Addiction specialists are very interested in any research that illuminates the brain’s reward system.
Because many drugs of abuse (cocaine, meth and others) trigger this system, information about how it works on a neurological level can have applications in treatment.
New research now links calorie restriction to an enhancement of the dopamine reward system in mice.
Calorie restriction linked to higher addiction rates
Scientists at the University of Texas Health Science Center found that fasting mice – mice which had been chronically underfed – had a greater response in their “reward circuits.” The effect showed up as a doubling of neuron firing when cocaine was administered. The phenomenon of calorie restriction leading to higher addiction rates in mice was already known, according to reporting in Science News Daily, but the specifics were missing.
The speculation is that mice (and by implication, humans) are wired by the dopamine system to motivate us to seek behaviors that are usually useful to us. In this light, pleasure triggers associated with food make sense. Enhanced pleasure when food has been lacking for some time also makes sense – if a behavior (eating) isn’t being triggered at one level of dopamine activity, the body might very well turn the dial up as a useful mechanism. Of course, the whole system is corrupted when cocaine enters the picture.
Implications for treatment
On the treatment side, there’s an interesting hypothesis that falls out of this new research. We know humans suffer impairment of the dopamine reward system while trying to kick cocaine. One of the significant effects of withdrawal is an inability to take pleasure in normal activities – without the cocaine pushing the buttons of our dopamine system, it’s much more difficult to experience positive feelings, including enjoying activities that were once pleasurable.
So what if you introduced calorie restriction? If dopaminergic neurons fired more frequently under fasting conditions, it might be a way to mitigate the effects of cocaine withdrawal until the brain returns to normal.
As always, the research invites more questions and comes with the caveat – mice aren’t people. But the hope remains that further understanding will lead to better treatments.