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?
A study by Ryan Newton and colleagues in mBio, the open access journal of the American Society for Microbiology, found that the bacterial composition of city sewage can almost precisely predict obesity rates in that city.
The researchers studied the microbial community of sewage from 71 US cities from 31 states using high-througput 165 rRNA gene sequencing technology.
Although on average only 15% of bacterial sequences in each sample represented bacteria known to occur in human stool, they were able to capture most (97%) of human fecal oligotypes.
Based on the distribution of three primary oligotypes representing different proportions of Bacteroidaceae, Prevotellaceae, or Lachnospiraceae/Ruminococcaceae, the researchers were able to predict whether samples came for cities with high or low prevalence of obesity with 81-89% accuracy.
No such relationship was found with non-fecal oligotypes, suggesting that this relationship was indeed due to the representation of human fecal bacteria in the sewage samples.
Obviously, it is very possible that the sewage bacterial composition reflects “lifestyles” associated with obesity rather than actual body weights, but the very fact that it was possible to identify important predictive differences in bacterial patterns between cities with varying obesity rates, together with the increasing recognition that gut bacteria may well play a role in obesity (and other metabolic diseases), is fascinating enough.
Should these findings be reproducible across other populations, I can only wonder whether sewage sampling may one day serve as a simple way to study changes in nutrition and obesity rates in whole populations.
Indeed, I can picture future public health scientists poring over sewage data to check if their public health policies to reduce obesity are in fact working.