Addicts’ brains depressed but normal users… normal.

A paper that’s about to be published in the journal Science has found at least part of the difference between the brains of addicted individuals and those that use recreationally.

The question as to why only some people get addicted to drugs has been a difficult one to answer. Still, there’s no doubt that only a relatively small fraction of those exposed to drugs develop the compulsive, often destructive pattern of use we associate with addiction. The pattern holds in animal research too – even though all the animals in an experiment get the same amount of drugs, delivered in the same way, only some of them develop addictive drug taking. It seems there’s something different about addicts’ brains, but what is it?

What’s different about addicts’ brains?

We’ve found quite a few things that differentiate addicts’ brains from those of normal research participants. These include lower density of a certain type of dopamine receptor (D2), reduced activity in specific brain parts like the OFC (orbitofrontal cortex) that are important in decision making and behavioral control. Still, if we start with what is supposed to be a pretty similar group of rats and give them all the same drug, for the same time, in the same amounts, why do only some get addicted?

This recent study found that a specific neuronal process called LTD (Long Term Depression), that is important in learning (or what we call plasticity) is suppressed in addicted animals for far longer than in animals that end up not not displaying addictive behavior. Even though all animals displayed this sort of deficiency in LTD right after learning to take drugs, only the addicted animals showed it when tested two months later.

Since the difference was seen in an area of addicts’ brains called the Nucleus Accumbens, a very important area for learning about rewards, it seems likely that it plays an important role in addicts’ inability to change their behavior after they’ve started using drugs. Past research has already identified this as a problem with something we call “reversal learning” but it seems we may have just found at least part of the mechanism.

Now we have to figure out why some animals show this sort of pattern and others don’t. Genetic variability seems like a good place to start here.

Citation:

F. Kasanetz, V. Deroche-Gamonet, N. Berson, E. Balado, M. Lafourcade, O. Manzoni, P. V. Piazza, Transition to addiction is associated with a persistent impairment in synaptic plasticity. Science 328, 1709–1712 (2010).

Obesity, drug addiction, and dopamine

Eating junk-food can be addictive, and apparently, it causes brain changes that look eerily similar to drug addiction. That’s the message not only from the rapidly fattening waistlines of Americans everywhere, but also from the Johnson and Kenny labs at the Scripps Institute.

Food and drug addiction

The idea that obesity is caused by a compulsive pattern of eating, and that there could be a similarity between such compulsive eating and drug addiction isn’t super new. In fact, Dr. Volkow from NIDA seemed to make research into this association her goal when taking  the helm of the addiction research kingdom.

When you think about it, the notion isn’t far-fetched: Drug addicts continue to take drugs, in increasing amounts, even though they’d often like to stop (at some point) and in the face of negative consequences and the common loss of other important life functions (like family, work, etc.). Obese individuals are quite the same, eating more and more food regardless of their desire to adopt a healthier diet and in-spite of ridicule, low self-esteem, and decreased functioning that often accompanies extreme weight gain.

The research by Johnson and Kenny examined whether exposure to the kind of high-fat, super high-calorie foods that floods the junk-food market are responsible for creating food-addicts in a similar way to drugs that alter the brain in ways that make stopping more difficult.

Dopamine, reward, and junk-food

The study took three groups of rats and gave them either the regular chow diet lab animals are used to or the worse kind of birthday party food: bacon, sausage, cheesecake, pound cake, frosting and chocolate. You can imagine the party going on in the rat cages that got to eat that! Of the two groups that got to eat the crazy-fat food, one had unlimited access while the other got to binge for only one hour a day.

The bottom line: Only the rats that got unlimited access to the fat-party food developed compulsive eating habits that resulted in roughly twice the weight gain of the other two groups and the ability to continue eating even in the face of signals for punishment (a light that they were trained to associate with shocks).

When the researchers looked deeper, they found that the brains of these rats suffered a significant reduction in the density of a specific kind of dopamine receptor (D2) in a brain part known as the striatum, the same kind of reduction common in drug addicted people and obese individuals. This receptor type is often thought to be important for regulation of impulses, both physical and otherwise. It therefore makes sense that losing this type of function would cause uncontrollable eating or drug taking.

Are drug- and food-addictions the same?

While this research isn’t saying that compulsive eating, or obesity, are the same as drug addiction, it does strongly suggest that there are common mechanisms in both. More importantly, it reveals a common process that unfolds when over-exposure to the reward, in this case food, occurs. This tells us that there can likely be common pathways to these different addictive disorders, though whether any specific person ended up a food- or drug-addict because of this kind of process is still an open question. I wonder if we’ll see something like this with sex addiction soon…

Citation:

Johnson and Kenny (2010) Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nature neuroscience, 13, 635-641.