Background: Desaturation of dietary α-linolenic acid (ALA) to omega-3 (n−3) long-chain fatty acids (FAs) is mediated through FA desaturases (FADS1-FADS2) and may be influenced by dietary FA composition.

Evidence suggests that short sleep duration may be a newly identified modifiable risk factor for obesity, yet there is a paucity of studies to investigate this. We assessed the feasibility of a personalized sleep extension protocol in adults aged 18–64 y who are habitually short sleepers (5 to <7 h), with sleep primarily measured by wrist actigraphy. In addition, we collected pilot data to assess the effects of extended sleep on dietary intake and quality measured by 7-d food diaries, resting and total energy expenditure, physical activity, and markers of cardiometabolic health. Forty-two normal-weight healthy participants who were habitually short sleepers completed this free-living, 4-wk, parallel-design randomized controlled trial. The sleep extension group (n = 21) received a behavioral consultation session targeting sleep hygiene. The control group (n = 21) maintained habitual short sleep. Rates of participation, attrition, and compliance were 100%, 6.5%, and 85.7%, respectively. The sleep extension group significantly increased time in bed [0:55 hours:minutes (h:mm); 95% CI: 0:37, 1:12 h:mm], sleep period (0:47 h:mm; 95% CI: 0:29, 1:05 h:mm), and sleep duration (0:21 h:mm; 95% CI: 0:06, 0:36 h:mm) compared with the control group. Sleep extension led to reduced intake of free sugars (–9.6 g; 95% CI: –16.0, –3.1 g) compared with control (0.7 g; 95% CI: –5.7, 7.2 g) (P = 0.042). A sensitivity analysis in plausible reporters showed that the sleep extension group reduced intakes of fat (percentage), carbohydrates (grams), and free sugars (grams) in comparison to the control group. There were no significant differences between groups in markers of energy balance or cardiometabolic health. We showed the feasibility of extending sleep in adult short sleepers. Sleep extension led to reduced free sugar intakes and may be a viable strategy to facilitate limiting excessive consumption of free sugars in an obesity-promoting environment. This trial was registered at www.clinicaltrials.gov as NCT02787577.

Underlying mechanisms responsible for the cholesterol-lowering effect ofβ-glucan have been proposed, yet have not been fully demonstrated. The primary aim of this study was to determine whether the consumption of barleyβ-glucan lowers cholesterol by affecting the cholesterol absorption, cholesterol synthesis or bile acid synthesis. In addition, this study was aimed to assess whether the underlying mechanisms are related to cholesterol 7αhydroxylase (CYP7A1) SNP rs3808607 as proposed by us earlier. In a controlled, randomised, cross-over study, participants with mild hypercholesterolaemia (n30) were randomly assigned to receive breakfast containing 3 g high-molecular weight (HMW), 5 g low-molecular weight (LMW), 3 g LMW barleyβ-glucan or a control diet, each for 5 weeks. Cholesterol absorption was determined by assessing the enrichment of circulating¹³C-cholesterol over 96 h following oral administration; fractional rate of synthesis for cholesterol was assessed by measuring the incorporation rate of²H derived from deuterium oxide within the body water pool into the erythrocyte cholesterol pool over 24 h; bile acid synthesis was determined by measuring serum 7α-hydroxy-4-cholesten-3-one concentrations. Consumption of 3 g HMWβ-glucan decreased total cholesterol (TC) levels (P=0·029), but did not affect cholesterol absorption (P=0·25) or cholesterol synthesis (P=0·14). Increased bile acid synthesis after consumption of 3 g HMWβ-glucan was observed in all participants (P=0·049), and more pronounced in individuals carrying homozygous G of rs3808607 (P=0·033). In addition, a linear relationship between log (viscosity) ofβ-glucan and serum 7α-HC concentration was observed in homozygous G allele carriers. Results indicate that increased bile acid synthesis rather than inhibition of cholesterol absorption or synthesis may be responsible for the cholesterol-lowering effect of barleyβ-glucan. The pronounced TC reduction in G allele carriers of rs3808607 observed in the previous study may be due to enhanced bile acid synthesis in response to high-viscosityβ-glucan consumption in those individuals.