At first glance, obesity and smoking may seem unrelated. In reality, they share far more connections than long assumed. Modern research shows that both conditions can involve overlapping brain mechanisms and parts of a person’s genetic makeup.
For many years, it was believed that smokers tend to be thinner mainly because nicotine suppresses appetite and slightly increases energy expenditure. It is true that many people gain several kilograms after quitting smoking (on average 4–5 kg in the first 3 months). Today, however, we know the explanation is much more complex.
When we eat something we enjoy (for example, sweet or fatty food), the brain activates its reward system. This creates a pleasant feeling and motivates us to repeat the experience.
Nicotine in cigarettes activates the same reward system, which helps explain why smoking can be so addictive.
This does not mean that food is a drug or that obesity is an addiction. It does mean, however, that some brain circuits controlling reward, motivation, and the urge to repeat certain behaviors partially overlap for eating and smoking.
Nicotine dampens hunger and at the same time slightly increases the amount of energy the body burns.
Once a person stops smoking, this effect disappears. Appetite increases, and many former smokers start reaching more often for sweets or fatty foods (often out of habit; they need something to hold in their hands and a new ritual to replace smoking). The body also burns slightly less energy than it did while smoking.
The result is usually an increase in body weight. On average, people gain 4–8 kilograms during the first year after quitting, although there are large differences between individuals.
Scientists asked whether the link between smoking and obesity might not be due solely to the effects of nicotine. They therefore analyzed genetic variants already known to be associated with a higher body mass index (BMI) and then examined whether the same variants were also related to smoking behavior.
The results were surprising.
People carrying certain genetic variants linked to higher BMI were, as a group, also more likely to start smoking, and among smokers, higher cigarette consumption was more common.
These findings were confirmed in more than 150,000 participants from several independent studies.
One of the most interesting findings was that this association did not depend only on how much a person weighed.
In other words, some genetic variants influenced the tendency to smoke even when body weight itself was taken into account. This suggests that some genes act on deeper biological mechanisms that affect both the regulation of food intake and the brain’s sensitivity to reward.
Not all genes behave the same way, however. For example, the well-known FTO gene, which strongly influences obesity risk, was not linked to a tendency to smoke. This shows that the genetics of obesity are very complex and that only certain genetic variants are shared by both traits.
These insights show that neither obesity nor nicotine dependence is simply a matter of willpower.
Their development involves a complex combination of genetic makeup, brain function, environment, and lifestyle.
A better understanding of these shared mechanisms may in the future help in developing new medications and more effective approaches that simultaneously support smoking cessation and assist with body weight regulation.
Although genetics is not destiny, it helps explain why some people struggle more than others with smoking or excess weight. Precisely this understanding of biological connections can lead to more effective and more individualized treatment.
I have been working in the field of addiction counselling for more than 10 years. I hold a bachelor’s degree in Addictology from the First Faculty of Medicine and a degree in General Medicine from the Second Faculty of Medicine, Charles University. In my research, I focus on preventive medicine and epidemiology.
In my work with clients, I combine evidence-based knowledge with a holistic approach to mental health. My medical background enables me to understand the broader clinical context and to better support each client’s individual needs.
