ľ¹Ï¸£ÀûÓ°ÊÓ

When people stop smoking, they often gain weight even when they are on the same diet. The reason for this is largely unknown. Leviel Fluhr and his colleagues from the Weizmann Institute of Science in Israel found that gut flora are important regulators of this weight gain in mice.

Quitters gain 4.5 kilos on average and 13% even gains 10 kilos within their first year of stopping. This is a serious problem as it prevents people from stopping and it induces quitters to start smoking again. Understanding how this weight gain happens will help to find a solution.

The of Fluhr recently published in Nature found that mice exposed to smoke gained weight when the exposure stopped compared to mice not exposed to smoke. When mice were given antibiotics, that deplete gut bacteria, they gained less weight after smoking cessation. This was supported by fecal transplantations, procedures in which mice without gut bacteria (recipient) receive stool from mice with gut bacteria (donor). When recipient mice received stool from donor mice that were exposed to smoke or recently ceased exposure, they gained weight. These results suggest an important role for gut bacteria in regulating the weight gain.   

Fluhr found that smoking alters the bacterial composition within the guts of mice, thereby creating an imbalance. Bacteria in this altered gut flora produce different levels of certain metabolites which results in greater energy uptake from food (hence more calories) and promotion of weight gain. Notably, these alterations were caused by other compounds within cigarettes than nicotine.

Bacteria in this altered gut flora produce different levels of certain metabolites which results in greater energy uptake from food (hence more calories) and promotion of weight gain.

The researchers propose the following model. Cigarette compounds induce anorexic signals that cause mice to lose weight, a characteristic of active smoking. Simultaneously, the gut flora changes and the bacteria produce different levels of metabolites. However, mice will not gain weight due to the anorexic signals. When quitting with smoking, the anorexic signals quickly disappear, while the gut flora and metabolite alterations reverse very slowly, ultimately leading to weight gain.

It is not clear yet whether this mechanism applies to humans as well. The study of Fluhr did find differences in gut flora between smokers and non-smokers. He also found altered levels of weight-gain inducing metabolites in their stools. However, other studies that investigate differences between gut flora in smokers and non-smokers find conflicting results. Large-scale human trials are therefore needed to study this mechanism in humans.

Nevertheless, this study sheds more light on mechanisms involved in weight gain after smoking cessation. This could be of help to create interventions that prevent weight gain in the future. Administrating drugs that block the production of the metabolites responsible for the weight gain might be such an intervention. Another possible solution could be to ban the compounds within cigarettes that induce changes in the gut flora.