Biology subjects

Weibel, J.

Publications and source records attributed to Weibel, J..

8 recordsLinked to original sources

bioRxiv2021

Time to recover from daily caffeine intake.

Caffeine elicits widespread effects in the central nervous system and is the most frequently consumed psychostimulant worldwide. First evidence indicates that, during daily intake, the elimination of caffeine may slow down and the primary metabolite, paraxanthine, may accumulate. The neural impact of such adaptions is virtually unexplored. In this report, we leveraged the data of a laboratory study with N= 20 participants and three within-subject conditions: caffeine (150 mg caffeine x 3/day x 10 days), placebo (150 mg mannitol x 3/day x 10 days), and withdrawal (caffeine x 9 days, afterwards placebo x 1 day). Using liquid chromatography-mass spectrometry coupled with tandem mass spectrometry, we determined the course of salivary caffeine and paraxanthine, measured regularly at day 10. We assessed grey matter (GM) intensity and cerebral blood flow (CBF) in the withdrawal condition as compared to their changes in caffeine in our previous report. The results indicate high remaining levels of paraxanthine and of caffeine carried overnight during daily intake, and the levels of paraxanthine remained higher than in placebo during withdrawal. After 36 h of withdrawal, the previously reported caffeine-induced GM reduction was partially mitigated, while CBF was elevated compared to placebo. Our findings unveil that conventional daily caffeine intake does not provide sufficient time to clear up psychoactive compounds and restore cerebral responses, even after 36 hours of abstinence. They also suggest investigating consequences of a paraxanthine accumulation during daily caffeine intake.

pharmacology and toxicology↗

bioRxiv2021

Working Memory Performance after Daily Caffeine Intake: Compromised Performance and Reduced Hippocampal Activity.

Neuroprotective effects of caffeine have been frequently reported in the context of disease and cognitive dysfunction as well as in epidemiological studies in humans. However, evidence on caffeine effects on neural and memory functions during daily intake in a healthy cognitive state remains scarce. This randomized double-blind placebo-controlled crossover study investigated working memory functions by N-back tasks and functional magnetic resonance imaging (fMRI) after daily caffeine intake compared to a placebo baseline and to acute caffeine withdrawal in 20 young healthy volunteers. Each volunteer was given 3 times 150 mg caffeine for 10 days in the daily caffeine condition, 3 times 150 mg mannitol for 10 days in the placebo condition, and 9-day caffeine plus 1-day mannitol in the acute withdrawal condition. During the 10th day, participants performed 4 N-back sessions (two loads each: 0- and 3-back) under controlled laboratory conditions. During the 4th session of N-Back (i.e. at 5.5 h, 36.5 h and > 10 days after the last caffeine intake in the caffeine, withdrawal, and placebo condition, respectively) we assessed blood-oxygen-level-dependent (BOLD) activity. During the entire 10th day, in 0-back tasks, we observed longer reaction times (RTs) in the withdrawal compared to the placebo (Cohens d = 0.7) and caffeine condition (Cohens d = 0.6), but no significant effects of conditions on error rates. In contrast, in 3-back tasks (controlled for 0-back), the RTs in the caffeine condition were longer compared to placebo (Cohens d = 0.6) and withdrawal (Cohens d = 0.5). Error rates were higher during both caffeine and withdrawal conditions compared to placebo (Cohens d of both contrasts = 0.4). Whole-brain analyses on fMRI data did not reveal significant condition-dependent differences in activities between task loads. Across task loads, however, we observed a reduced hippocampal activation (Cohens d = -1.3) during the caffeine condition compared to placebo, while no significant difference in brain activities between withdrawal and placebo conditions. Taken together, the worse working memory function and the hippocampal hypoactivation implicate a potential detrimental effect of daily caffeine intake on neurocognitive functions of healthy adults. Moreover, they echo the hippocampal volumetric reduction reported previously in the same volunteers. Lastly, acute withdrawal from daily caffeine intake impairs both low-order cognitive processes and working memory performance. Taking earlier studies on acute caffeine effects into account, our findings indicate that daily caffeine intake elicits a dynamic change in cerebral activities during the course of repeated consumption, with unknown consequences in the long run.

neuroscience↗

bioRxiv2020

Regular caffeine intake attenuates REM sleep promotion and sleep quality in healthy men

