Neuroimaging reveals a shared basis for chocoholia and drug addiction
This article explains clearly how "natural reinforcers" like food (and sex) can become addictive.
Mounting evidence shows that compulsive eating and drug abuse engage some of the same brain circuits in similar ways, offering a new angle for understanding and treating obesity. In an interview with Scientific American, Nora D. Volkow, director of the National Institute on Drug Abuse and a pioneer in the study of addiction, explains.
How do foods and drugs affect the brain in the same way?
The system in the brain that both drugs and food activate is basically the circuitry that evolved to reward behaviors that are essential for our survival. One of the reasons why humans are attracted to food is because of its rewarding, pleasurable properties. When we experience pleasure, our brains learn to associate the pleasurable experience with the cues and conditions that predict it. In other words, the brain remembers not just what the food tasted like but also the sensation of pleasure itself, and the cues or behaviors that preceded it. That memory becomes stronger and stronger as the cycle of predicting, seeking and obtaining pleasure becomes more reliable. When you remember that food, you also automatically expect the pleasure that comes from it. So when you like something very much, the mere fact of being re-exposed to it, even if it is out of reach, will trigger the desire to get it. In scientific terms, we call this process conditioning.
Conditioned cues or memories are very powerful and can profoundly affect our behavior. And when conditioning occurs to a positive stimulus, such as food, you are much more likely to repeat a particular action to obtain it. Drugs are particularly effective as conditioning stimuli, primarily by virtue of their chemical properties. They can directly stimulate areas of the brain involved with pleasure in a way that is more efficient than natural reinforcers, such as food or sex. You get an exaggerated response (supraphysiological) partly because the drug can get to the brain very fast, in a matter of seconds. With natural reinforcers the process of activating the reward pathway is more prolonged. Importantly, the conditioning that takes place links the behavior not just to the stimulus itself but to the environment and other cues that might have been only peripherally associated with it.
That’s exactly what nature intended: if the behavior necessary to seek a pleasurable experience was triggered exclusively by the object, the conditioned response would be very ineffective indeed; think about the need to find food to survive, for example: say we are primitive creatures in the jungle and you by pure chance taste a banana. The banana tastes good, but if you were just conditioned to remember that it tasted good—and not to the smell, the shape, the color, or the location of the banana—your ability to find it again would be impaired. Once you create this conditioned memory, though, it’s just like Pavlov’s dogs; the response becomes a reflex. This conditioned response underlies both the drive in drug addiction and the drive in compulsive eating.
What’s going on in the brain during cravings?
Had Pavlov been able to see inside the dog’s brain, he would have very likely seen that there is an increase in dopamine in the brains of those dogs when they get exposed to the sound previously paired with the meat. Dopamine tells us what's important—the unexpected bits of new information we need to pay attention to in order to survive, like alerts about sex, food and pleasure, as well as danger and pain. Indeed we’ve tested these in humans using brain imaging technologies. The human brain is highly sensitive to food stimuli. We’ve documented that when you show people favorite foods, to which they’ve been conditioned, there is an increase in dopamine in the striatum which is a brain region involved with reward and behavioral motivation. Mind you, this increase is just from smelling and looking at the food, because we tell study participants that they will not be able to eat it. And this is the very same neurochemical response that happens when addicts see a video of other people taking drugs, or anything to do with their drug of choice, like where they normally take it or with whom they take it.
Also in the brains of both drug addicts and obese people we typically find a reduced number of D2 dopamine receptors in the striatum, compared to non-abusers and non-obese controls, respectively. Perhaps these findings reveal that the brain is somehow trying to compensate for the repeated surges inn dopamine stimulation from continuous stimulation with drugs or food. Another possibility is that these individuals had lower numbers of receptors to begin with, a biological feature that may put them at increased risk for diseases of addiction, in general. Low numbers of D2 receptors are well documented in people addicted to cocaine, alcohol, opiates and other drugs. Interestingly, a study by Dr. Gene Jack Wang and colleagues found the same type of relationship between the availability of D2 receptors and Body Mass Index (BMI) in obese individuals. In other words, the more obese a person is, the fewer receptors they have. By contrast, in normal weight subjects, the levels of D2 receptors are not associated with their BMI.
Now the chronic use of drugs—by repeatedly stimulating the dopamine and other systems--eventually leads to a disruption of function in frontal cortical areas involved with inhibiting behaviours and emotions. It is also possible that this circuit is weaker in people who are addicted to drugs from the start, but we don’t know that yet. In obesity, however, we do not have evidence, to my knowledge, that the frontal cortex is similarly disrupted. What has been documented instead is that the drive for food is so powerful that it overrides any ability to exert inhibitory control.
Are particular foods more reinforcing than others? Why?
