Rough night of sleep? Relying on caffeine to get you through the day isn’t always the answer, says a new study from Michigan State University.
Researchers from MSU’s Sleep and Learning Lab, led by psychology associate professor Kimberly Fenn, assessed how effective caffeine was in counteracting the negative effects of sleep deprivation on cognition. As it turns out, caffeine can only get you so far.
The study – published in the most recent edition of Journal of Experimental Psychology: Learning, Memory, & Cognition – assessed the impact of caffeine after a night of sleep deprivation.
More than 275 participants were asked to complete a simple attention task as well as a more challenging “placekeeping” task that required completion of tasks in a specific order without skipping or repeating steps.
Fenn’s study is the first to investigate the effect of caffeine on placekeeping after a period of sleep deprivation.
She added, “Caffeine may improve the ability to stay awake and attend to a task, but it doesn’t do much to prevent the sort of procedural errors that can cause things like medical mistakes and car accidents.”
Insufficient sleep is pervasive in the United States, a problem that has intensified during the pandemic, Fenn said. Consistently lacking adequate sleep not only affects cognition and alters mood, but can eventually take a toll on immunity.
“Although people may feel as if they can combat sleep deprivation with caffeine, their performance on higher-level tasks will likely still be impaired. This is one of the reasons why sleep deprivation can be so dangerous.”
Fenn said that the study has the potential to inform both theory and practice.
“If we had found that caffeine significantly reduced procedural errors under conditions of sleep deprivation, this would have broad implications for individuals who must perform high stakes procedures with insufficient sleep, like surgeons, pilots and police officers,” Fenn said.
“Instead, our findings underscore the importance of prioritizing sleep.”
Sleep deprivation (SD) is common in the current society, with a prevalence of approximately 35% (Bandyopadhyay and Sigua, 2019). SD refers to the state that occurs when there is a loss of sleep and increased wakefulness that is maintained for a certain time (Roca et al., 2012; Kusztor et al., 2019), and total sleep deprivation (TSD) is the elimination of sleep for some time (at least one night) to significantly prolong wakefulness (Reynolds and Banks, 2010).
TSD is one of the main reasons for a low arousal level, reduced cognitive function, and increased reaction times, among other things. Since TSD has serious effects on human cognitive brain function, studies on interventions for mitigating the impact of TSD have become increasingly prevalent in this research field.
Recently, there has been a trend toward the use of caffeine (1,3,7-trimethylxanthine) to alleviate the effects of TSD and maintain arousal levels (Spaeth et al., 2014; Burrows et al., 2020). Worldwide, caffeine is the most widely consumed central nervous stimulant (Colombo and Papetti, 2020).
Caffeine has been classified by pharmacologists as a central nervous system stimulant affecting, with increasing doses, the cortex, the medulla, and finally the spinal cord (Arnaud, 1987). Caffeine acts in the brain as a non-specific potent inhibitor of the actions of A1 and A2 Adenosine receptors (Ribeiro and Sebastiao, 2010; Nehlig, 2016).
It seems particularly effective in improving alertness in situations of reduced arousal. Caffeine maintains a higher dopamine concentration especially in those brain areas linked with “attention.” Depending on the neurotransmitter system, caffeine can affect different brain areas with different functions (Meeusen et al., 2013).
Usually, caffeine has delayed effect about 3–4 h of half-life (Knutti et al., 1981, 1982; Nehlig, 2016), caffeine’s behavioral effects and the significant increase in psychomotor performance it causes have been documented in a large body of literature, in addition to improvements in attention- (Temido-Ferreira et al., 2019; Alasmari, 2020; Franceschini et al., 2020; Irwin et al., 2020; Jahrami et al., 2020), mood-, and vigor-based tasks (Dietz and Dekker, 2017; Shabir et al., 2018; Alasmari, 2020).
Moreover, Beaumont et al. (2005) found that the action of caffeine both shortened response times and reduced the number of errors on psychomotor tests, which indicates that caffeine has a global action on information processing and divided attention management (Beaumont et al., 2005; Wilhelmus et al., 2017).
Although caffeine has been studied for more than a 100 years, more research is necessary to better understand how brain activity is affected by caffeine consumption (Meng et al., 2017; van Son et al., 2018; Franco-Alvarenga et al., 2019; Tarafdar et al., 2019; Ueda and Nakao, 2019). Electrophysiological technology with event-related-potential (ERP) component detection, such as P50, N200, and P300, has been used for the measurement of brain activity.
This technology allows for the measurement of neuroelectric activity related to cognitive processes, such as attention allocation and activation of short-term memory. Specific electrical patterns as measured using electroencephalography (EEG) can be evoked by sensory stimulation, such as visual and auditory stimulation.
This evoked activity, or ERP, typically consists of several positive and negative peaks (Jin et al., 2015). ERPs are time-locked and can reflect both endogenously and exogenously driven cognitive processes. Concerning ERP components that reflect stimulus processing, a general arousal effect of caffeine would thus be expected to affect all components similarly, acting broadly as a stimulant amplifying all aspects of brain function (Kahathuduwa et al., 2017; Barry et al., 2019).
