Abstract
As we explore another topic in our second Day In The Life of My Brain Essay, we should consider the fundamental importance of lessons learned from our last examination of a Day In The Life of My Brain. Most importantly, we will remember this time to effectively cover both the cytoarchitectonic and functional view of research on taking a nap in the afternoon. Then, we will connect this research to the health benefits and detractions of taking an afternoon nap.
This phenomenon, the afternoon nap or siesta, is an occurrence that is familiar to many throughout their lifetime. Research, however, suggests that a paradox exists in the balance of the positive and negative outcomes of napping. As we work through our research topic, we will generally explore this paradox, aiming to answer whether taking a siesta has become commonplace for a good cause and biological reasons or simply a habit of a lazy society. Why do we nap, specifically in the afternoon? This paper aims to investigate our brain and body’s desire for an afternoon nap.
Research Perspectives
Midday naps offer a variety of health benefits, including memory consolidation, preparation for subsequent learning, executive functioning enhancement, and a boost in emotional stability (Mantura & Spencer, 2017). Exploring naps first from a cytoarchitectonic and functional approach may offer a breadth of understanding as to why afternoon naps appear commonplace.
Considering these two research approach objectives, a cytoarchitectonic study of the afternoon nap would consider the brain structures necessary to engage in the task of an afternoon nap. In this specific vein, from our learning this semester and prior ones, neurochemicals are appropriate to consider when discussing a cytoarchitectonic study (The Pennsylvania State University, 2023a). Considering this approach, we might also assess the health benefits of napping and how, from a functional perspective, they may explain why we engage in an afternoon nap.
Throughout this semester, I have learned that frequently, it’s beneficial to explain the functional causes of behavior and then determine the cytoarchitecture utilized in engaging it. From this perspective, the functional explanation of taking an afternoon nap may look at the positive health benefits as the origin of the desire to nap in the first place. This view, however, must be balanced somewhat with the neurochemical correlates we understand to signal our bodies to crave a nap.
We understand that our daily or circadian rhythms seem to control the urge to sleep, depending on our internal clock’s schedule. To narrow the focus of this paper, we must consider that sleep is being discussed in the context of a nap. Unlike sleep occurring once daily such as overnight, according to our biological clocks, (The Pennsylvania State University, 2023b) a nap can occur at various times throughout the day, predominately in the afternoon hours. There is further evidence that homeostatic pressure (Process S) and circadian rhythmicity (Process C) are correlated in regulating sleep. For instance, process S has been hypothesized to result from extracellular adenosine accumulation (Borbely, 2982), which we will discuss in more detail.
The idea of napping in the afternoon needs to be further narrowed. For our functional exploration, we are exploring rest, which is less than 30 minutes long. Naps promote restorative functions in the executive domain, memory formation, learning, and emotional processing (Mantura & Spencer, 2017).
This concept is so basically and eloquently defined within the context of the research into the cognitive health benefits and detractions of napping, which this paper mainly rests. Essentially, in one study, following sleep deprivation, restriction, or even a normal night of sleep, cognitive abilities such as working memory (executive function), decrease throughout the day, however following a midday nap, they recover. This is clear evidence of the restorative functions of a nap in an overview of a behavioral intervention.
Understanding basic experimental design is necessary to fully understand the scope of the cause-effect relationship the research initiative is attempting to explain. In the most basic form, we must realize that biology, in a somatic intervention, is the independent variable and the resulting behavior is the dependent variable. Generally, researchers aim to measure outcomes by manipulating some component of a biological system (the independent variable) and then measure the outcome of the manipulation on behavior (the dependent variable). Conversely, in behavioral intervention, the roles are reversed. Behavior (the independent variable) is manipulated, and biology (the dependent variable) is measured.
Within the context of this behavioral intervention, researchers investigated the differences between nap lengths, ranging from 10-30 minutes, finding that a 10-minute nap increased immediate alertness to a greater extent than other nap lengths. Researchers restricted sleep to five hours for participants, followed by a nap in the afternoon and three hours of post-nap testing and diagnostics performed within a laboratory environment. The researchers aimed to investigate the relationship between sleepiness and stages of sleep based on the length of the experiment.
