As many are well aware, obesity in the United States has reached "epidemic" proportions (Centers for Disease Control), with about two-thirds of us overweight. Helpful consequence-based approaches are discussed in my book. But wouldn’t it be easier just to pop a pill that would reduce appetite?
The drug rimonabant did just that, first for animals, and then in human clinical trials. It was on the market as a prescription drug only briefly, though: As you might have guessed, it was too good to be true, and came with problematic side effects. But suppose we could better understand how it works? And how it interacts with some of the relevant genes?
A particular genetic strain of rats is primed for obesity, and has been used for decades as a model for related human problems, such as diabetes and high blood pressure. These rats still don’t necessarily become obese, they’re just more likely to. Erin Rasmussen and colleagues, for example, studied these rats working for sucrose pellets--table sugar. They showed that when the schedule of reinforcement became lean enough (that is, required a lot more work per sucrose pellet), these rats worked no harder and earned no more rewards than normal rats. As always, nature-and-nurture systems offer lots of interactions and flexibility.
It’s probably obvious that increasing the amount of work to get a consequence is similar to increasing its price--making the economic demand likely to decrease. If it’s something we can’t live without, though, like water in a desert, we’ll do whatever we need to: Demand is "inelastic" in that case. My own demand level for premium breakfast cereals is seriously elastic: I don’t buy one unless it’s on sale! It's simply not a powerful enough reward to overcome a high price. Mathematical relations let scientists compare demand levels and degree of elasticity in precise ways.
In a follow-up article that appeared this year in the journal Physiology and Behavior, Rasmussen and colleagues checked out the effects of rimonabant on food reward value and elasticity in the normal and "obese" variants of this rat strain. Sucrose was again the reward, and these nuggets of pure sugar are usually as desirable to rats as they are to us. The schedule of reinforcement was a "fixed ratio," which means it was work-based: just 1 lever press per pellet at first, then 15, 30, 50, 90, 150, and 300 (whew). At the lower prices (lower ratio values), the overweight rats worked harder and earned significantly more sweet rewards than the normal ones, as we might expect. But, when the going got tough, as in the earlier study, all the rats behaved similarly: The obese rats were no longer working more and eating more. Now add the appetite-reducing drug, with its known effects on neurophysiology. Not surprisingly, all the rats stopped working as hard as they had before: Sucrose wasn’t as rewarding. Mathematically, elasticity increased for both groups.
What a great example of interdisciplinary work, including behavioral economics, neuroscience, schedules of reinforcement, reward value, genetics, and more. Research like this helps us understand how all these factors interact, and may lead to practical applications in preventing and treating obesity.
Meanwhile, check out the effective consequence-based methods that already exist if you want to work on your weight. David Freedman's recent articles offer a good, accessible introduction (for example, here).
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