No abstract

Obesity rates have increased dramatically in recent decades, and it has proven difficult to treat. An attentional bias towards food cues may be implicated in the aetiology of obesity and influence cravings and food consumption. This review systematically investigated whether attentional biases to food cues exist in overweight/obese compared with healthy weight individuals. Electronic database were searched for relevant papers from inception to October 2014. Only studies reporting food-related attentional bias between either overweight (body mass index [BMI] 25.0-29.9 kg m(-2)) or obese (BMI ≥ 30) participants and healthy weight participants (BMI 18.5-24.9) were included. The findings of 19 studies were reported in this review. Results of the literature are suggestive of differences in attentional bias, with all but four studies supporting the notion of enhanced reactivity to food stimuli in overweight individuals and individuals with obesity. This support for attentional bias was observed primarily in studies that employed psychophysiological techniques (i.e. electroencephalogram, eye-tracking and functional magnetic resonance imaging). Despite the heterogeneous methodology within the featured studies, all measures of attentional bias demonstrated altered cue-reactivity in individuals with obesity. Considering the theorized implications of attentional biases on obesity pathology, researchers are encouraged to replicate flagship studies to strengthen these inferences.

Aerobic exercise (AE) has been widely praised for its potential benefits to cognition and overall brain and mental health. In particular, AE has a potent impact on promoting the function of the hippocampus and stimulating neuroplasticity. As the evidence-base rapidly builds, and given most of the supporting work can be readily translated from animal models to humans, the potential for AE to be applied as a therapeutic or adjunctive intervention for a range of human conditions appears ever more promising. Notably, many psychiatric and neurological disorders have been associated with hippocampal dysfunction, which may underlie the expression of certain symptoms common to these disorders, including (aspects of) cognitive dysfunction. Augmenting existing treatment approaches using AE based interventions may promote hippocampal function and alleviate cognitive deficits in various psychiatric disorders that currently remain untreated. Incorporating non-pharmacological interventions into clinical treatment may also have a number of other benefits to patient well being, such as limiting the risk of adverse side effects. This review incorporates both animal and human literature to comprehensively detail how AE is associated with cognitive enhancements and stimulates a cascade of neuroplastic mechanisms that support improvements in hippocampal functioning. Using the examples of schizophrenia and major depressive disorder, the utility and implementation of an AE intervention to the clinical domain will be proposed, aimed to reduce cognitive deficits in these, and related disorders.

Key pointsr Magnetic resonance spectroscopy was conducted before and after high-intensity interval exercise.r Sensorimotor cortex GABA concentration increased by 20%. r The increase was positively correlated with the increase in blood lactate. r There was no change in dorsolateral prefrontal cortex. r There were no changes in the glutamate-glutamine-glutathione peak.Abstract High-intensity exercise increases the concentration of circulating lactate. Cortical uptake of blood borne lactate increases during and after exercise; however, the potential relationship with changes in the concentration of neurometabolites remains unclear. Although changes in neurometabolite concentration have previously been demonstrated in primary visual cortex after exercise, it remains unknown whether these changes extend to regions such as the sensorimotor cortex (SM) or executive regions such as the dorsolateral prefrontal cortex (DLPFC). In the present study, we explored the acute after-effects of high-intensity interval training (HIIT) on the concentration of gamma-Aminobutyric acid (GABA) and the combined glutamate-glutamine-glutathione (Glx) spectral peak in the SM and DLPFC, as well as the relationship with blood lactate levels. Following HIIT, there was a robust increase in GABA concentration in the SM, as evident across the majority of participants. This change was not observed in the DLPFC. Furthermore, the increase in SM GABA was positively correlated with an increase in blood lactate. There were no changes in Glx concentration in either region. The observed increase in SM GABA concentration implies functional relevance, whereas the correlation with lactate levels may relate to the metabolic fate of exercise-derived lactate that crosses the blood-brain barrier.

There is a growing view that certain foods, particularly those high in refined sugars and fats, are addictive and that some forms of obesity can usefully be treated as a food addiction. This perspective is supported by a growing body of neuroscience research demonstrating that the chronic consumption of energy-dense foods causes changes in the brain's reward pathway that are central to the development and maintenance of drug addiction. Obese and overweight individuals also display patterns of eating behavior that resemble the ways in which addicted individuals consume drugs. We critically review the evidence that some forms of obesity or overeating could be considered a food addiction and argue that the use of food addiction as a diagnostic category is premature. We also examine some of the potential positive and negative clinical, social, and public policy implications of describing obesity as a food addiction that require further investigation.