Sleep restriction leads to increased activation of brain regions sensitive to food stimuli.

BACKGROUND: Epidemiologic evidence shows an increase in obesity concurrent with a reduction in average sleep duration among Americans. Although clinical studies propose that restricted sleep affects hormones related to appetite, neuronal activity in response to food stimuli after restricted and habitual sleep has not been investigated. OBJECTIVE: The objective of this study was to determine the effects of partial sleep restriction on neuronal activation in response to food stimuli. DESIGN: Thirty healthy, normal-weight [BMI (in kg/m²): 22-26] men and women were recruited (26 completed) to participate in a 2-phase inpatient crossover study in which they spent either 4 h/night (restricted sleep) or 9 h/night (habitual sleep) in bed. Each phase lasted 6 d, and functional magnetic resonance imaging was performed in the fasted state on day 6. RESULTS: Overall neuronal activity in response to food stimuli was greater after restricted sleep than after habitual sleep. In addition, a relative increase in brain activity in areas associated with reward, including the putamen, nucleus accumbens, thalamus, insula, and prefrontal cortex in response to food stimuli, was observed. CONCLUSION: The findings of this study link restricted sleep and susceptibility to food stimuli and are consistent with the notion that reduced sleep may lead to greater propensity to overeat.

Neural response to eye contact and paroxetine treatment in generalized social anxiety disorder.

Generalized social anxiety disorder (GSAD) is characterized by excessive fears of scrutiny and negative evaluation, but neural circuitry related to scrutiny in GSAD has been little studied. In this study, 16 unmedicated adults with GSAD and 16 matched healthy comparison (HC) participants underwent functional magnetic resonance imaging to assess neural response to viewed images of faces simulating movement into eye contact versus away from eye contact. GSAD patients were then treated for 8 weeks with paroxetine, and 15 patients were re-imaged. At baseline, GSAD patients had elevated neural response to eye contact in parahippocampal cortex, inferior parietal lobule, supramarginal gyrus, posterior cingulate and middle occipital cortex. During paroxetine treatment, symptomatic improvement was associated with decreased neural response to eye contact in regions including inferior and middle frontal gyri, anterior cingulate, posterior cingulate, precuneus and inferior parietal lobule. Both the magnitude of GSAD symptom reduction with paroxetine treatment and the baseline comparison of GSAD vs. HCs were associated with neural processing of eye contact in distributed networks that included regions involved in self-referential processing. These findings demonstrate that eye contact in GSAD engages neurocircuitry consistent with the heightened self-conscious emotional states known to characterize GSAD patients during scrutiny.

Brain tissue volume changes following weight gain in adults with anorexia nervosa.

OBJECTIVE: To measure brain volume deficits among underweight patients with anorexia nervosa (AN) compared to control participants and evaluate the reversibility of these deficits with short-term weight restoration. METHOD: Brain volume changes in gray matter (GM), white matter (WM), and cerebrospinal fluid (CSF) were examined in 32 adult women with AN and compared to 21, age and body mass index-range matched control women. RESULTS: Patients with AN had a significant increase in GM (p = .006, η(2) = 0.14) and WM volume (p = .001, η(2) = 0.19) following weight restoration. Patients on average had lower levels of GM at low weight (647.63 ± 62.07 ml) compared to controls (679.93 ± 53.31 ml), which increased with weight restoration (662.64 ± 69.71 ml), but did not fully normalize. DISCUSSION: This study suggests that underweight adult patients with AN have reduced GM and WM volumes that increase with short-term weight restoration.

Leptin reverses weight loss-induced changes in regional neural activity responses to visual food stimuli.

Increased hunger and food intake during attempts to maintain weight loss are a critical problem in clinical management of obesity. To determine whether reduced body weight maintenance is accompanied by leptin-sensitive changes in neural activity in brain regions affecting regulatory and hedonic aspects of energy homeostasis, we examined brain region-specific neural activity elicited by food-related visual cues using functional MRI in 6 inpatient obese subjects. Subjects were assessed at their usual weight and, following stabilization at a 10% reduced body weight, while receiving either twice daily subcutaneous injections of leptin or placebo. Following weight loss, there were predictable changes in neural activity, many of which were reversed by leptin, in brain areas known to be involved in the regulatory, emotional, and cognitive control of food intake. Specifically, following weight loss there were leptin-reversible increases in neural activity in response to visual food cues in the brainstem, culmen, parahippocampal gyrus, inferior and middle frontal gyri, middle temporal gyrus, and lingual gyrus. There were also leptin-reversible decreases in activity in response to food cues in the hypothalamus, cingulate gyrus, and middle frontal gyrus. These data are consistent with a model of the weight-reduced state as one of relative leptin deficiency.

Human cortical specialization for food: a functional magnetic resonance imaging investigation.

Although specialized cortical pathways that process specific sensory stimuli and/or execute cognitive functions have been identified, the neuro-specificity for food-related stimuli has not been clearly demonstrated. We employed functional magnetic resonance imaging (fMRI) to compare neural systems associated with the appreciation of foods and nonfoods. Healthy, normal weight, right-handed men and women (n = 12; age 29.8 +/- 1.8 y, BMI 21.8 +/- 0.8 kg/m(2)) were imaged by fMRI while fasting. Real food and nonfood items were presented to subjects both visually and tactilely, during scanning. Subjects were instructed to pay attention to the items. A randomized 2 x 2 block design consisted of 4 conditions: visual food, visual nonfood, tactile food, and tactile nonfood. Brain regions that were significantly activated to a greater extent during the presentation of foods compared with nonfood items included the anterior cingulate, superior temporal gyrus, parahippocampal gyrus, hippocampus, and the insula. These findings support the claim that the presence of food (either seen or felt) elicits a unique cortical response that is differentiated from nonfood items. This neural substrate specialized for processing of foods informs models of food-related behavior.