representative cohorts recruited as kindergarteners during the 1998 to 1999 and 2010 to 2011 school years, which includes approximately 17,000 and 15,560 kindergarteners, respectively.
Between 1998 and 2010, with a nearly 20% overall increase in obesity prevalence, obesity decreased nonsignificantly for the highest quintile of socioeconomic class, increased nonsignificantly for the second-highest quintile, and increased significantly for the lowest three quintiles. The greatest increase was seen in non-Hispanic black kids.
Thus, the authors point out that not only have childhood obesity rates substantially increased during the time periods of this study, but also that this increase was accompanied by a substantial increase in socioeconomic disparities as obesity decreased in children with higher socioeconomic backgrounds but increased among children with lower socioeconomic backgrounds.
Perhaps our childhood prevention measures are not reaching the kids who need them the most?