For specific stimuli in certain response inhibition tasks, such as Go and No-Go stimuli in Go/No-Go tasks, corresponding evoked potentials can be generated during brain processing. Go-related potential changes are mainly related to automatic response processing, while No-Go-related potential changes are related to response inhibition.
Several ERP studies have examined the impact of TSD on vigilant attention during target detection and selective attention as it interacts with working and visuomotor memory (Zhang et al., 2014; Jin et al., 2015). These studies have found that TSD reduces early (~160–200 ms) or late (>250 ms) ERP component amplitudes, or delays the latencies of these components. Jin et al. (2015) found that TSD induces a dose-dependent functional decline in response inhibition (No-Go-N2 and No-Go P3 amplitudes), and 8 h of recovery sleep resulted in a partial recovery or maintenance of response inhibition (Jin et al., 2015).
Tieges et al. (2009) examined the effects of caffeine in a task-switching paradigm and reported that caffeine increased N2 amplitude, but did not affect N2 latency. By contrast, P2 and P3 latencies were reduced, with no amplitude effects, indicating the difficulty in conceptualizing such inconsistent effects between components (Tieges et al., 2009).
In an auditory Go/No-Go task, Barry et al. (2007) found that a single oral dose of caffeine (250 mg) resulted in focal rather than global increases in P1, P2, and P3b amplitudes to Go stimuli with no changes in latency, suggesting that caffeine differentially improves aspects of processing related to response production and task performance (Barry et al., 2007).
Within the visual Go/NoGo paradigm, ERP studies have suggested that the N2 component reflects stimulus perception (Dulinskas and Ruksenas, 2019; Song et al., 2019), cognitive control, and response inhibition (Magnuson et al., 2019; Quaglia et al., 2019). P300 is the largest positive-going peak amplitude of the waveform within a time window of 300–400 ms and is considered to represent the allocation of attentional resources to rare salient stimuli (Cote et al., 2001; Marhöfer et al., 2015). P300 amplitude and latency are thought to reflect cognitive processing, such as stimulus identification and evaluation (Feng et al., 2019; Wang et al., 2019; Gao et al., 2020; Khedr et al., 2020).
Studies have also suggested that higher-order cognitive stimuli-elicited P300 components are generated from the anterior cortex, and these components reflect the response inhibition process (de Bruijn et al., 2020; Paul et al., 2020). However, Deslandes et al. (2006) and Tieges et al. (2009) have found no significant alteration of ERP indices or other neuropsychomotor results following caffeine administration after TSD, indicating that there is still a lack of knowledge of caffeine’s effects on the human brain.
By comparing ERPs related to response inhibition tasks before and after TSD, we can understand how the brain’s automatic response or response inhibition is affected by TSD. In the present study, we utilized ERP techniques to analyze behavioral, cognitive, and electrophysiological changes produced by caffeine administration after TSD.
Based on previous studies, we hypothesized that TSD would induce a decrease in amplitude and a prolonged latency of the N2/P3 components. We also hypothesized that caffeine consumption would attenuate the decline in response accuracy and prolongation of reaction time (RT) caused by TSD. Because caffeine mainly enhances the alertness level of individuals, we supposed that ingesting caffeine after TSD can improve the process of automatic response and response inhibition, which will be reflected in increased amplitude and prolonged latency of ERP involving Go or No-Go stimulation.
We chose 36 h of TSD to induce a moderate intensity of fatigue in subjects, to better observe the effect of caffeine intervention. To address these problems clearly, a visual Go/No-Go task with simultaneous EEG recording was used to evaluate caffeine’s effect on brain function before and after 36 h of TSD.
Conclusion
These results suggest that caffeine may be beneficial to cognitive processes related to response selection and inhibition. Higher-level cognitive brain functions appeared to be improved by the administration of caffeine (Han et al., 2015; Satterfield et al., 2018). By utilizing an electrophysiological technique, the most notable results of the present study were concerning changes to the P2 component. After TSD, there was an obvious change in the N2 and P3 component amplitudes.
Also, a change in the P2 amplitude was seen following caffeine ingestion. This could be explained by the fact that caffeine is related to individual arousal and accelerated response-related decisions rather than higher-level recognition (Bocca and Denise, 2006; Czisch et al., 2012).
Thus, the ingestion of caffeine seems to counteract the TSD effect, which did not occur in the placebo condition. EEG studies have shown an absolute increase in the P2 amplitude after caffeine ingestion compared with the N2 and P3 components after 36 h of TSD.
It reflects neuroelectric activity related to cognitive processes such as attention allocation and activation of short-term memory. Caffeine is related to the preservation of an individual’s arousal level and accelerated response-related decisions, while subjects’ higher-level recognition has limited improvement with prolonged awareness.
reference link : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7347038/
Michelle E. Stepan et al, Caffeine selectively mitigates cognitive deficits caused by sleep deprivation., Journal of Experimental Psychology: Learning, Memory, and Cognition (2021). DOI: 10.1037/xlm0001023
Alison J. Day et al, Is it worth it? The costs and benefits of bringing a laptop to a university class, PLOS ONE (2021). DOI: 10.1371/journal.pone.0251792
