So tomorrow is the big lecture covering some of the biology of obesity.  My attempt to provide a more comprehensive and better integrated view than Kolata’s Rethinking Thin, at least from an anthropological view (which includes both biological and cultural viewpoints, and for me, also brings in a qualitative focus on people’s experiences and behaviors).  Tonight I will cover three topics—the health risks of obesity, the role of activity and exercise in weight, and the mind vs. metabolism debate.  These complement previous posts on the Behavioral Biology of Obesity and Obesity and Genetics. 

Being fat kills, right?  That’s the predominant health message of the past decade or so.  Extra weight is as bad as smoking, and should be as vilified.  There’s just one problem.  The science doesn’t back up such a blanket statement.  Right now it looks like having a few (yes, a few) extra pounds is actually healthier than being too skinny, at least at the population level. 

Some of Kolata’s best writing tells us about the work of Katherine Flegal and colleagues, who used sophisticated population data and statistical work to ask a basic question, What is the health risk of being overweight?  Based on research published in 2005 by the Journal of American Medical Association, Flegal found that individuals who were overweight but not obese (a BMI between 25 and 30) had lower mortality rates than people considered “normal” by BMI standards (86,000 deaths less than expected).  For people with a BMI of 30 or greater, obesity accounted for 112,000 deaths per year, a very large number but quite less than previous estimates of around 400,000 per year. 

This research is well-summarized in this Medical News Today article, which states “the net U.S. death toll from excess weight is 26,000 per year. By contrast, researchers found that being underweight results in 34,000 deaths per year.”  Flegal and colleagues have gone on to provide a wealth of evidence, their own and others’, that confirms their basic point that being overweight is different from being obese, and less risky than generally assumed in the highly charged moral debate in the United States.  As always, there is criticism and controversy over the methods and results, which are well summarized in this piece at Partnership for Prevention and also at The Center for Consumer Freedom. 

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With activity, Greg made a powerful argument that the difference in today’s environment is so much eating as dramatic differences in levels of physical activity.  The foraging and agricultural lifestyles were physically demanding, in ways that are hard to imagine in today’s sedentary world.  For example, among the Amish walking 25 miles a day behind a plow is a rather ordinary feat.  I count myself lucky if I only have to walk 5 minutes to class. 

Exercise is not the same thing as level of activity.  US guidelines point to thirty minutes of physical activity “most days” of the week, i.e., a very class oriented view of doing a work-out.  For sustaining weight loss, the guidelines recommend ninety minutes of exercise a day. 

Certainly there are people ready to push an entirely environmental activity-oriented approach to our obesity problem.  This website, An Epidemic of Obesity Myths, highlights a number of questionable points often made about obesity, for example, that soda causes childhood obesity.  In one summary, they highlight a series of activity-related issues in our modern environment: labor saving appliances, being couch potatoes, driving everywhere, climate-controlled environments, and jobs that emphasize sitting.  It all ends up to less calories burnt per day. 

And, indeed, when we look at twin studies that examine why one identical twin might weigh significant less than another, the prime mover is physical activity.  As this blog relates, “the biggest predictor of weight gain in these genetically identical but weight-discordant co-twins was a markedly lower physical activity level, which in turn, declined even further as the obese co-twins packed on the pounds.” 

But this “increasing activity” approach is a bit too environmental.  The counter-argument is genetics and having enough calories anyways.  But what if activity drives changes in our biological function, say, through allostatic mechanisms that change our weight range and basic metabolic function?  How could such a thing happen?

Levels of physical activity that go beyond simple “exercise” have two effects.  First, in terms of appetite and energy regulation, your brain-body systems orient to having enough energy to maintain adequate daily function every day, thus bypassing significant storage of energy in fat.  In turn, without an increase in adipose tissue, the person is unlikely to have as much leptin release, providing a further buffer against weight gain.  This synergistic effect maintains weight at a much lower allostatic level. 

So, remember, exercise, in terms of low-level activity according to US guidelines, is not a necessary answer to the obesity epidemic, as recent research shows.  Going back to a hunter-gatherer or an agricultural lifestyle is not an option for most people either.  Or working out like a professional athlete.  So, just as overweight and obese are not the same, neither are a lifestyle of activity and a sedentary lifestyle.  We live in the second option.  It might not be bad for most.  But for some, it is not at all good. 

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I’ll end by discussing the mind-versus-metabolism debate.  Hans-Rudolf Berthoud has a 2004 article where he appears to set up a mind/body argument, but it is more subtle than that.  In sedentary environments with rich food available, genetically predisposed individuals suffer, largely due to body weight regulatory systems.  However, Berthoud argues that these systems interface with the environment through neural processes involving the limbic systems and frontal cortices, which “are involved in the initiation, procurement, and appetitive phases of ingestive behavior and associative learning before, during, and after the consummatory phase.”  In other words, these are the systems that the genetics point to as being compromised or vulnerable—appetite and eating, rather than energy regulation.  As Berthoud writes, “learned and unlearned representations of foods and food cues in the orbitofrontal and other cortical areas are filtered for affective/emotional value in the amygdala and for motivational salience in the nucleus accumbens/ventral striatum to initiate goal-directed motor programs.” 

Schwartz and Newsender (2004) argue that this sort of argument can distinguish between “absence of protection” (obesity as the natural result of an obesogenic environment) or “central resistance” (where homeostasis normally protects against weight gain or loss, but genetic or acquired deficiencies make regulatory systems malfunction).  In my mind, we need both types of argument—how environments push us and how our appetitive and regulatory systems push back, with synergistic outcomes.  These outcomes are neither “natural” nor “deficient,” the two basic options the normal/pathological biomedical model provides us.  Rather, they are dynamic outcomes, building from environment/biology interaction. 

And even that is likely not a good enough conceptualization, but I’ll write more about that later…