Addiction, Food and Your Brain

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. Full Article

Extract:

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.

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.

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.

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.

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.

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