Anorexia and the Diet-Exercise Trap

It is commonly assumed that eating disorders like anorexia nervosa are driven purely by modern social pressures and distorted body images. And while yes, these psychological factors play a powerful association with restriction, behavioral psychology specifically the research detailed in Chapter 12 of Introduction to Learning and Behavior (Powell et al., 2016) suggests a biological mechanism that can keep someone trapped in the disorder. Being vulnerable and looking back at my personal struggles with anorexia when I was 17 years old, I used to think it was just a battle of willpower and restriction. I used to think it was all about trying to match a specific body standard. But learning about activity anorexia altered how I view the struggle. It showed me that the disorder is less simply about willpower and more about a brutal cycle where evolutionary adaptations and brain chemistry are able to drown out rational thought (Powell et al., 2016). Which makes sense in retrospect, as I knew what I was doing to myself was illogical and harmful, yet I couldn't stop and felt addicted. In a lab, behaviorists can actually recreate this exact human behavior in lab rats using a simple yet sad trick. They limit the rats to just one 1.5-hour feeding window a day, but let them use a running wheel as much as they want during the 22.5 hours between meals. (Pierce & Epling, 1991) What follows is a pretty crazy behavioral loop: The less the rats eat, the more they compulsively run; and the more they run, the less they want to eat when their food window finally opens. Within a single week, this whole cycle completely spirals out of control. The rats end up running up to 12 miles a day while refusing to touch their food, which obviously leads to severe emaciation. Interestingly, rats on the same strict diet without a wheel do just fine, and so do rats with a wheel but no diet restriction. It's purely the combination of severe dieting and a sudden spike in exercise that snaps the trap shut. 

So, why does the brain lock into a cycle of self destruction? It makes sense when simply looking on a neurophysiological level, the mechanism is heavily driven by endorphins, similar to morphine-like substances in the brain, which are naturally associated with pain reduction as well as the euphoric feeling we call a "runner's high". Research shows that when rats in a state of food deprivation run excessively, it triggers a massive endorphin release. Because drugs that block endorphins will temporarily stop the wheel running, scientists are able to conclude that both activity anorexia in rats and anorexia nervosa in humans are maintained by essentially an addiction to an endorphin high. When I was 17, I vividly remember how the empty sensation of hunger and the exhaustion of exercise I forced myself to endure daily would bizarrely keep me in an intoxicating "high” with many others who have faced the same disorder frequently reporting this. From an evolutionary perspective, this connection between starvation and high levels of activity actually served an adaptive purpose. In the wild, an animal faced with a sudden, severe scarcity of food supplies cannot survive by sitting still and waiting to starve. Instead, their internal feeding system kicks off a general search program, triggering the animal to get hyperactive so it can travel long distances to find a brand new food supply. Under extreme evolutionary pressure, the brain is even wired to ignore small, low energy food prompts along the way so the animal stays completely focused on migrating until it hits a rich resource zone. However, when a modern human uncovers this ancient evolutionary survival software through a voluntary diet, the brain misinterprets the restriction as a localized famine. The biological system commands us to run and move, creating intense restlessness while the endorphin release also makes starvation feel less distressing.  We tend to look at this constant movement as a willful strategy to burn up calories. But even if it starts out as a conscious decision, the routine eventually becomes autonomous. It shifts from being something under your control to a purely biological reflex that completely overrides your actual choices (Boakes, 2007). Figuring out the mechanics behind activity anorexia completely changes how we look at treatment and prevention. Behavioral therapy has to focus just as much on bringing extreme activity levels down to a normal baseline level as it does on getting someone to eat normally again. Looking back at these struggles with this behavioral understanding shows that what feels like a purely emotional or psychological battle is often a manifestation of our biology and evolutionary conditioning playing out. (Guisinger, S., 2003)

My critique: While understanding the evolutionary and biological side of activity anorexia feels incredibly eyeopening,  my main critique is that a purely behaviorist solution is too narrow for real world recovery. In a lab, you can cure a rat simply by taking away its wheel and changing its feeding schedule. But with humans, you can't just fix the physical routine and expect the disorder to vanish. Treating anorexia strictly as an outdated biological glitch ignores the deep anxiety and distress as well as the very mindset behind it. Behavioral conditioning models can be great at explaining the physical cycle of a disorder, but ultimately in situations like anorexia disorder they fall short because they try to treat a deeply emotional human struggle like a purely mechanical issue. 

References

• Epling, W. F., & Pierce, W. D. (1991). Solving the anorexia puzzle: A scientific approach. Hogrefe & Huber Publishers.

• Powell, R. A., Symbaluk, D. G., & Honey, P. L. (2016). Introduction to Learning and Behavior. Cengage Learning. 

• Boakes RA. Self-Starvation in the Rat: Running versus Eating. The Spanish Journal of Psychology. 2007;10(2):251-257. doi:10.1017/S113874160000651X 

• Guisinger, S. (2003). Adapted to flee famine: Adding an evolutionary perspective on anorexia nervosa. Psychological Review, 110(4), 745–761. https://doi.org/10.1037/0033-295X.110.4.745