Obesity prevalence: nothing new but something weird

 I’ll admit to being blasé about the rising U.S. and global obesity prevalence.  It’s a huge public health problem, of course, but it just seems like I’ve been waiting for someone to tell me more than just:  “We have a big problem here…it’s getting worse…we’re not sure why…we’re not taking enough public health measures to control it.”  What you don’t hear very often:  “Even if we do take strong public health measures to control obesity’s scourge, we’re not at all sure they’ll have any effect, because we don’t understand the cause of the problem to begin with, and behavioral manipulations are unlikely to have a large impact of themselves.”

Unfortunately, I’m not going to be the one to tell you something Earth-shatteringly new.  So, I’ll just ruminate about something old–the obesity prevalence trends.  Have you taken a look at them closely?  They’re rather startling, and not in the ways that make headlines. 

What we learned back in April (from the JAMA article by CDC personnel describing 6-year (1999-2004) trends in NHANES obesity-prevalence data) was that obesity prevalence is on the rise generally, affecting an astonishing 32% of adults over age 20.  The small bit of good news from that study was that the rise appeared confined to men–the rise in women appeared to be leveling off–although all ethnic and age groups were affected.

What we’re hearing today is a bit different.  In today’s MMWR (mm5536.pdf), CDC is reporting longitudinal 11-year data (1995-2005) from the BRFSS, which relies on self-reported height and weight to calculate BMI, rather than actual measurements, like NHANES.  BRFSS generally underestimates BMI substantially, but trends in self-reported and measured BMI usually closely parallel each other.  In the case of the BRFSS results, however, there was no apparent leveling off of rising prevalence of obesity in females.  How to explain this discrepancy in survey findings?  I really don’t know.  Normally, I’d say that the measurements more likely reflect reality, but height and weight measurement techniques have likely changed subtly over time, so in this case, I’d say that the self-reported results from BRFSS are at least as likely to reflect the truth.

This one issue aside, what strikes me as weird about obesity prevalence trends in the U.S. generally is how they are affecting everyone, everywhere.  What I mean by this is that the prevalence of obesity is on the rise in every geographic region of the country, in every self-reported ethnic group, in every age group, and probably in both sexes.  What other chronic disease (or condition, if you prefer), unrelated to obesity, has proliferated as relentlessly in modern times without regard to one of these factors?  I can’t think of one.

Think a bit about the implications of these observations.  They suggest that the underlying cause of obesity is more than meets the eye–more than vending machines in schools; more than the proliferation of Starbucks, McDonald’s and their ilk; more than the sowing of a nation of couch potatoes.  If these “lifestyle” factors alone were necessary and sufficient for the growth in obesity prevalence across-the-board, we would expect to see unequal growth according to behavioral patterns that would likely be reflected in both age and ethnic groups.  That we don’t see this pattern is, for lack of a better description, weird.  It suggests to me that lifestyle alone is not sufficient to explain the rise in obesity prevalence in the U.S.; necessary perhaps, but not sufficient.

So, where else to look?  Left with no obvious explanations, more attention should be paid to non-obvious environmental factors, particularly infectious (e.g. viral, prion) and toxic.  Some work is being done in these areas but not nearly enough.  Scientists used to laugh at the notion that such agents are potentially important actors in chronic disease, until the early 90’s when peptic ulcers were found to be caused by bacteria.  Now, scientists don’t mock these notions, but they’re usually investigated as last resorts, after the “obvious” actors have been ruled out.  With as much as a third of the nation obese, it’s time to delve deep into the non-obvious, the weird.

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1 Comment »

  1. Pharma’s Cutting Edge » New evidence linking viruses to obesity said,

    August 21, 2007 at 12:49 pm

    […] Last September, I noted that the epidemiology of modern obesity (in the last couple decades) strongly suggests transmissible or pervasive environmental factors–more persavive even than junk food and sedentary behavior–at work in its etiology.  Now, Magdalena Pasarica, M.D., Ph.D., of the Pennington Biomedical Research Center and her colleagues are reporting at the American Chemical Society meeting that adenovirus-36 (Ad-36), a common form of this common human-infecting virus, is capable of differentiating adult human stem cells into fat: In the current study, Pasarica and her associates obtained adult stem cells from fatty tissue from a broad cross-section of patients who had undergone liposuction. Half of the stem cells were exposed to Ad-36 and the other half were not exposed to the virus.  After about a week of growth in tissue culture, most of the virus-infected adult stem cells developed into fat cells, whereas the non-infected stem cells did not, the researchers say.  Funded by the National Institutes of Health (NIH), Dr. Dhurandhar’s group recently identified a gene in the Ad-36 virus that appears to be involved in causing fat accumulation observed in infected animals. That gene, called E4Orfl, is now emerging as a promising target for future human therapies, such as vaccines and anti-viral medicines, aimed at preventing or inhibiting the obesity virus, she says. […]

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