Yes, absolutely. High calorie foods—particularly foods that are high in fat or sugar—are more likely to trigger compulsive eating. Again, that makes sense from nature’s perspective. As hunters, we didn’t always succeed at finding something to eat and so high-calorie foods, which pack a lot of energy, offered a survival advantage. In that environment, it was in our best interest to consume as much of this type of food as we could find. So they are very reinforcing. But today when we open up our refrigerators, we have a 100 percent chance of succeeding at finding food.
Our genes have changed little, but in our environment, we are now surrounded by high-fat, high-sugar foods. And this abundance is undoubtedly a major factor contributing to the rise in obesity Conditioning responses are incredibly powerful with food: when I go past a vending machine and I see chocolates I like very much, I desire the chocolate even though I’m not hungry. But if those chocolates weren’t there, it would be the last thing on my mind.
Are certain people at greater risk for drug or food addictions?
We know from twin studies that approximately 50 percent of the risk for both addiction and obesity is genetic. But the genes involved come into play on many different levels—from differences in the efficiency with which we metabolize drugs (or food) to differences in our likelihood of engaging in risk-taking or exploratory behaviors to more specific risks, such as the underlying sensitivity of the reward system.
In obesity, some people may be at a greater risk for compulsive eating because they may be overly sensitive to the rewarding properties of food. One study showed that some obese people have increased brain activity in response to mouth, lip and tongue sensations. For them, eating may be much more pleasurable than other natural reinforcers. Likewise, some people are not very efficient at registering or responding to internal signals of satiety, so they are possibly going to be more vulnerable to cravings triggered by food cues in their environment.
For example, in a recent study we looked at obese people who had an Implantable Gastric Stimulator (IGS), which electrically activates the vagus nerve and causes the stomach to expand and feel full. And even with this implant, these people still only manage to lose about five percent of their body weight. On a higher level, they have powerful conditioned responses that can apparently override other regulating signals
Does the overlap between addiction and obesity reveal any new targets for treatment?
There are pharmacological interventions to explore, such as medications that increase the dopamine response in the brain. Rimonabant, which boosts dopamine levels by dampening the endocannabinoid system, has shown promise in helping people who are obese and those who are smokers.
Another exciting development is the recent synthesis and preliminary testing of an orally administered drug that blocks orexin, a peptide that reinforces the “high” associated with drinking alcohol and is thought to regulate feeding. This drug could be extremely helpful in the treatment of specific brain disorders that involve aberrant food and drug taking behaviors. Also, because of the stigma associated with both of these conditions, obesity and drug addiction can lead to a deep sense of isolation, which is very stressful. This is an area where group therapy could help.
Yet another exciting area NIDA is researching is the use of functional magnetic resonance imaging (or fMRI) in biofeedback to train people to exercise specific parts of their brains, just like muscles. Sean Mackey of Stanford University, neuroscientist Christopher De Charms of Omneuron [in SanFrancisco] and their colleagues have similarly trained healthy subjects and chronic-pain sufferers to control their brain activity to actually modulate their experience of pain. So NIDA is exploring the possibility that you might use this kind of biofeedback to train people to control a region of the brain called the insula, which has been implicated in food and drug cravings. Smokers who have a lesion in the insula after a stroke, for instance, seem to lose the desire to smoke.
But one of the major and distinct obstacles for a person trying to recover from compulsive eating is the obvious fact that you have to eat in order to survive whereas, if you are addicted to an illegal substance, you are in a way protected by the fact that that drug is not going to be environmentally available everywhere. One of the therapeutic interventions for drug addicts is to teach them to avoid places associated with their habit. But how do you do that with food? It’s impossible.
And these people suffer. In rats, it has been shown that, if you give them very high-sugar diets and then make them give them an opioid antagonist (naloxone), you can trigger a withdrawal that is similar to that you observe when you give naloxone to an animal that has received repeated injections of morphinel. This indicated that chronic exposure to high sugar diets generated physical dependence. If similar processes happen in humans then interventions to mitigate the appearance of withdrawal symptoms during dieting may benefit the discomfort to the subject and improve outcomes.
Addiction is not a choice. It is a reflexive response. Do you think that Pavlov’s dogs had a choice of salivating when they heard the sound that had been conditioned to the meat? They did not and had you seen inside their brains you would probably have observed that the sound would trigger dopamine increases in their striatum that would be signalling to expect the reward of the meat. The message that you get when dopamine is liberated in striatum—in this case, the dorsal striatum—is that you need to get into action to achieve a certain goal. It is a powerful motivator. It is extremely hard to overcome these impulses with sheer willpower.
Original article at 'Scientific American.com' by Kristin Leutwyler Ozelli