Obesely Speaking

The brain and obesity

Compulsive Overeating and Habit Formation

How a thread becomes a cable
Joseph Troncale, M.D. FASAM
This post is a response to Your Lizard Brain by Joseph Troncale, M.D.

Welcome to the first post of Obesely Speaking: The Brain And Obesity. Question: Why am I doing this? Answer: I am black, morbidly obese, and have a Ph.D. in neuroscience. It’s an elite group, and not by choice.  According to The Centers for Disease Control, (2009–2010) 35.9% of Americans over 20 were morbidly obese, with Blacks and Hispanics comprising the lion share.  Next to smoking, morbid obesity is the leading “preventable” cause of death. The compulsive overeater in me says, “Define preventable; sounds like ‘one size fits all’ to me”.  The neuroscientist in me says, “The issue is not defining ‘preventable’, but defining how to prevent overeating.” On this blog, I will speak from both perspectives. 

I have been struggling with compulsive overeating since I learned to feed myself.  Compulsive overeating resulting in morbid obesity has essentially deconstructed my life.  My top weight was nearly 1,000 pounds; 973 pounds to be exact, according to the bulk-mail scale at the Post Office (or in my case the bulk-male scale). I am now in the low 500’s. I’ve learned some things along the way.  I want to share them here. They may save my life. But, if I fall short of that goal, then at least I will have had this forum to give a small voice to a large, silently suffering, population.  Having said that, thank-you for being here, and let’s get to it.  

If the brain were a television network, addictive, compulsive behavior would be a reality show called, “Habits Gone Wild,” starring Compulsive Overeating. But, the brain is not a TV network and addictive, compulsive behaviors are not celebrities. They are just habits.

Human habits are simple forms of learning that are frequently repeated and tend to occur subconsciously.  For example, when you walk into a dark room you flip the light switch because you want to turn on the light and you’ve learned flipping a light switch does that.  This habit is a goal-oriented behavior; you flip the switch to achieve the goal of having more light.  This, like all goal-directed habits, is motivated by consequence.

But have you ever had a bulb burn out, and forgot to change it, but every time you walk into that room, you flick the light switch anyway? This habit is a stimulus-response behavior. The stimulus of entering a dark room causes the automatic response of flipping the light switch. So, stimulus-response habits differ from goal-directed habits because they are motivated by stimuli as opposed to outcomes.

Neuroscientists have long understood the distinction between goal-directed behaviors and stimulus-response behaviors. Normal eating is goal-directed behavior; compulsive overeating is not. Even Ray Charles can see that, and he’s dead and blind.

Compulsive overeating is a complex stimulus-response behavior. The stimulus may vary. For example, the stimulus could be boredom, anger, happiness, sexual frustration, fear, or anxiety.  The strength of the response may also differ.  It could range from eating until your stomach feels slightly uncomfortable to eating until you vomit.  The consequence of compulsive overeating can run the gamut from being slightly overweight to morbid obesity or bulimia nervosa. I know; I’ve been there and done all three.  Regardless of where the specific elements fall on the spectrum, or what eventuates, at the end of the day, compulsive overeating is still a goal-directed behavior that has become a stimulus-response habit gone horribly awry.  Why does this happen, and how does this neuro-drama unfold in the brain?

Once neuroscientists believed goal-directed behaviors began in the prefrontal cortex and repetition caused them to encode in the basal ganglia in the dorsal striatum. For example, your pre-frontal cortex makes the decision “I want to exercise in the morning.” So, every morning you wake up and think, “I decided to exercise in the morning” and you get out of bed and do 20 push-ups. Eventually repetition encodes that goal-directed behavior in your dorsal striatum.  Once a goal-directed behavior is encoded in the dorsal striatum, it becomes a stimulus-response behavior. In this example, when that occurs you will no longer need the pre-frontal cortex to initiate the goal-directed behavior of exercising in the morning. When you wake up, you will automatically do 20 push-ups because waking up is the stimulus and doing 20-push ups is the response.

While the neuroscientist in me knew this was true, the compulsive overeater in me knew it could not be whole the truth. Far too many of my goal-directed decisions regarding diet and exercise did not encode in my dorsal striatum as healthy stimulus-response habits. Regrettably, it was the repetition of unhealthy habits that my dorsal striatum latched on to. Repeatedly, I had made the decision to exercise regularly and eat healthy foods. Yet, I always found myself in Mickey D’s drive-thru line with “super-size me” on my lips and a Big Mac on my breath. Where was my prefrontal cortex when I was going from “no pain no gain” to “no pickles no onions?”

Well, as it turns out goal-directed behavior doesn’t always begin in the prefrontal cortex. There are actually two goal-directed behavior sources contributing to habit formation in the dorsal striatum: the pre-frontal cortex, and the ventral striatum.  When the pre-frontal cortex initiates a goal-directed behavior, the more it is repeated the more deeply it is encoded by the dorsal striatum. When the ventral striatum generates a goal-directed behavior, dopamine is released by the mesolimbic pathway, which makes the dorsal striatum more likely to repeat the action in the future. This is because both the ventral and dorsal striatum are dopaminergic, although they utilize dopamine differently and serve different purposes in the brain. In the dorsal striatum, dopamine initiates action, but in the ventral striatum, it signals reward.  