Researchers equipped participants with electroencephalograms and electromyogram electrodes to record sleep stages associated with the nap. The nap commenced when participants reached the first of three consecutive epochs below the 50% alpha baseline of the sleep cycle. Following the identification and stage of sleep, researchers awakened participants at precisely 5, 10, 20, or 30 minutes of sleep, then observed their findings. In this context, the independent variable is represented by the varying degrees of time subjects were allowed to sleep, then subsequently measured outcomes in the arenas of sleep latency, subjective sleepiness, fatigue, vigor, and cognitive performance (Brooks & Leon, 2006). Together, these ratings encompassed the dependent variable.
Mantura & Spencer have guided us through their research into an understanding of the significant cognitive functions that together seem to form a good basis for investigating the cytoarchitectonic correlation to napping. As discussed, naps promote the restoration of function in the executive decision-making processes, memory formation, learning, and emotional regulation and processing. Conversely, our text illustrates the correlation between cortical and subcortical regions and their associated functions. Considering this, we understand the hippocampus to be responsible for memory formation, the thalamus to be primarily responsible for sensory processing information, including memory and learning, the PFC or prefrontal cortex to be closely integrated with executive functioning, and the amygdala which is a structure highly involved in the coordination of certain emotional responses, (Freberg, 2018, p. 54) .
In an endeavor to explore the cytoarchitecture of a nap, the author requests a little latitude to draw a potential biological cause for the desire to take a nap and then the cortical structures that benefit as a result. Following a restful night’s sleep, as demonstrated through the author’s first term paper, the first wake-up decision is to consume a cup of coffee. Within the context of that paper, the author described the benefits the morning pick-me-up offers. What the author did not discuss was his habit of consuming coffee multiple times during the day and his unstable sleep patterns as a product of education, work-related, and family endeavors. Considering this notion, the author must consider that some individuals get along fine with 5-6 hours of sleep, while others require 9-10 hours to avoid feeling lethargic the following day. Due to the demands of children and family atop the author’s already demanding schedule, sleep frequently comes around 2:30 am. The following morning begins around 6:30 am. Daily, the author takes a two-hour nap at 2:30 pm. The author’s cumulative sleep in any circadian period is 6 hours, or frequently less.
Considering this, the desire to nap in the afternoon is already high, and we will discuss shortly how this phenomenon is correlated to our circadian cycles. Since the average adult human desires roughly eight hours of sleep to function the next day, it is the author’s suspicion that his desire to nap is a combination of a substantial cliff after 11:00 am, when he no longer consumes coffee, and 2:30, when the napping period occurs.
First, we understand from previous research that caffeine promotes wakefulness by blocking or antagonizing the activation of adenosine’s A1 and A2a receptors (Holst & Landolt, 2015). Considering this notion, in the afternoon, the release of these receptors increases sleep drive or sleep pressure. Homeostatic sleep drive is the pressure to sleep that increases with time awake and decreases after sleep occurs, (Hayashi & Motoyoshi, 2005). It could be posited that this author’s sleep pressure is internally highest after the abatement of caffeine’s antagonism of adenosine, around 2:30 pm daily. When sleep pressure is highest, the desire to sleep is strongest (CDC, 2023).
The brain then approaches and enters sleep associated with our napping condition. We understand from our lectures that two types of sleep predominately occur. REM and NREM. REM, the rapid eye movement stage of sleep, is the dreaming phase and the most active of all sleep cycles. Conversely, NREM is the most restorative. It is slow in nature where synchronicity occurs in neuronal activity. Considering once again our teachings, REM stages may only last fifteen minutes while NREM is a longer, slower cycle of sleep. The entire cycle, typically, repeats every 90 minutes. Considering this notion, the author’s sleep cycle accommodates two cycles of minimally restorative REM sleep, and two cycles of highly restorative NREM sleep.
Further consideration of our lectures identifies the reticular formation within the medulla as being a maintainer of wakeful states. The idea is that this pathway, originating within the reticular formation, within the medulla and projected superiorly through the posterior hypothalamus, synapsing at the basal forebrain, together is responsible for wakeful states. Once again, from the author’s learning this semester, the discovery of inverse biological operations frequently lead to the discovery of systems involved in the process under investigation. Central to this idea is that within these pathways, particularly within the basal forebrain, GABA can be released onto awake structures, thereby inhibiting them, essentially encouraging sleep. Relevant to this notion is the idea that researchers have found electronic stimulation to the region of the basal forebrain encourages or stimulates sleep while lesion studies have revealed that severe insomnia can occur in patients with damage to this region of the brain, (The Pennsylvania State University, 2023b).
