Eating during the night may increase the risk for obesity and type 2 diabetes in shift workers. This study examined the impact of either eating or not eating a meal at night on glucose metabolism. Participants underwent four nights of simulated night work (SW1-4, 16:00-10:00 h, <50 lux) with a daytime sleep opportunity each day (10:00-16:00 h, <3 lux). Healthy males were assigned to an eating at night (NE; n = 4, meals; 07:00, 19:00 and 01:30 h) or not eating at night (NEN; n = 7, meals; 07:00 h, 09:30, 16:10 and 19:00 h) condition. Meal tolerance tests were conducted post breakfast on pre-night shift (PRE), SW4 and following return to day shift (RTDS), and glucose and insulin area under the curve (AUC) were calculated. Mixed-effects ANOVAs were used with fixed effects of condition and day, and their interactions, and a random effect of subject identifier on the intercept. Fasting glucose and insulin were not altered by day or condition. There were significant effects of day and condition × day (both p < 0.001) for glucose AUC, with increased glucose AUC observed solely in the NE condition from PRE to SW4 (p = 0.05) and PRE to RTDS (p < 0.001). There was also a significant effect of day (p = 0.007) but not condition × day (p = 0.825) for insulin AUC, with increased insulin from PRE to RTDS in both eating at night (p = 0.040) and not eating at night (p = 0.006) conditions. Results in this small, healthy sample suggest that not eating at night may limit the metabolic consequences of simulated night work. Further study is needed to explore whether matching food intake to the biological clock could reduce the burden of type 2 diabetes in shift workers.

This study examined the impact of eating during simulated night shift on performance and subjective complaints. Subjects were randomized to eating at night (n=5; 23.2 ± 5.5 y) or not eating at night (n=5; 26.2 ± 6.4 y). All participants were given one sleep opportunity of 8 h (22:00 h-06:00 h) before transitioning to the night shift protocol. During the four days of simulated night shift participants were awake from 16:00 h-10:00 h with a daytime sleep of 6 h (10:00 h-16:00 h). In the simulated night shift protocol, meals were provided at ≈0700 h, 1900 h and 0130 h (eating at night); or ≈0700 h, 0930 h, 1410 h and 1900 h (not eating at night). Subjects completed sleepiness, hunger and gastric complaint scales, a Digit Symbol Substitution Task and a 10-min Psychomotor Vigilance Task. Increased sleepiness and performance impairment was evident in both conditions at 0400 h (p<0.05). Performance impairment at 0400 h was exacerbated when eating at night. Not eating at night was associated with elevated hunger and a small but significant elevation in stomach upset across the night (p<0.026). Eating at night was associated with elevated bloating on night one, which decreased across the protocol. Restricting food intake may limit performance impairments at night. Dietary recommendations to improve night-shift performance must also consider worker comfort.

Shiftworkers have impaired performance when driving at night and they also alter their eating patterns during nightshifts. However, it is unknown whether driving at night is influenced by the timing of eating. This study aims to explore the effects of timing of eating on simulated driving performance across four simulated nightshifts. Healthy, non-shiftworking males aged 18-35 years (n = 10) were allocated to either an eating at night (n = 5) or no eating at night (n = 5) condition. During the simulated nightshifts at 1730, 2030 and 0300 h, participants performed a 40-min driving simulation, 3-min Psychomotor Vigilance Task (PVT-B), and recorded their ratings of sleepiness on a subjective scale. Participants had a 6-h sleep opportunity during the day (1000-1600 h). Total 24-h food intake was consistent across groups; however, those in the eating at night condition ate a large meal (30% of 24-h intake) during the nightshift at 0130 h. It was found that participants in both conditions experienced increased sleepiness and PVT-B impairments at 0300 h compared to 1730 and 2030 h (p < 0.001). Further, at 0300 h, those in the eating condition displayed a significant decrease in time spent in the safe zone (p < 0.05; percentage of time within 10 km/h of the speed limit and 0.8 m of the centre of the lane) and significant increases in speed variability (p < 0.001), subjective sleepiness (p < 0.01) and number of crashes (p < 0.01) compared to those in the no eating condition. Results suggest that, for optimal performance, shiftworkers should consider restricting food intake during the night.

