In recent years, anti-obesity drugs have achieved unprecedented success, with clinically relevant and sustained weight reductions. Active ingredients such as semaglutide —marketed as Ozempic and Wegovy—, a GLP-1 receptor agonist, and more recently tirzepatide —Mounjaro and Zepbound—, a dual GLP-1/GIP agonist, have marked a turning point.
These drugs mimic the action of incretins, intestinal hormones that regulate appetite, satiety and energy metabolism. Their high efficacy and manageable safety profile consolidate a new stage in the treatment of obesity.
What began as a strategy to control blood glucose in type 2 diabetes, and later to reduce weight, has a much broader scope due to its direct influence on the brain circuits involved in desire, reward and compulsion.
Based on the repeated clinical observation of patients treated with these drugs, who not only eat less but also smoke less or lose interest in other addictive behaviours, such as alcohol consumption, science now confirms this with solid evidence.
The brain’s reward system is a complex network of regions and neurotransmitters that regulate motivation and pleasure, including dopamine, which is activated both by natural food-related stimuli and by addictive substances. It is precisely there, at this shared nexus between metabolism and addiction, that GLP-1 and GIP agonists act.
A few months ago, the observational data were already difficult to ignore. A study of more than 600,000 patients with type 2 diabetes, published in the British Medical Journal, showed significant reductions not only in the onset of new addictions, but also in their serious complications. But one essential element was still missing: proving causality.
And that arrived on the first of May, marking a before and after: a clinical trial published in The Lancet —one of the highest-impact medical journals—, with a randomised, double-blind, placebo-controlled design; the most rigorous standard, in which neither patients nor researchers know who is receiving the treatment and allocation is random, allowing the real effect of the drug to be isolated.
The result: semaglutide, administered once a week, significantly reduces excessive alcohol consumption in people with obesity: fewer episodes of heavy drinking, lower desire to drink and better clinical outcomes. We are no longer talking about association, but about causality. Its application in other patient profiles remains to be clarified, but the decisive step has already been taken.
The implications are profound and go beyond obesity: the possibility of safely and sustainably modulating the reward system opens the door to earlier intervention, better prevention and fewer relapses in alcohol addiction and, perhaps, in other addictions.
And the conceptual advance can be extended to other diseases: integrating processes that until now had been treated separately into a single medical and scientific vision, with potential application in clinical practice.
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