Human Biology and Models for Obesity

In reviewing the research and public debates, I have come away startled by the depths of politics and misappraisal about the problem, and the need for human biology to counter this mix of science and morality.  So tonight I’ll write about three problematic things I outlined to my class today, and then show how human biology can provide a useful counter. 

Mind/body and nature/nurture dichotomies run rampant in both public and scholarly discussions of debate.  If it’s not willpower, then it is a biological deficiency.  Genetics causes obesity, or super-size-me environments.  These dichotomies are based on philosophical distinctions that are now centuries old.  They do not match up well with how our bodies, minds, and environments actually work. 

The moralization of fat and the politics of diet produce a tremendous incentive for bias, whether explicit or implicit.  Rhetorical arguments are never really rhetorical in the domain of obesity.  Results are tinged by claims of good and bad, of what’s ideal and what needs to be done.  Since thin-is-in, obesity must be bad, no matter the data; finding that miracle cure, whether it is a diet or surgery or drug, promises huge financial gains, so convenient theories are propped up. 

Suspect science results from both old dichotomies and from the moral politics of obesity.  The moral politics is heightened by the uses of science in establishing authority over a problem, whether it is the government, a medical association, restaurant businesses or soda companies. 

So suspicion grows, and is, in my view, the science becomes quite compromised by the prevailing conceptual model for understanding of obesity—the homeostatic model.  People are not homes, with thermostats.  People do things in their environments; they need to respond to challenges, whether an active lifestyle, a famine, or the demands of growth.   Feedback and feedforward processes do not overturn the basic assumption—stasis, rather than adaptation.  While maintaining internal conditions within favorable limits, a static approach can not account for either weight gain or weight loss (both require change).  Nor can a homeostatic approach deal well with the central issue of appetite, of hunger and temptation and environmental cues.  Something more dynamic is needed. 

So, what does human biology offer?  The first point is easy.  Rather than mind/body and nature/nurture dichotomies, human biology highlights the necessity to consider mechanisms and environment together—the interaction is what matters, for example, a genetically predisposed individual who gains weight in a food-rich environment, with weight maintained (in part) by the concerted action of leptin and gherlin on the brain. 

The second point is more important—variability.  Human variability is rarely considered in obesity debates.  The use of Body Mass Index is a good example—irrespective of sex, build and history of physical activity, people are assigned to a number class: underweight, normal, overweight, and obese.  These classifications then fed into how authority is established in deciding what is a good or bad weight, and what sorts of people “need” to lose weight according to the standards made by others.  The initial promise of treating leptin deficiency as the cause of obesity quickly gave way to the recognition that leptin deficiency accounts for a very-small percentage of obese individuals. 

Finally, human biology has long used the concept of “canalization,” or a focus on how variation gets shaped into certain forms due to organism-environment interactions.  Canalization is a very different model than homeostasis or cause-and-effect, and is an apt metaphor for genetics, fetal programming, or brain systems.  In particular, canalization forces us to think about how to account for the range of variation that we observe.  And it also points to the limits of variation, that once a biological system gets pushed in a certain direction, it is hard to get back to that original state of greater potential variation.  Large weight gain appears to have a canalizing effect for many individuals. 

In the end, human biology offers a series of contrasts to normal thinking about obesity: 

Categorical Thinking vs. Variability
Cause/Effect vs. Canalization

Homeostasis vs. Allostasis

Rather than categories like “obese” or “nature,” we need to start with an assumption of variability.  Our present categories dictate our results too much.  Variability, in both the processes that account for obesity and the health effects of excess weight, is the norm, not the exception. 

Rather than a cause/effect model, say genes or environment, we can think about how the flow of genes gets shaped by the gates of environment, sending the rush of water in one direction or another.  In a highly active environment, most individuals will have their energy regulatory systems canalized around meeting on-going demands.  In a sedentary environment, energy storage can take precedence, and in an eating-promoted and food-rich environment, that storage can get gated to even further extremes.

Allostasis, rather than homeostasis, represents a better conceptual starting point for thinking about obesity.  Allostasis encompasses both change and stability, hence can deal with appetite and weight.  Rapid weight gain through a combination of high-calorie eating and stress can then become a stable point once the stress is gone.  The homeostatic model offers the illusion that you can simply turn up or down the thermostat, thus regulating weight according a person’s or society’s ideals.  But the science and the frustration of millions attest to different dynamics.

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