Desorption ionisation on porous silicon mass spectrometry imaging (DIOS-MSI) was used on fingerprints to map the distribution of exogenous and endogenous molecules present in sweat. Our attention was focused on the proof-of-principle to detect illicit drugs and their metabolites to exemplify the technique's potential in the area of forensic and workplace testing.

Object and action naming and comprehension were tested in frontotemporal dementia (frontal variant, FTD), in Alzheimer’s disease (AD) and in controls. Although lower scores were obtained by all groups, we can confirm that actions were proportionally more impaired in FTD. The correlation between action naming deficit and severity of dementia was stronger in this group than in AD. The correlation analysis also suggested that the naming disorder was different in nature in FTD (mostly a dysexecutive deficit) and in AD (mostly a linguistic disorder). Our explanation is that since verbs are supposed to be more demanding of executive resources than nouns, a higher sensitivity to verbs should be expected in any brain pathology, but mostly in FTD in which executive resources are typically reduced.

Use of illicit stimulants such as methamphetamine, cocaine, and ecstasy is an increasing health problem. Chronic use can cause neurotoxicity in animals and humans but the long-term consequences are not well understood. The aim of the current study was to investigate the long-term effect of stimulant use on the morphology of the human substantia nigra. We hypothesised that history of illicit stimulant use is associated with an abnormally bright and enlarged substantia nigra (termed ‘hyperechogenicity’) when viewed with transcranial sonography. Substantia nigra morphology was assessed in abstinent stimulant users (n = 36; 31±9 yrs) and in two groups of control subjects: non-drug users (n = 29; 24±5 yrs) and cannabis users (n = 12; 25±7 yrs). Substantia nigra morphology was viewed with transcranial sonography and the area of echogenicity at the anatomical site of the substantia nigra was measured at its greatest extent. The area of substantia nigra echogenicity was significantly larger in the stimulant group (0.273±0.078 cm2) than in the control (0.201±0.054 cm2; P<0.001) and cannabis (0.202±0.045 cm2; P<0.007) groups. 53% of stimulant users exhibited echogenicity that exceeded the 90th percentile for the control group. The results of the current study suggest that individuals with a history of illicit stimulant use exhibit abnormal substantia nigra morphology. Substantia nigra hyperechogenicity is a strong risk factor for developing Parkinson's disease later in life and further research is required to determine if the observed abnormality in stimulant users is associated with a functional deficit of the nigro-striatal system.

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The current study investigated the effects of repeated caffeine administration on performance and subjective reports of sleepiness and fatigue during 50h extended wakefulness. Twenty-four, non-smokers aged 22.5±2.9y (mean±SD) remained awake for two nights (50h) in a controlled laboratory environment. During this period, 200mg of caffeine or placebo gum was administered at 01:00, 03:00, 05:00 and 07:00 on both nights (total of 800mg/night). Neurobehavioral performance and subjective reports were assessed throughout the wake period. Caffeine improved performance compared to placebo, but did not affect overall ratings of subjective sleepiness and fatigue. Performance and sleepiness worsened with increasing time awake for both conditions. However, caffeine slowed performance impairments such that after 50h of wakefulness performance was better following caffeine administration compared to placebo. Caffeine also slowed the increase in subjective sleepiness and performance ratings, but only during the first night of wakefulness. After two nights of sleep deprivation, there was no difference in sleepiness ratings between the two conditions. These results demonstrate that strategic administration of caffeine effectively mitigates performance impairments associated with 50h wakefulness but does not improve overall subjective assessments of sleepiness, fatigue and performance. Results indicate that while performance impairment is alleviated, individuals may continue to report feelings of sleepiness. Individuals who use caffeine as a countermeasure in sustained operations may feel as though caffeine is not effective despite impairments in objective performance being largely mitigated.