CHICAGO — Childhood obesity is associated with a number of adverse complications, ranging from serious physiological conditions like diabetes or heart disease, to psychological stress caused by negative self-image or poor performance in physical activities. However, a new study finds that childhood obesity may even cause brain damage, affecting the areas of children’s brains in control of emotions, cognitive functions, and appetite control.
It’s no secret that childhood obesity is on the rise, especially in the United States. Since the 1970s, the percentage of American children classified as obese has more than tripled. Recently, evidence has begun to surface indicating that obesity can also cause inflammation in the nervous system, which could consequently damage integral brain areas.
New developments in MRI technology, such as diffusion tensor imaging (DTI), allowed researchers from the University of São Paulo in Brazil to investigate this matter more thoroughly. DTI enables scientists to track the diffusion of water within the human brain’s signal carrying white-matter pathways.
For their research, the study’s authors analyzed DTI results from 59 obese children and 61 children of normal weight, all between the ages of 12-16. Using these DTI results, they constructed their own unit of measure called fractional anisotropy (FA), designed to serve as a reading of the brain’s white matter. The lower a child’s FA score, the more observed damage to their white matter.
The research team discovered lower FA scores among the obese adolescents, within brain regions located in the corpus callosum. The corpus callosum is incredibly important; it connects the brain’s left and right hemispheres. Lower FA scores were also noted in the middle orbitofrontal gyrus, an area of the brain associated with emotional control and the reward circuit. In total, not a single brain area among any of the obese adolescents showed increased FA scores.
“Brain changes found in obese adolescents related to important regions responsible for control of appetite, emotions and cognitive functions,” says study co-author Pamela Bertolazzi, a biomedical scientist and Ph.D. student from the University of São Paulo, in a release.
This observed neural damage in obese adolescents also corresponded with the presence of a few inflammatory markers, such as leptin. This hormone is produced by fat cells and aids in the regulation of energy levels and fat storage. Some obese people’s brains don’t seem to respond to leptin, causing them to continue eating despite storing more than enough energy and fat. This condition, referred to as leptin resistance, causes a vicious cycle in which fat cells start producing even more leptin.
Furthermore, poor white matter quality was also linked to insulin levels. Insulin helps to regulate blood sugar, and it’s common for obese individuals to experience insulin resistance.
“Our maps showed a positive correlation between brain changes and hormones such as leptin and insulin,” Dr. Bertolazzi adds. “Furthermore, we found a positive association with inflammatory markers, which leads us to believe in a process of neuroinflammation besides insulin and leptin resistance.”
“In the future, we would like to repeat brain MRI in these adolescents after multi-professional treatment for weight loss to assess if the brain changes are reversible or not,” she concludes.
The study is set to be presented this week at the annual meeting of the Radiological Society of North America in Chicago.