En full appeal trial of the Mediator case, it may seem paradoxical to be interested the use, still diverted, of a drug to fight against obesity. Semaglutide, an agonist of the glucagon-like peptide-1 (GLP-1) receptor, used in the treatment of type 2 diabetes, has seen its indication extended, at higher doses, in that of severe obesity. Would history stutter, unable to take into account the mistakes of the past? Wouldn’t it be time to question the relevance of a pharmacological approach to obesity?
The pharmacology of obesity has appeared recently, under the influence of a double determination: on the one hand, the mediatized development of the cult of thinness; on the other, the growing prevalence of overweight and obesity, which results from an increased sedentary lifestyle and an increasingly fatty and sugary diet, of which fast food is the emblem. These are primarily amphetamine derivatives that have been registered or diverted for their anorectic effect (which temporarily suppresses hunger) and their action on the hunger-satiety balance, with dramatic consequences.
Rimonabant, a cannabinoid type 1 (CB1) receptor antagonist, was thus withdrawn from the market because of a risk of depression greater than the very modest benefit on the weight curve. Orlistat, an intestinal lipase inhibitor, combines low efficacy with a risk of drug interactions and sometimes severe digestive adverse effects. Finally, some monoamine reuptake inhibitors (serotonin, norepinephrine, dopamine) have also positioned themselves in the treatment of obesity with mixed effects.
In most of these situations, the pharmacological response to obesity consists in inhibiting the feeling of hunger, accelerating the feeling of satiety or modifying the craving for certain foods. This is also the case for GLP-1 agonists. The goal is thus to modify one of the most basic behaviors of the human species as of all species.
Prevention, the best approach
But the development of overweight and obesity has above all been concomitant with that of industrialized food and a social change in eating habits, most often linked to the price of the least qualitative foods from a nutritional point of view. Obesity and overweight, with its galloping epidemiology, therefore constitutes a social disease, which we try to justify from a medical point of view, in particular by looking at all costs for genetic susceptibility factors. Non-alcoholic fatty liver disease, for which we are also looking for a pharmacological answer, isn’t it nicknamed the “soda disease”?
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