Obesity has been identified as a significant risk factor for neurodegenerative diseases such as Alzheimer’s Disease in humans, and animal studies have shown obesity to increase susceptibility to brain dysfunction and degeneration. However, less is known about the specific effects of obesity on the human brain. To address this, researchers compared MRI brain scans of 23 morbidly obese individuals to the brains of nonobese individuals, looking at obesity’s impact on both gray and white matter in the brain.
Although some prior research had examined the impact of obesity on gray matter in the human brain, little has been known about how white matter was impacted. Gray matter refers mostly to the cell bodies of neurons in the brain, while white matter refers to the tissue surrounding the axons that connect one nerve cell to another. This white matter is responsible for the rapid and efficient communication that is necessary between neurons.
In comparing the scans of obese and nonobese individuals, the researchers found that differences were observed in brain regions governing reward seeking, inhibitory control of impulses, and appetite. Each of these areas was smaller in obese individuals, and the researchers suggest that these differences could underlie at least some of the excessive food consumption among obese individuals. No brain regions were shown to be larger in obese individuals compared to the nonobese. In obese individuals, gray matter density was significantly lower in frontal lobe areas that govern executive functions; temporal lobe areas that subserve long-term memory and the processing of visual, auditory, and speech information; and in the visual cortex. White matter density was lower in limbic regions that govern emotional functions and that have been associated with motivation and processing the pleasantness of food, as well as in the bundles of axons below the temporal lobes.
In addition to examining differences in brain regions between obese and nonobese individuals, the researchers also aimed to determine which clinical variables were associated with the observed brain abnormalities in obese individuals. In this analysis, they found that the greater the individual’s body mass index (BMI), the greater the likely reduction of brain matter density. They also found that the changes in brain structure were mainly associated with percentage of fat. The amount of abdominal subcutaneous fat tissue was also associated with brain changes among the obese, and triglycerides had a minor contribution in some regions. However, in this study, systolic and diastolic blood pressure were not associated with altered brain structure, nor were blood glucose levels.
In discussing their findings that body fat percentage was the critical factor explaining brain volume reductions, these researchers suggest that the body’s inflammatory response to fat tissue may be responsible for the decrease in brain volume. This is supported by other research on the correlation between obesity-mediated inflammation and reduced brain integrity, as well as by the lack of significant association of glucose and blood pressure measurements with the observed brain changes in this study. From this research, it appears that managing blood pressure and glucose levels alone in obese individuals may not be sufficient to counteract the impact of obesity on the brain and the greater risk of neurodegenerative disease associated with obesity.
However, many questions remain. It is unclear whether these observed brain differences precede obesity or occur as a consequence of obesity. It could be that differences in these brain regions increase the risk of developing obesity, that these differences reflect changes that occur as a result of overeating, or that both of these possibilities play a role. The authors suggest that research on the impact of weight loss on brain structure could provide important insight into the relationship of weight and brain structure.
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