Image courtesy of Wikimedia Commons.
Whether it is pizza or steak, pudding or cake, the taste, smell, and even the idea of something we love eating can unleash an intoxicating rush of pleasure. Some might compare it to a “high,” describing their fondness as an “addiction.” Even though that qualification might seem hyperbolic, it turns out that the neurological bases behind addiction and excessive eating could have more in common than one would imagine.
Intrigued by a potential connection between addiction and excessive eating, a team of Yale researchers led by Thang Le, a postdoctoral associate at the Department of Psychiatry in the Yale School of Medicine, decided to investigate the brain mechanisms that could lead to overeating and, consequently, obesity. “People engage in addictive behaviors for different reasons, with the pursuit of pleasure being one of the primary motivating factors,” Le said. “In a similar way, the reward component [in eating] is fundamental because, even though we eat to survive, we also eat to enjoy the pleasure it gives us.”
Inspired by this idea, the group decided to probe the association between body mass index (BMI), the hypothalamus’s grey matter volume (GMV) (the volume of the hypothalamic region in the brain with the highest neuronal cell body density) and resting state functional connectivity, a measure that observes correlations in brain activity in the hypothalamus and different regions to map out functional networks. “The hypothalamus influences how we approach eating, how we respond to rewards, and how we control ourselves in terms of feeding behavior,” Le said. In the study, the authors report that BMI is affected by how the hypothalamus communicates with areas that govern motivation, motor function, and self-control. They postulated that it was worth observing how brain activity and the physical form of the hypothalamus varied in relation to BMI.
The group found that greater BMI values were associated with increased connectivity between the hypothalamus and the globus pallidus, cerebellum, insula, and thalamus––areas that play important roles in motivated feeding. Higher BMI was also linked to a decreased connectivity between the hypothalamus and the superior parietal lobule––a region engaged with the cognitive control of our eating behaviors. Additionally, a positive association was observed between the hypothalamus’s GMV and its connectivity to the posterior insula, an area of the brain that plays a role in the control of food intake and the intensity coding of sensory experiences. This could explain why subjects with higher BMI were generally found to have greater difficulty controlling how much they ate. Higher BMI values were also connected to higher hypothalamic GMV.
Dubbed similar to “the chicken and the egg problem” by Le, the remaining question is whether the habits that lead to obesity prompt the observed changes in the hypothalamus, or whether differences in hypothalamus morphology are actually responsible for the disease. “Overeating can create alterations in the hypothalamus, and changes in the hypothalamus are going to have an impact on how it regulates eating, so this could be a vicious cycle where you start eating and cannot stop, leading your brain function and anatomy to change in a way that promotes even more eating,” Le said.
With obesity on a rampant rise around the world, deciphering the cryptic nature of its causal mechanisms is a primary concern. The path towards combating obesity begins with studies like this one, which can help us reach a more scientific understanding of the pathophysiology of obesity.