Executive function and dietary intake in youth: A systematic review of the literature.

Despite increasing evidence that childhood obesity may be related to impairments in executive function, the evidence supporting the relation between executive function (EF) and dietary intake, a key factor linked to obesity, is mixed. Although research from the obesity literature often interprets EF as a factor that may influence dietary intake, there is also evidence that dietary intake may influence EF. Drawing on a developmental perspective, this systematic review examines the literature on the link between executive function (i.e., inhibition, working memory, and cognitive flexibility) and dietary intake in youth through the inclusion of cross-sectional, longitudinal, and intervention studies aimed at altering either dietary intake or EF as a way to influence the other. In total, 5650 studies were screened for eligibility. Twenty-six studies met inclusion criteria and were included in the review. Results indicated that the relation between executive function and dietary intake is equivocal. Although there is some support for a cross-sectional relation between executive function and dietary intake, the lack of longitudinal studies makes it difficult to make conclusions about directionality. Findings from intervention studies do not support the effectiveness of short-term manipulations on dietary intake to change subsequent EF, and few intervention studies exist that explicitly aim to "train" EF to change subsequent dietary intake. Furthermore, the wide variety of measures used to assess EF and dietary intake, and the lack of consideration of the role that weight status may play in the relation between EF and dietary intake, make overall interpretation of the literature more difficult. In sum, there is a need for more prospective research examining a variety of ages, domains of EF, and weight statuses, taking into account developmental factors.

Independent association of resting energy expenditure with blood pressure: confirmation in populations of the African diaspora.

BACKGROUND: Obesity is a major risk factor for hypertension, however, the physiologic mechanisms linking increased adiposity to elevations in blood pressure are not well described. An increase in resting energy expenditure (REE) is an obligatory consequence of obesity. Previous survey research has demonstrated that REE is an independent predictor of blood pressure, and eliminates the co-linear association of body mass index. This observation has received little attention and there have been no attempts to provide a causal explanation. METHODS: At baseline in an international comparative study on obesity, 289 participants aged 25-44 were recruited from communities in the US, the Seychelles, Ghana and South Africa and had REE measured with indirect calorimetry. All participants were thought to be free of major illness. RESULTS: In multivariate regression models, both systolic and diastolic blood pressure were positively associated with REE (p < 0.01), while body mass index and fat mass were negatively correlated with systolic blood pressure (p < 0.01, and p < 0.05 respectively), but not diastolic blood pressure. CONCLUSIONS: These data confirm previous reports and suggest that a common physiologic abnormality links REE and blood pressure. Elevated catecholamines, a putative metabolic characteristic of obesity, is a possible candidate to explain this association. The direct role of excess adipose tissue is open to question.