Food Satiety Disorders refers to a group of conditions in which the body’s ability to regulate hunger is disrupted. This can lead to excessive hunger and obesity or, in some cases, reduced hunger and underweight. The brain plays a crucial role in hunger regulation control by processing signals from hormones and food to control appetite. Genetic defects can disturb this system of hunger regulation.

Currently, our research is primarily focused on genetic obesity disorders. Individuals with these disorders have excessive hunger, putting them at risk of developing severe early-onset obesity. Many children affected by a genetic obesity disorder develop obesity in the first year of life.

At our Center of Expertise for Genetic Obesity (Amsterdam UMC & Erasmus MC), we have successfully diagnosed genetic obesity in 13% of children (1).

Conditions we frequently encounter include:

• Genetic defects in the leptin-melanocortin pathway, for example in the MC4R gene or LEPR gene

• 16p11.2 deletion/duplication syndrome

• Chung-Jansen syndrome

• Bardet-Biedl syndrome

Recently, there have been many developments in drug therapy for obesity. We are studying whether these treatments are also effective for various forms of genetic obesity disorders, or if specific treatments targeting the underlying genetic defect are required.

At the Emma CPM, we are dedicated to advancing the understanding of Food Satiety Disorders. By studying the genetic, hormonal, and neurological pathways involved, we aim to uncover novel therapeutic strategies to help patients more effectively.