Acute caffeine intake can attenuate homeostatic sleep pressure and worsen sleep quality. Besides, caffeine intake - particularly in high doses and close to bedtime - may also affect circadian-regulated REM sleep promotion, an important determinant of subjective sleep quality. However, it is not known whether such changes persist under chronic caffeine consumption during daytime. Twenty male caffeine consumers (26.4 {+/-} 4 years old, habitual caffeine intake 478.1 {+/-} 102.8 mg/day) participated in a double-blind crossover study. Each volunteer completed a caffeine (3 x 150 mg caffeine daily), a withdrawal (3 x 150 mg caffeine for eight days then placebo), and a placebo condition. After ten days of controlled intake and a fixed sleep-wake cycle, we recorded 8 h of electroencephalography starting 5 h after habitual bedtime (i.e., start on average at 04:22 am which is around the peak of circadian REM sleep promotion). A 60 min evening nap preceded each sleep episode and reduced high sleep pressure levels. While total sleep time and sleep architecture did not significantly differ between the three conditions, REM latency was longer after daily caffeine intake compared to both placebo and withdrawal. Moreover, the accumulation of REM sleep proportion was slower, and volunteers reported more difficulties at awakening after sleep and feeling more tired upon wake-up in the caffeine condition compared to placebo. Our data indicate that besides acute also regular daytime caffeine intake affects REM sleep regulation in men. We have evidence that regular caffeine intake during daytime weakens circadian sleep promotion when compared to placebo. Moreover, the observed caffeine-induced deterioration in the quality of awakening may suggest a potential motive to reinstate caffeine intake after sleep.

neuroscience↗

bioRxiv2020

The impact of daily caffeine intake on nighttime sleep: signs of overnight withdrawal?

Acute caffeine intake can delay sleep initiation and reduce sleep intensity, particularly when consumed in the evening. However, it is not clear whether these sleep disturbances disappear when caffeine is continuously consumed during daytime, which is common for most coffee drinkers. To address this question, we investigated the sleep of twenty male young habitual caffeine consumers during a double-blind, randomized, crossover study including three 10-day conditions: caffeine (3 x 150 mg caffeine daily), withdrawal (3 x 150 mg caffeine for eight days, then switch to placebo), and placebo (3 x placebo daily). After nine days of continuous treatment, electroencephalographically (EEG)-derived sleep structure and intensity were recorded during a scheduled 8-h nighttime sleep episode starting 8 (caffeine condition) and 15 h (withdrawal condition) after the last caffeine intake. Upon scheduled wake up time, subjective sleep quality and caffeine withdrawal symptoms were assessed. Unexpectedly, neither polysomnography-derived total sleep time, sleep latency, sleep architecture, nor subjective sleep quality differed among placebo, caffeine, and withdrawal conditions. Nevertheless, EEG power density in the sigma frequencies (12-16 Hz) during non-rapid eye movement (NREM) sleep was reduced in both caffeine and withdrawal conditions when compared to placebo. These results indicate that daily caffeine intake in the morning and afternoon hours does not strongly impair nighttime sleep structure or subjective sleep quality in healthy good sleepers who regularly consume caffeine. The reduced EEG power density in the sigma range might represent early signs of overnight withdrawal from the continuous presence of the stimulant during the day. Statement of SignificanceCaffeine consumption is highly prevalent worldwide and has been repeatedly shown to acutely disrupt sleep, particularly when consumed after several days of abstinence or close to bedtime. However, commonly, caffeine is consumed daily and during daytime. Our well-controlled laboratory study revealed that this common pattern of intake affects nighttime sleep differently: While slow-wave sleep duration or slow-wave activity were rather similar compared to placebo, caffeine intake surprisingly reduced EEG power density in the sigma frequencies. In the light of earlier studies, this might present early signs of caffeine withdrawal which occurs due to overnight caffeine abstinence. The present findings provide novel insights into the impact of daily presence and nightly abstinence of caffeine on nighttime sleep in regular consumers.

neuroscience↗

bioRxiv2020

Changing color and intensity of LED lighting across the day impacts on human circadian physiology, sleep, visual comfort and cognitive performance

We examined whether dynamic light across a scheduled 16-h waking day influences cognitive performance, visual comfort, melatonin secretion, sleepiness and sleep under strictly controlled laboratory conditions of 49-h duration. Participants spent the first 5-h in the evening under standard lighting, followed by an 8-h nocturnal sleep episode at habitual bedtimes. Thereafter volunteers either woke up with static daylight LED (100 lux and 4000 Kelvin) or with a dynamic daylight LED that changed color (2700 - 5000 Kelvin) and intensity (0 - 100 lux) across the scheduled 16-h waking day. This was followed by an 8-h nocturnal treatment sleep episode at habitual bedtimes. Thereafter, volunteers spent another 12-h either under static or dynamic light during scheduled wakefulness. Under dynamic light, evening melatonin levels were less suppressed 1.5hours prior to usual bedtime, and participants felt less vigilant in the evening compared to static light. Sleep latency was significantly shorter in both the baseline and treatment night compared to the static light condition while sleep structure, sleep quality, cognitive performance and visual comfort did not significantly change. Our results support the recommendation of using blue-depleted light and low illuminances in the late evening, which can be achieved by a dynamically changing daylight LED solution.

