Obesity is a worldwide epidemic and is becoming an issue of concern in certain contact sports like football.1, 3, 5, 15
Previously, we have demonstrated significant global decreases in blood flow in a population of retired NFL players compared with healthy subjects,7
and we have observed decreases in blood flow to the prefrontal cortex in a group of healthy, cognitively normal individuals who were overweight.8
Here, we show that retired, overweight NFL players have significantly more decreases in blood flow in the prefrontal cortex and temporal pole, and greater cognitive impairment than those retired NFL players categorized as normal weight. It appears that both playing professional football and being overweight result in additive risk factors for decreasing blood flow and cognition.
The prefrontal cortex is the brain's executive processing center, allowing for cognitive flexibility, planning and forethought. This circuitry is involved in gathering and consolidating input required for complex behavior, thus allowing for a top–down processing of information.16, 17
In essence, the prefrontal cortex functions as a highly tuned processing center with projections to the sensory and motor cortical systems, ultimately allowing for the output of proper goal-oriented behavior. When this connectivity becomes disrupted, deficits in cognitive flexibility, information processing speed, reasoning and attention ultimately result. In our cohort of overweight NFL players, we observed significant blood flow deficits specifically in the dorsolateral prefrontal cortex (Brodmann areas 8, 9), regions involved with processing of visuospatial and motor information and the anterior prefrontal cortex (BA 10), a region involved in memory retrieval and executive function. We also observed significant hypometabolism in the left temporal pole, which is associated with a variety of higher-order cognitive processes including emotion, attention, behavior and memory. As the temporal pole has extensive connectivity with the hippocampus and the frontal lobes, the blood flow deficits observed in the overweight players correlate well with the cognitive processing impairments present on the neuropsychiatric examinations.
Mild traumatic brain injury results from repetitive subconcussive impacts to the head and football players at the high school, collegiate and professional level are vulnerable to the cognitive deficits and long-term neurodegenerative complications that may accompany it. It is without question that NFL players are at a heightened risk for cognitive impairment18
and dementia. Although the pathogenesis underlying traumatic brain injury is not clearly understood, histological data demonstrate that the deposition of tau proteins, amyloid plaques and neurofibrillary tangles following repetitive head injury can increase susceptibility to chronic traumatic encephalopathy, a progressive neurological disorder documented in the autopsied brains of professional athletes involved in contact sports.19, 20, 21
The mechanical forces from repetitive head trauma rupture delicate cell membranes and alter the fidelity of the electrical signal that has been observed by our group7
These subtle neurobiological changes that can influence cognition may ultimately usher in the more chronic effects of traumatic brain injury, including diffuse axonal injury, ischemia, synaptic loss and demyelination. The combined metabolic changes and alterations in neuronal integrity result in the global hypometabolism that we have previously reported in this population of athletes.7
In addition to the obvious risk factors from playing contact sports, the additive impact of having excess body mass increases the propensity for further metabolic and neurological complications. Anstey et al.23
reported the results of a comprehensive meta-analysis on the association between body mass index and dementia, and found that categorization in the overweight or obese range in midlife is a risk factor for dementia later in life. Obesity results in an upregulation of pro-inflammatory cytokines (C-reactive protein, tumor necrosis factor α or interleukin-6) with a corresponding decrease in beneficial adipokines, triggering a cascade of apoptosis, neuroinflammation, microglia activation and blood–brain barrier damage often observed with metabolic syndrome. Brain imaging studies have reported the deleterious effects of having a high body mass index being associated with lower brain volume24
and impaired frontal lobe function.4, 8, 25
Therefore, it is clear that obesity has a role in compromised brain function, and we report here that retired NFL players who are overweight have greater cognitive impairment and blood flow deficits in the prefrontal cortex and temporal pole as compared with their normal-weight cohorts.
Obesity has been linked to executive dysfunction,4, 13, 25
and our cohort of overweight NFL players demonstrate decreased performance in the areas of attention and cognitive functioning upon neuropsychological evaluation. These observations may correlate with the decrements in metabolic activity to the prefrontal cortex and temporal pole that we observe in our overweight athletes. Alternatively, the cognitive deficits may be attributed to the elevated circulation of pro-inflammatory cytokines and biomarkers that result in myelin abnormalities, which have been documented in the frontal lobes of obese individuals.26
With the heightened prevalence of obesity3
and cardiovascular disease risk factors27
in NFL players, our results suggest this trend will have negative, long-term consequences on brain health and may lead to complications due to stoke or chronic traumatic encephalopathy. If this finding is replicated it indicates that proper weight education and management may be essential to the future health of athletes who have been exposed to repetitive brain trauma.