Chronic sleep restriction during adolescence appears to cause increased consumption of foods with a high glycemic index, particularly desserts/sweets. The chronic sleep restriction common in adolescence may cause changes in dietary behaviors that increase risk of obesity and associated morbidity.

The frequency of selective eating and nutritional deficiency was studied among 22 children with autism and an age matched typically developing control group. Children with autism ate fewer foods on average than typically developing children. (33.5 vs. 54.5 foods, P < .001) As compared to typical controls, children with autism had a higher average intake of magnesium, and lower average intake of protein, calcium, vitamin B12, and vitamin D. Selective eaters were significantly more likely than typical controls to be at risk for at least one serious nutrient deficiency (P < .001).

OBJECTIVE -The purpose of this study was to compare the effects of highmonounsaturated fatty acid (MUFA) and high-carbohydrate (CHO) diets on body weight and glycemic control in men and women with type 2 diabetes.RESEARCH DESIGN AND METHODS -Overweight/obese participants with type 2 diabetes (n ϭ 124, age ϭ 56.5 Ϯ 0.8 years, BMI ϭ 35.9 Ϯ 0.3 kg/m 2 , and A1C ϭ 7.3 Ϯ 0.1%) were randomly assigned to 1 year of a high-MUFA or high-CHO diet. Anthropometric and metabolic parameters were assessed at baseline and after 4, 8, and 12 months of dieting.RESULTS -Baseline characteristics were similar between the treatment groups. The overall retention rate for 1 year was 77% (69% for the high-MUFA group and 84% for the high-CHO group; P ϭ 0.06). Based on food records, both groups had similar energy intake but a significant difference in MUFA intake. Both groups had similar weight loss over 1 year (Ϫ4.0 Ϯ 0.8 vs. Ϫ3.8 Ϯ 0.6 kg) and comparable improvement in body fat, waist circumference, diastolic blood pressure, HDL cholesterol, A1C, and fasting glucose and insulin. There were no differences in these parameters between the groups. A follow-up assessment of a subset of participants (n ϭ 36) was conducted 18 months after completion of the 52-week diet. These participants maintained their weight loss and A1C during the follow-up period.CONCLUSIONS -In individuals with type 2 diabetes, high-MUFA diets are an alternative to conventional lower-fat, high-CHO diets with comparable beneficial effects on body weight, body composition, cardiovascular risk factors, and glycemic control. Diabetes Care 32:215-220, 2009

Objectives: Preclinical studies have shown that blueberry supplementation can improve cognitive performance and neuronal function in aged animals and have identified associations between anthocyanins and such benefits. Preliminary human trials also suggest cognitive improvement in older adults, although direct evidence of enhancement of brain function has not been demonstrated. In this study, we investigated the effect of blueberry supplementation on regional brain activation in older adults at risk for dementia. Methods: In a randomized, double-blind, placebo-controlled trial we performed pre- and post-intervention functional magnetic resonance imaging during a working memory task to assess the effect of blueberry supplementation on blood oxygen level-dependent (BOLD) signal in older adults with mild cognitive impairment, a risk condition for dementia. Results: Following daily supplementation for 16 weeks, blueberry-treated participants exhibited increased BOLD activation in the left pre-central gyrus, left middle frontal gyrus, and left inferior parietal lobe during working memory load conditions (corrected p < 0.01). There was no clear indication of working memory enhancement associated with blueberry supplementation. Diet records indicated no between-group difference in anthocyanin consumption external to the intervention. Discussion: These data demonstrate, for the first time, enhanced neuronal response during working memory challenge in blueberry-treated older adults with cognitive decline and are consistent with prior trials showing neurocognitive benefit with blueberry supplementation in this at-risk population.

Given evidence that eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and anthocyanin-rich blueberries provide neurocognitive benefit, we investigated long-term supplementation in older adults with cognitive complaints. In a 24-week randomized, double-blind, placebo-controlled trial, elderly men and women received daily fish oil (FO) or blueberry (BB) or both. Diet records confirmed that participants reduced background consumption of EPA, DHA, and anthocyanins as prescribed. Erythrocyte EPA + DHA composition increased in the FO groups (p = 0.0001). Total urinary anthocyanins did not differ between the groups after supplementation but glycoside and native (food) forms increased only in the BB-supplemented groups. The FO (p = 0.03) and BB (p = 0.05) groups reported fewer cognitive symptoms, and the BB group showed improved memory discrimination (p = 0.04), indicating that supplementation improved cognition. Cognitive benefit in the BB group was associated with the presence of urinary anthocyanins reflecting recent BB intake but not with anthocyanin metabolites. However, combined FO + BB treatment was not associated with cognitive enhancement as expected.

