According to the World Health Organization, obesity has almost tripled since 1975.

In 2016, 13% of adults worldwide were classified as obese. Some countries have higher rates of obesity, such as the United States, where 41.9% of people were obese in 2020.

While obesity has multiple possible causes, it is believed to be caused by poor dietary choices and maladaptive eating behavior such as hedonic eating—eating when not hungry—and lack of physical activity.

Obesity, however, is not easily treated with caloric restriction and an exercise routine. When treated this way, the body’s metabolism often counterbalances and restores prior body weight.

Pharmaceutical interventions may eventually prove useful for treating obesity, although many that are currently available cause significant side effects due to the pathways on which they work.

Research seeking to identify brain networks that shape dietary choice and self-control is thus critical for understanding mechanisms to develop new treatment approaches to obesity.

Recently, researchers discovered that a group of neurons in the amygdala—a part of the brain involved in experiencing emotions and decision-making—may also trigger hedonic eating.

The study was published in Nature Neuroscience.

“The identification of the neuronal substrates mediating overeating could provide new molecular targets for devising new anti-obesity treatments,” Alessandro Furlan, assistant professor at the Department of Neuroscience at Karolinska Institutet, Sweden, one of the study’s authors, told Medical News Today.

For the study, the researchers conducted several experiments on mice to observe their neuronal behavior.

From the first set of experiments, they observed their neural activity in response to eating regular chow or a high-fat diet (HFD) after food restriction.

After an HFD, but not chow, the researchers noted higher activity levels among certain neurons in a part of the amygdala known as the interstitial nucleus of the posterior limb of the anterior commissure (IPAC).

The findings, they wrote, indicated that certain neurons of the IPAC may be activated following the consumption of palatable food, and not necessarily an energy deficit.

Further tests demonstrated that these IPAC neurons could also be activated in the presence of fatty and sugary food and smells in the absence of hunger.

The researchers next conducted an experiment to see whether activating these neurons would lead to overfeeding. They found that ‘switching’ these neurons on increased sated mice’s intake of all foods and liquids.

The effect, however, was larger for coconut and olive oil-flavored HFDs and white chocolate than for chow and dark chocolate. Meanwhile, switching the neurons off then resulted in reduced feeding.