Stopping smoking: how to avoid weight gain?

Three-quarters of people who quit smoking gain weight in the months after quitting, even when their caloric intake remains stable. These extra pounds would be caused by a major modification of the intestinal flora which improves the absorption of energy contained in food.

Smokers are often thinner than non-smokers due to the many metabolic effects of tobacco nicotine, such as decreased appetite, inhibition of enzymes involved in fat assimilation, and increased body energy expenditure.

Quitting smoking makes you gain between 3 and 10 kg

These metabolic impacts mean that it is very common for people to gain weight after quitting smoking: 80% of ex-smokers gain three to four kilos in the period following their last cigarette, this excess can even be over 10 kilos in some. This potential weight gain represents for many people, especially young women, an important factor in the decision to continue or to start smoking again. This is a very poor body weight control strategy given the many catastrophic health effects of smoking! A better understanding of the factors involved in weight gain following smoking cessation is therefore of great importance to improve the effectiveness of anti-smoking strategies.

Ex-smokers and obese: an identical intestinal flora

An increase in appetite and caloric intake following nicotine withdrawal is generally singled out to explain the weight gain in ex-smokers, especially if they adopt poor eating habits to compensate for the lack of tobacco. . This is undoubtedly true for some, but it is well documented that a large number of ex-smokers gain weight by several pounds without having changed their diet, and sometimes even despite a reduction in their caloric intake. How can a constant or even lower number of calories be associated with weight gain?

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To answer this question, a team of Swiss researchers looked at the potential role of the intestinal flora. These bacteria break down substances that we are unable to digest on our own (eg dietary fibre), and the energy thus released is subsequently assimilated by the body. This is a phenomenon of great importance: for example, studies have shown that the population of bacteria present in the intestine of obese people is more efficient in extracting the energy contained in food and contributes by does even at calorie overload. To determine if a similar phenomenon was at work in ex-smokers, the researchers analyzed the composition of their bacterial flora and compared it to that of smokers.

They first noticed that smoking was associated with a marked reduction in the diversity of microbial flora, which could explain the known negative impact of tobacco on inflammatory bowel disease. On the other hand, they observed that stopping smoking was associated with remarkable changes in the composition of this flora, the proportion of the different bacteria that compose it approaching that found in obese people. It therefore seems that stopping smoking promotes the establishment of a flora better able to extract the energy contained in food, which could explain the weight gain in ex-smokers.

Quit smoking without weight gain

The discovery of the important role of the intestinal flora in the weight gain of ex-smokers suggests that the adoption of dietary habits known to influence the composition and diversity of this flora could make it possible to reduce this weight gain. In this sense, a diet rich in fiber (fruits, vegetables, whole grains) and low in fat and industrial sugar is possibly the best strategy to adopt to allow the optimal functioning of the flora.

Keep in mind that the benefits of quitting smoking are so important that the fear of gaining a few pounds should not be a limiting factor in the decision to quit smoking!

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Tobacco remains the leading cause of death.


Biedermann L et al. Smoking cessation induces profound changes in the composition of the intestinal microbiota in humans. PLoS One; 8: e59260.

Cotillard A et al. Dietary intervention impact on gut microbial gene richness. Nature; 500: 585-8.


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