Also, the nucleus accumbens, home of the brain’s reward system, is in the ventral striatum.  Addiction was born and raised in this brain region. Incentive salience is a key component of addiction. Incentive salience is your brain’s reward utility. It works by using sensory cues, associated with memory or imagination, to motivate you to want to do something based on anticipating the reward of doing it. For example, wanting to eat signals the reward of eating, thereby causing dopamine release and alteration to neurons, neural pathways, and other structural and functional elements of the brain. 

The brain releases more dopamine when you want to do something than it does when you actually do it. That’s because in the brain’s reward game, the trick is to get you to want to do something enough to do it; once that happens, game over. That’s messy because suddenly, due to the larger amounts of dopamine released in wanting to eat, wanting to eat potentially becomes more pleasurable than eating. This is partially why compulsive overeaters eat beyond the point of a pleasant, healthy experience. It is not the eating that is driving the compulsive, addictive behavior but the obsession with wanting to do it. Actually, it is the obsession with the extra dopamine that is released when you want to do something because of a reward cue. Compulsive overeaters, like all addicts, are not in it for their substance of choice. They are in it for the dopamine. This is not news.  It happens in alcoholics and drug addicts, 24/7/365. It is the signature of addiction. 

However, in normal eaters, the pre-frontal cortex, like a nagging mother, imposes impulse control. “Don’t eat any more, you’ve had enough,” “Get some exercise, you look like a bean bag chair with lips,” “don’t even think about ordering a meat-lovers' pizza” etc.  However, if you have pre-frontal cortex damage, reduced serotonin, or excessive stress, the prefrontal cortex’s ability to impose impulse control decreases. Even if you’re experiencing a major distraction in your life the prefrontal cortex’s functionality is compromised. This inability to exercise impulse control allows a behavior like eating to transform from being a hedonic goal-oriented habit in the ventral striatum to a compulsive stimulus-response habit in the dorsal striatum. 

Also, since the normal eater’s prefrontal cortex is capable of imposing impulse control, often he or she can’t understand why compulsive overeaters cannot do the same. That is why people think compulsive overeating is a character flaw, as opposed to a functional brain issue. This is harmful because self-perception is partly determined by how we believe others perceive us, based on how we are treated. Thus, this social stigma erodes self-esteem, thereby increasing stress, decreasing serotonin, which further compromises prefrontal cortex function, and feeds (no pun intended) compulsive overeating behaviors.

Regrettably, researchers cannot conduct functional MRI studies on the morbidly obese, because there are no machines capable of producing worthy data that can accommodate us. On a more positive note, historically, compulsive overeating has been virtually identical to alcoholism in studies where both alcoholics and the morbidly obese can participate. Thus, I suspect study findings about alcoholics probably hold true for compulsive overeaters as well.  

Studies have shown that alcohol cues cause greater activity in the ventral striatum in light drinkers compared to heavy drinkers. However, heavy drinkers show greater activity than light drinkers in the dorsal striatum in response to alcohol cues. This is probably because heavy drinkers are drinking to satisfy an addictive, stimulus-response habit, whereas social drinkers are drinking for pleasure. If you have ever seen an alcoholic drink, you know pleasure has nothing to do with it. I also, know from personal experience, as well as witnessing others, that pleasure has nothing to do with compulsive overeating.

While addictive compulsive behaviors are goal-directed habits from the ventral striatum that have turned into stimulus-response habits gone wild in the dorsal striatum, they are only part of the problem in compulsive over eating.

Like all compulsive addictive behaviors, many factors contribute to compulsive overeating.  Some of the science is simple, much of it is complex, and even more remains unknown.  Fundamental neuroanatomy is universal in humans. However, individual brain function is contextual and singular. Early life experience has a considerable influence on this and is the principal architect of one’s perspective. 

Perspective, not reality, determines how our brains negotiate daily living. Early learning and memory are the chief currencies of that enterprise. If you learn to self-medicate with food as a child, this habit will surely encode in the dorsal striatum. A habit is a cable and each day it weaves a thread. Eventually it is so strong, it seems impossible to break. But there are no cables that cannot be broken, and in the case of compulsive overeating, the cable must be broken.

We all have our buckets of woe and private demons. The onus is on each of us to slay our private demon and reconstruct the concerns that deconstruct our lives. One of the keys in my moving towards some higher ground has been learning how my brain specifically works, hence my interest in habit formation. The greater lesson I’ve learned in exploring this is never to value what my brain has not done, or cannot do, more than I value what my brain has done and is capable of doing. 

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Billi Gordon, Ph.D., is  Co-Investigator in the  Ingestive Behaviors & Obesity Program, Center for the Neurobiology of Stress, David Geffen School of Medicine at UCLA.


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