Alcoholics are usually smokers, too, and that presents something of a problem for someone trying to get back on the wagon. It seems that smoking makes it harder to quit drinking. Puzzlingly, it’s not nicotine but rather an as yet unknown component of tobacco smoke that’s to blame, according to research published today.
Both alcohol and nicotine dependence result from complex processes in the brain, involving a number of different chemicals, known as neurotransmitters, that help regulate signals sent from neuron to neuron and across regions of the brain. At the same time, tobacco smoke in particular has many different components, making it tough to sort out how alcohol and nicotine interact. One known point of overlap between alcohol and nicotine addiction, however, is a neurotransmitter called gamma-aminobutyric acid A. GABA-A actually slows down signals as they spread through the brain, but it’s thought that it underlies the particular kind of high one gets when drinking and that nicotine similarly stimulates production of the chemical.
Both alcohol and nicotine dependence result from complex processes in the brain, involving a number of different chemicals, known as neurotransmitters, that help regulate signals sent from neuron to neuron and across regions of the brain.
Complicated brain chemistry aside, the connection led Yale University’s Kelly Cosgrove and her team to wonder what would happen if someone went through alcohol withdrawal while either continuing or quitting smoking. They studied 22 alcohol-dependent men and five alcohol-dependent women along with 20 men and five women who weren’t addicted to alcohol. About three-fifths of both groups were smokers. Doctors admitted the alcoholic group into the Department of Veterans Affairs’ Clinical Neuroscience Research Unit for a treatment program, during which time they underwent PET scans to measure the availability of GABA-A receptors—basically, the number of spots where a GABA-A molecule could attach and do its work—in different parts of the brain.
Over a four-week period, alcohol withdrawal led to higher levels of GABA-A receptor availability in both smokers and non-smokers, and at the same time, cravings for alcohol declined in both groups. However, alcohol-dependent non-smokers’ levels returned to that of the non-smoking controls by the end of four weeks. Alcoholic smokers’ levels remained level throughout the treatment period. Meanwhile, while both alcoholic smokers’ and non-smokers’ displayed less desire to drink as the treatment went on, smokers generally had about twice as much desire to drink compared with non-smokers. An additional analysis suggested that there was a connection between GABA-A receptor availability and cravings for alcohol, but only among smokers. Finally, a study using rhesus monkeys found that nicotine didn’t play a role in GABA-A receptor availability, leaving exactly how smoking affected GABA-A unclear.
“Continued smoking during withdrawal interfered with the subsequent normalization of the GABA-A receptors and was associated with higher levels of craving, which may increase relapse risk,” the authors write in Proceedings of the National Academy of Sciences. The team also concluded that researchers looking to treat alcoholism should focus on the GABA-A system in future studies.