physiology↗

bioRxiv2020

Wide awake at bedtime? The effects of caffeine on sleep and circadian timing in teenagers - a randomized crossover trial

BackgroundAdolescents frequently consume caffeine with unknown consequences on sleep and circadian rhythms. In adults, the evidence indicates that caffeine acutely reduces homeostatic sleep pressure and delays the circadian timing system. ObjectiveHere, we investigated the acute effects of caffeine intake on the developing sleep-wake regulatory system of teenagers. DesignIn a double-blind randomized crossover laboratory study, 18 teenagers (16.1 {+/-} 1 years old, pubertal development scale [PDS]: 2.76 {+/-} 0.35) ingested 80 mg caffeine (vs placebo) four hours prior to bedtime. Until bedtime, participants regularly filled in the Karolinska Sleepiness Scale and gave saliva samples to measure melatonin secretion. During nighttime, we quantified homeostatic sleep need by the electroencephalographically derived amount of slow wave sleep duration (SWS). After sleep, participants rated sleep quality by the Leeds Sleep Evaluation Questionnaire. ResultsWhile participants felt less sleepy after caffeine vs. placebo (P=0.038), their ratings of sleep quality were not strongly affected by the treatment. However, objectively, SWS was on average reduced by [~]20 min after caffeine vs. placebo (P=0.026). This caffeine-induced reduction was more pronounced in those individuals with more SWS under placebo (regression: P=0.042; standardized beta=0.622, P=0.011), even if controlling for habitual caffeine intake or pubertal stage (PDS). In melatonin onsets we observed both delays and advances in response to caffeine. This variance could partly be explained by differences in relative dose (i.e., mg caffeine/kg of bodyweight): the higher the relative dose, the more likely were delays (regression: P=0.01; standardized beta=0.592, P=0.01). ConclusionsIn teenagers, evening caffeine intake of already 80 mg (i.e. [~]8fl oz of common energy drinks) is sufficient to promote alertness at the costs of subsequent sleep. These costs might be more pronounced in adolescents with a higher need for SWS. Moreover, caffeine might disturb the circadian timing system, consequently hampering the balanced interplay of sleep-wake regulatory components. Sources of SupportMarie-Heim-Voegtlin Grant of the Swiss National Science Foundation (SNSF) PMPDP1_171364

neuroscience↗

bioRxiv2019

Caffeine-induced Plasticity of Grey Matter Volume in Healthy Brains: A placebo-controlled multimodal within-subject study

Disturbed sleep homeostatic states have been found to alter neuronal homeostasis and reduce grey matter (GM) volume. Caffeine intake that interferes with sleep homeostasis through antagonizing adenosine receptors can impair hippocampal synaptic strength, neurogenesis, as well as memory and learning in rats. In this study, reduced medial temporal GM volume was observed after daily caffeine intake in humans (3 x 150 mg x 10 days compared to 10-day placebo administration). The potential bias from reduced cerebral blood flow was controlled, and the GM reduction was independent of the change in sleep pressure. A decrease in working memory during daily caffeine intake was observed, albeit no association with the magnitude of GM changes. The findings indicate that daily caffeine intake might induce rapid cerebral plasticity and be detrimental for higher order cognitive performance in the long run. They may call into question whether the neuroprotective effects of caffeine found in acute or low dose administration in animals are generalizable onto the daily usage in humans.

neuroscience↗

bioRxiv2019

Caffeine-dependent changes of sleep-wake regulation: evidence for adaptation after repeated intake

To enhance wakefulness, daily consumption of caffeine in the morning and afternoon is highly common. However, it is unknown whether such a regular intake pattern affects timing and quality of wakefulness, as regulated by an interplay of circadian and sleep-homeostatic mechanisms. Thus, we investigated the effects of daily caffeine intake and its withdrawal on circadian rhythms and wake-promotion in 20 male young habitual caffeine consumers. We applied a double-blind, within-subject design with a caffeine (150 mg, 3 x daily), a placebo, and a withdrawal condition each lasting ten days. Starting on day nine of treatment, salivary melatonin and cortisol, evening nap sleep, as well as sleepiness and vigilance performance throughout day and night were quantified during 43 h under controlled laboratory conditions. Neither the time course of melatonin (i.e., onset, amplitude, or area under the curve) nor the time course of cortisol were significantly affected by caffeine intake or its withdrawal. During withdrawal, however, volunteers reported increased sleepiness, showed more attentional lapses, as well as polysomnography-derived markers of elevated sleep propensity in the late evening compared to both, placebo and caffeine conditions. Thus, the typical timing of habitual caffeine intake in humans may not necessarily shift circadian phase nor lead to clear-cut benefits in alertness. The time-of-day independent effects of caffeine withdrawal suggest an adaptation to the substance, presumably in the homeostatic aspect of sleep-wake regulation.

neuroscience↗