Nevertheless, for what it is worth, a publication by Ruth Brown and colleagues from York University, Toronto, published in Obesity Research and Clinical Practice, suggests that people today may be more susceptible to obesity than just a few decades ago.
The study looks at self-reported dietary from 36,377 U.S. adults from the National Health and Nutrition Survey (NHANES) between 1971 and 2008 and physical activity frequency data from 14,419 adults between 1988 and 2006 (no activity data was available from earlier years).
Between 1971 and 2008, BMI, total caloric intake and carbohydrate intake increased 10-14%, and fat and protein intake decreased 5-9%.
Between 1988 and 2006, frequency of leisure time physical activity increased 47-120%.
However, for a given amount of caloric intake, macronutrient intake or leisure time physical activity, the predicted BMI was up to 2.3kg/m2 higher in 2006 that in 1988.
So unless there was some major systematic shift in what people were reporting (which seems somewhat unlikely) it is clear that factors other than diet and physical activity may be contributing to the increase in BMI over time – or in other words, it appears that people today, for the same caloric intake and physical activity, are more likely to have a higher BMI than people living a few decades ago.
There are of course several plausible biological explanations for these findings including epigenetics, obesogenic environmental toxins, alterations in gut microbiota to name a few.
If nothing else, these data support the notion that there is more to the obesity epidemic than just eating too much and not moving enough.
Yesterday, I suggested that using a cost-saving argument to justify treatments for obesity reeks of discrimination. I argued that even if obesity treatment costs the system money, it needs to be delivered in the same way that we deliver treatments for other conditions – not because they save money, but because that’s what people living with those conditions deserve.
But the “cost-saving” argument is not just used to justify treatment for obesity – it is also regularly and widely used to justify spending money on obesity prevention. The usual line of argumentation is that x dollars spent on obesity prevention will save y times x dollars in healthcare spending, which is why we need to prevent obesity.
This is nonsense. We should be preventing obesity whether or not it saves money for the healthcare system, simply because obesity (defined here as excess weight that actually causes health problems) negatively impacts health and well-being. If this costs money, so be it.
Obviously, no one is asking anyone to simply pay for everything (prevention or treatment) just because it is the right thing to do, no matter the cost.
In real life cost does matter and there is a fiscal responsibility to spend money on things that are effective and deliver real benefits – but let us not wander into weighing one disease against another in making that decision.
And most certainly the question of “fault and responsibility” leads to a very slippery slope, given that so much of what affects our health (from infections to cancer, from accidents to chronic diseases) is often avoidable.
The question really boils down to whether or not there are effective ways to prevent obesity – if there are, they need to be funded, whether they save money or not.
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 be a “U” or “J” shaped relationship between family size and obesity in the offspring – if anyone has data on this, I’d certainly be interested.
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.
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).