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) 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. My compulsive overeating resulting in morbid obesity has radically 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 500’s. I’ve learned some things along the way. I want to share them here, so let’s get to it.
Habits are simple forms of frequently repeated learning that often occur subconsciously. For example, you walk into a dark room and flip the light switch because you want to turn on the light, and you’ve learned to flip a light switch to accomplish that. This habit is a goal-oriented behavior; you flip the switch to achieve the goal of having more light. Flipping the light switch, like all goal-directed habits, is motivated by consequence. But have you ever had a bulb burn out, and forgotten to change it? Yet, every time you walk into that room, you still flick the light switch. 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 stimulus, as opposed to outcome motivated.
Neuroscientists have long understood the distinction between goal-directed behaviors and stimulus-response behaviors. Normal eating is goal-directed behavior. Compulsive overeating is a complex stimulus-response behavior. (1-4) The stimulus may vary (boredom, anger, happiness, sexual frustration, fear, or anxiety). The strength of the response may also differ (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 morbidly obesity or bulimia nervosa. 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 work out 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 knows this is true, the compulsive overeater in me knows it cannot 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. Conversely, it was the repetition of unhealthy habits that my dorsal striatum developed. Repeatedly, I had made the decision to exercise regularly and eat healthy foods. Still, 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. Two goal-directed behaviors contribute 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.1 The reason this is liable to happen is that 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.3,4
Incentive Salience and Addiction
The nucleus accumbens, the epicenter of reward, is also in the ventral striatum. Incentive salience is a fundamental 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.
Hence, the brain releases more dopamine when you want to do something than it does when you do it. That’s because, in the reward game, the trick is getting you to want to do something enough to do it; once that happens, game over. That’s problematic because the larger amounts of dopamine released in wanting to eat, make wanting to eat more pleasurable than eating. Hence, compulsive overeaters can eat beyond the point of a pleasant, healthy experience. It is not the eating experience that is driving the compulsive, addictive behavior but the extra dopamine derived from wanting to do it because of the reward cue.4 This scenario is the signature of any and all addiction.
However, in regular eaters, the pre-frontal cortex, like a nagging mother, imposes impulse control. “Don’t even think about eating more food; you look like a bean bag chair with lips.” 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. Addictive, Compulsive goal-directed behaviors in the ventral striatum turning into stimulus-response habits in the dorsal striatum are only part of the problem. 5,6
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 main 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; the cable is impossible to break." my mother used to say. She was wrong. There are no cables that we cannot break; Compulsive overeating is a cable that we must break.
We all have our buckets of woe and private demons. The onus is on each of us to slay our private demon and reconstruct our lives. One of the keys to my moving towards that higher ground is learning how your brain specifically works. More importantly, it is learning never to value what your brain cannot do than what it can do. Remain fabulous and phenomenal!
1. Jog, M.S., et al., Building neural representations of habits. Science, 1999. 286(5445): p. 1745-9.
2. O'Tousa, D. and N. Grahame, Habit formation: implications for alcoholism research. Alcohol, 2014. 48(4): p. 327-35.
3. Sturman, D.A. and B. Moghaddam, Striatum processes reward differently in adolescents versus adults. Proc Natl Acad Sci U S A, 2012. 109(5): p. 1719-24.
4. Wise, R.A., Brain reward circuitry: insights from unsensed incentives. Neuron, 2002. 36(2): p. 229-40.
5. Fineberg, N.A., et al., Probing compulsive and impulsive behaviors, from animal models to endophenotypes: a narrative review. Neuropsychopharmacology, 2010. 35(3): p. 591-604.
6. King, J.A., et al., Neural substrates underlying impulsivity. Ann N Y Acad Sci, 2003. 1008: p. 160-9.