Cravings and binges are created in the brain, and that is where the new generation of . This is what explains research published this Monday in the scientific journal. Neurologists from the University of Pennsylvania have had the rare opportunity to peer into the brains of four obese people affected by the so-called binge eating disorder. One of them was being treated with . This slimming drug was shown to suppress neuronal activity in the nucleus accumbensa region associated with pleasure, motivation and reward. The drug demonstrated a short-term or incomplete effect, warranting further research.
The findings represent the first research in humans on the impact of this compound on brain activity. “Now we can begin to understand what the medications are doing in this region of the brain,” explains a neurologist at the University of Pennsylvania and lead author of the study in conversation with this newspaper. The desire to eat, whether for pleasure or to obtain energy, involves the complex interaction between different areas of the brain. Investigating how these drugs modify brain activity could contribute to the development of new treatments for eating disorders.
Slimming drugs, such as tirzepatide, promote weight loss in a surprising way that we do not fully understand. The basic mechanism would be something like this: when food reaches our intestine, incretins are naturally secreted, hormones whose main function is to stimulate the secretion of insulin and notify the brain that food has already arrived, giving a feeling of satiety. The two most important incretins are GLP-1 and GIP. In people with type 2 diabetes and those with obesity, these hormones do not work as well. That’s why they continue eating, even if they are physically full.
“Incretin analogs mimic the effects of these molecules,” explains in an exchange of messages, coordinator of the comprehensive obesity treatment unit at the Vall Hebron University Hospital. They trick your pancreas and brain by telling them that you have already eaten, giving you a feeling of eternal satiety. The first generation of drugs, semaglutide (sold under brands such as Ozempic or Wegovy) mimicked only one molecule, GLP1. “But the new compositions add the effect of GIP, creating a much more powerful dual compound,” says the endocrinologist. This is the case of tirzeptad, included in commercial brands such as Mounjaro. “It is the most effective drug that has been available so far in weight loss,” he explains. The first versions of semaglutide involved an average loss of 15% of body weight. Tirzeptaide shoots that percentage up to 22%. “One of the hypotheses is that GIP acts at other levels in the brain, enhancing the effect of GLP1,” says the expert.
Until now, there had been speculation that these molecules manipulated the neuronal mechanisms of pleasure and addiction. It had been demonstrated in mice. It had been seen in observational studies, such as the one published last year , highlighting that there was a 50% lower risk of incidence or recurrence of alcohol use disorder among semaglutide users. This suggested a strong association, but did not prove causality.
This is what the present study does, by analyzing the brain activity, recorded directly with electrodes, of four participants with severe obesity and difficulties controlling their eating habits. “Brain surgery to implant the electrodes is invasive, so it is extremely rare to study human brain activity in this way,” explains Halpern.
Initially, the study aimed to implant electrodes in people with binge eating disorders, to interact with the brain with the goal of stopping cravings before they occurred. But one of the four participants, a 60-year-old woman identified as “patient three,” was being treated with tirzepatide, so the neurologists decided to also observe how the drug acted in her brain and compare its activity with that of the rest of the patients. “This rare opportunity to study the underlying physiology of agonists in the brain might not be repeated,” says Halpern, so she decided to take advantage of it.
In doing so, they found that episodes of intense preoccupation with food and cravings were related to stronger low-frequency brain signals (called brain activity). delta-theta) in the core accumbens. And the consumption of tirzepatide suppressed that signal, which resulted in reduced cravings and weight loss. “This discovery could be useful in treating a wide range of conditions related to impulse control, such as,” notes the author.
Binge eating disorder was recognized as a mental illness in 2013, it is estimated that it affects 3% of the Spanish population, being the most common eating disorder in the adult population. Understanding the brain mechanisms that cause it could change the way we approach it. “This can also mean a revolution in the field of mental health, eating disorders and addictions,” says Ciudin. “Perhaps many of these diagnoses are based on a biological alteration, and you give the replacement treatment and the pathology is over.”
