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Moderate Physical Activity Mediates the Association between White Matter Lesion Volume and Memory Recall in Breast Cancer Survivors.
Cooke, GE, Wetter, NC, Banducci, SE, Mackenzie, MJ, Zuniga, KE, Awick, EA, Roberts, SA, Sutton, BP, McAuley, E, Kramer, AF
PloS one. 2016;11(2):e0149552
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Plain language summary
As survival rates of breast cancer increase, the long-term cognitive effects of disease and required treatment are emerging. The underlying pathways of cancer-related cognitive impairment involve accelerated aging of the brain, low levels of physical activity and decreased cognitive function, however these links have not been adequately explored. The aim of this study was to investigate the link between physical activity, white matter lesion volume and cognition in 30 breast cancer survivors and 28 age-matched controls. The results of this study showed that brain structure significantly predicted cognitive function. This study provided evidence suggesting that moderate physical activity may help reduce the treatment related risks associated with breast cancer.
Abstract
Increased survival rates among breast cancer patients have drawn significant attention to consequences of both the presence of cancer, and the subsequent treatment-related impact on the brain. The incidence of breast cancer and the effects of treatment often result in alterations in the microstructure of white matter and impaired cognitive functioning. However, physical activity is proving to be a successful modifiable lifestyle factor in many studies that could prove beneficial to breast cancer survivors. This study investigates the link between white matter lesion volume, moderate physical activity, and cognition in breast cancer survivors following treatment compared to non-cancer age-matched controls. Results revealed that brain structure significantly predicted cognitive function via mediation of physical activity in breast cancer survivors. Overall, the study provided preliminary evidence suggesting moderate physical activity may help reduce the treatment related risks associated with breast cancer, including changes to WM integrity and cognitive impairment.
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Circulating glucose levels modulate neural control of desire for high-calorie foods in humans.
Page, KA, Seo, D, Belfort-DeAguiar, R, Lacadie, C, Dzuira, J, Naik, S, Amarnath, S, Constable, RT, Sherwin, RS, Sinha, R
The Journal of clinical investigation. 2011;121(10):4161-9
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Glucose is an important fuel source for the brain. Specialised sensors in brain areas such as the hypothalamus, hindbrain and forebrain are essential for optimal blood glucose control and feeding. Low blood glucose results in hunger, although the specific neurological mechanisms causing this drive for food under these conditions is unclear. This trial performed functional MRI (fMRI) scans of 14 healthy non-obese (9) and obese (5) subjects in a mild low or normal blood glucose state. The study found that low blood sugar increases the activation of the reward and motivation regions of the brain (the hypothalamus, insula and striatum). It also found that circulating glucose levels interact with external food cues (i.e. the presence of food), stimulate the reward related brain regions and motivate an individual to eat high-calorie foods. In normal weight subjects, the pre-frontal cortex (PFC) (the brain region known for impulse control) was stimulated under normal blood sugar levels and caused less interest in food stimuli. Interestingly, obese subjects under normal blood sugar levels did not see this PFC stimulation. The authors conclude that this may contribute to overeating and a preference for high-calorie foods in obese people, which is worsened in low blood glucose conditions.
Abstract
Obesity is a worldwide epidemic resulting in part from the ubiquity of high-calorie foods and food images. Whether obese and nonobese individuals regulate their desire to consume high-calorie foods differently is not clear. We set out to investigate the hypothesis that circulating levels of glucose, the primary fuel source for the brain, influence brain regions that regulate the motivation to consume high-calorie foods. Using functional MRI (fMRI) combined with a stepped hyperinsulinemic euglycemic-hypoglycemic clamp and behavioral measures of interest in food, we have shown here that mild hypoglycemia preferentially activates limbic-striatal brain regions in response to food cues to produce a greater desire for high-calorie foods. In contrast, euglycemia preferentially activated the medial prefrontal cortex and resulted in less interest in food stimuli. Indeed, higher circulating glucose levels predicted greater medial prefrontal cortex activation, and this response was absent in obese subjects. These findings demonstrate that circulating glucose modulates neural stimulatory and inhibitory control over food motivation and suggest that this glucose-linked restraining influence is lost in obesity. Strategies that temper postprandial reductions in glucose levels might reduce the risk of overeating, particularly in environments inundated with visual cues of high-calorie foods.