Scientists say they've finally discovered why smokers tend to gain some weight when they kick the habit.
It turns out that nicotine can rev up brain cells that normally signal people to stop eating when they're full, researchers report in Friday's edition of the journal Science.
The weight connection isn't huge: On average, quitters gain less than 10 pounds. Still, it's a worry that many smokers cite when asked why they don't try to quit. Now the question is whether the discovery might lead to better treatments to help them quit without worrying about weight.
Yale University associate research scientist Yann Mineur stumbled onto the connection while studying a nicotine-related substance in mice - and the animals suddenly started eating less.
Nicotine hooks onto a variety of receptors, or docking sites, on the surface of cells. That's how it triggers addiction in one part of the brain.
But when it comes to weight, the Yale research found that both nicotine and the related drug cytisine were activating a different receptor than the one involved in addiction. This one is located on a small set of neurons in the hypothalamus, a region that regulates appetite.
When they gave nicotine to mice without that cellular pathway, it didn't help them lose weight like it did normal mice.
Smoking causes cancer, heart attacks and a host of other ailments so worry about modest weight gain shouldn't deter someone from quitting. But smokers who do have that concern should try nicotine-based smoking-cessation treatments, said study senior author Marina Picciotto, a Yale professor of psychiatry and neurobiology.
The other drug used in the mouse experiments, cytisine, is sold in Eastern Europe for smoking cessation but not in the U.S., and she'd like to see if there's data on the weight of smokers abroad who've used it.
Developing a drug to target only these specific receptors would be difficult, she cautions, because they're also involved in the body's stress responses in ways that could lead to such side effects as high blood pressure.