The Genetics of Human Behavior: Why Are Obesity and Smoking Linked?

25/08/2026

At first glance, obesity and smoking may seem to have nothing in common. In reality, however, they share more than researchers once thought. Modern research suggests that both conditions may involve some of the same mechanisms in the brain, as well as parts of our genetic makeup.

For many years, it was believed that smokers tend to be slimmer mainly because nicotine suppresses appetite and slightly increases energy expenditure. It is true that many people gain several kilograms after quitting smoking, with an average weight gain of around 4–5 kg during the first three months after quitting. Today, however, we know that the explanation is much more complex.

The Brain Responds Similarly to Food and Nicotine

When we eat something we enjoy, such as sweet or fatty foods, the brain activates its reward system. This creates a pleasurable sensation and makes us want to repeat the experience.

Nicotine in cigarettes activates the same reward system. This is one of the reasons smoking can be so addictive.

This does not mean that food is a drug or that obesity is an addiction. It does, however, mean that some of the brain circuits involved in reward, motivation, and the desire to repeat certain behaviors overlap between eating and smoking.

Why Do People Gain Weight After Quitting Smoking?

Nicotine suppresses appetite while also slightly increasing the amount of energy the body burns.

Once a person stops smoking, these effects disappear. Appetite increases, and many former smokers start reaching for sweets or high-fat foods more often, sometimes simply out of habit. They may also need something to hold in their hands or a new ritual to replace smoking. At the same time, the body burns slightly less energy than it did while smoking.

The result is often an increase in body weight. On average, people gain around 4–8 kg during the first year after quitting, although there is considerable variation between individuals.

What Has Genetics Revealed?

Scientists began asking whether the connection between smoking and obesity could be explained by more than just the effects of nicotine. They therefore analyzed genetic variants that had previously been associated with a higher body mass index (BMI). They then investigated whether the same genetic variants were also associated with smoking behavior.

The results were surprising.

People carrying certain genetic variants associated with a higher BMI were, as a group, also more likely to start smoking, and smokers carrying these variants tended to have higher cigarette consumption.

These findings were confirmed in more than 150,000 participants across several independent studies.

It's Not Just About Body Weight

One of the most interesting findings was that this association did not depend solely on how much a person weighed.

In other words, some genetic variants were associated with a greater tendency to smoke even after taking body weight into account. This suggests that some genes may influence deeper biological mechanisms involved in both appetite regulation and the brain's sensitivity to reward.

Not all genes behave in the same way, however. For example, the well-known FTO gene, which has a strong influence on obesity risk, was not associated with a greater tendency to smoke. This shows just how complex the genetics of obesity are and that only certain genetic variants are shared between the two traits.

What Does This Mean?

These findings suggest that neither obesity nor nicotine addiction is simply a matter of willpower.

Both are influenced by a complex combination of genetics, brain function, environment, and lifestyle.

A better understanding of these shared mechanisms could eventually help researchers develop new medications and more effective approaches that support smoking cessation while also helping people manage their body weight.

Genetics is not destiny, but it can help explain why some people struggle more with smoking or excess weight than others. Understanding these biological connections may ultimately lead to more effective and personalized approaches to treatment.

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