Unacylated ghrelin (UAG) is the predominant ghrelin isoform in the circulation. Despite its inability to activate the classical ghrelin receptor, preclinical studies suggest that UAG may promote β-cell function. We hypothesized that UAG would oppose the effects of acylated ghrelin (AG) on insulin secretion and glucose tolerance. AG (1 µg/kg/h), UAG (4 µg/kg/h), combined AG+UAG, or saline were infused to 17 healthy subjects (9 men and 8 women) on four occasions in randomized order. Ghrelin was infused for 30 min to achieve steady-state levels and continued through a 3-h intravenous glucose tolerance test. The acute insulin response to glucose (AIRg), insulin sensitivity index (SI), disposition index (DI), and intravenous glucose tolerance (kg) were compared for each subject during the four infusions. AG infusion raised fasting glucose levels but had no effect on fasting plasma insulin. Compared with the saline control, AG and AG+UAG both decreased AIRg, but UAG alone had no effect. SI did not differ among the treatments. AG, but not UAG, reduced DI and kg and increased plasma growth hormone. UAG did not alter growth hormone, cortisol, glucagon, or free fatty acid levels. UAG selectively decreased glucose and fructose consumption compared with the other treatments. In contrast to previous reports, acute administration of UAG does not have independent effects on glucose tolerance or β-cell function and neither augments nor antagonizes the effects of AG.

Introduction Glucose hypometabolism and insulin resistance increase risk for and accelerate progression in Parkinson's disease and neurocognitive disorders. We conducted a proof of concept trial to determine whether ketogenesis, a metabolic adaptation induced by dietary carbohydrate restriction, can improve cognitive performance in Parkinson's disease patients with mild cognitive impairment. Methods We enrolled patients with mild cognitive impairment associated with Parkinson's disease in an eight-week nutritional intervention with random assignment to either high-carbohydrate consumption typical of the Western dietary pattern ( n = 7) or to a low-carbohydrate, ketogenic regimen ( n = 7). We assessed changes in cognitive performance as well as motor function, anthropometrics, and metabolic parameters. Results Relative to the high-carbohydrate group, the low-carbohydrate group demonstrated improvements in lexical access ( p = 0.02, Cohen's f effect size = 0.76) and memory ( p = 0.01, f = 0.87) and as well as a trend for reduced interference in memory ( p = 0.06, f = 0.60). The low-carbohydrate group also exhibited reduced body weight ( p < 0.0001, f = 1.89) and increased circulation of beta-hydroxybutyrate ( p = 0.01, f = 0.90). Change in body weight was strongly associated with memory performance ( p = 0.001). Motor function was not affected by the intervention. Conclusion Nutritional ketosis enhanced cognitive performance in Parkinson's disease-associated mild cognitive impairment in this pilot study. This metabolic intervention and its mechanisms deserve further investigation in the context of neurodegeneration.

Adiponectin is an adipose‐derived protein with beneficial metabolic effects. Low adiponectin is associated with obesity and related diseases. Significant weight loss increases adiponectin, reducing disease risk. This study compared the effects of two weight‐loss diets with different macronutrient compositions on adiponectin. Eighty‐one obese women in two cohorts were randomized to a low‐fat (LF) or a low‐carbohydrate (LC) diet. All subjects underwent equivalent weight‐loss intervention, with weight and other measures assessed at baseline and after 6 (cohort I) or 4 (cohort II) months. Body fat was measured by dual energy X‐ray absorptiometry. Adiponectin was measured by radioimmunoassay. Diet intake was assessed using 24‐h recalls and 3‐day diet records. Data were analyzed via t‐tests and repeated‐measures factorial ANOVA using time, diet, and replicate (cohort I vs. cohort II) as factors. Age, weight, body fat, BMI, adiponectin, and diet were similar at baseline. Following intervention, macronutrient composition of the diet was vastly different between the groups, reflecting the assigned diet. Both groups lost weight and body fat (P < 0.001), with effect in LC dieters greater than LF dieters (−9.1 kg vs. −4.97 kg weight, P < 0.05 and −5.45 kg vs. −2.62 kg fat, P < 0.001). Adiponectin increased in the LC (+1.92 mcg/ml, P < 0.01), but not the LF (+0.86 mcg/ml, P = 0.81), group. There was no correlation between weight loss and increase in adiponectin. These results confirm that diet‐induced loss of weight and body fat is associated with increased adiponectin concentrations. This effect is evident with weight loss of 10% or more, and may be greater with LC diets.