It seems, biochemically, several neuromodulators, including serotonin, acetylcholine, histamine, orexin, noradrenaline (Yokoi, 2018), and even adenosine, play a role in sleep-wake cycles. GABA seems to also be involved in the inhibition of certain cortical structures in the region of the basal forebrain. The author would postulate that dopamine (DA) could and should be involved in this group also. DA inhibits neuronal activity and excites wake-promoting circadian neurons; accordingly, DA should be considered another neuromodulator that has significant ties to wakefulness through the circadian neuronal networks, (Fernandez-Chiappe, 2020).
Research supports restorative sleep benefits memory formation, emotional regulation, executive functioning, and learning. When antagonized by caffeine, adenosine suppresses sleep drive, otherwise known as homeostatic sleep drive, or the pressure to sleep. With the reduction of caffeine and its impact on adenosine, the author posits that homeostatic pressure increases, encouraging sleep. Accordingly, adenosine seems central to maintaining wakeful states and correlated to encouraging sleepful states. Finally, one final view considers reversing neurological logic. Wakeful states seem to be controlled initially by the reticular formation of the medulla and maintained through several down pathways. Stimulation of the down pathway in the basal forebrain results in sleep stimulation, whereas damage to this pathway results in insomnia (The Pennsylvania State University, 2023b).
Research Methods
First, it seems the somatic benefits of a siesta may outweigh the health detractors, at least at first blush (Hayashi & Motoyoshi, 2005). In this psychophysiological study, researchers aimed to measure naps’ impact on cognitive function. Hayashi et al. aimed to confirm the recuperative effect of a nap of fewer than 30 minutes. Researchers presented seven women and three men aged 18-24 with a questionnaire that examined their sleep-wake habits. The group reported sleeping between six and eight hours as their baseline sleep measurement; the group was not overly weighted with larks and owls[1], and each took naps less than once weekly.
Subjects were equipped with electroencephalograms (EEG) to measure stages of sleep. Slow eye movements were noted as transition sequences between stages of sleep, and increased sleepiness indicated alertness. Special care was taken to identify stages 1 and 2 of sleep. Subjects were awakened after precisely five minutes of stage 1 sleep (S1-nap-condition) and three minutes of stage 2 sleep (S2-nap-condition). It seems relevant to note that subjects received eight minutes of rest in the measured period compared to zero in the no-nap condition.
Before initiating the task, free from alcohol or caffeine for twelve hours before the experiment, subjects participated in three experimental conditions highlighting the associated stages of sleep (S1 and S2) and no-nap conditions, with measurements recorded to establish baseline functioning. Before the experiment day, subjects reduced their daily sleep patterns by 1.5 hours precisely.
Subjects then engaged in the experiment with baseline measurements recorded. Following the criterion for the achievement of the S1 and S2 sleep stages, participants were awakened. Participants were then asked to perform a visual detection task and a symbol-digit task. In this arena, no significant difference was observed immediately before and after napping, within those only experiencing the S1-nap condition. Within the S2-nap condition, misses were infrequent pre-nap and post-nap, however, the number of errors during the last half of the post-nap session showed significant increases in errors in both the no-nap and S1-nap conditions. This lends support to the restorative effects of naps of the S2-persuasion, even when the time within this stage of the nap is less than half of the time spent in the S1-nap condition.
Subjects also completed subjective mood measurements as related to S1, S2, and no-nap conditions. Findings within this domain supported that sleepiness and fatigue decreased in the S1 nap condition but significantly decreased in the S2-nap condition. This area seems ripe for additional research. In other words, does the overall time that it takes one to achieve stage two sleep impact processing performance?
There was no reported change in the no-nap condition as one might expect, accordingly, the totality of the evidence reported by Hayashi et al, confirms the restorative or recuperative effect of a daytime nap, within the domain of associative and sequential memory performance. S1 and S2 nap conditions vary to some degree in their restorative effect but clearly, the no-nap condition illustrates that a nap of any variety does benefit cognition but those of the S2 persuasion are substantially more restorative than naps only containing S1 sleep.
As we have discussed, sleep deprivation can occur with damage to certain cortical structures, especially those located in the basal forebrain. The author felt it necessary to tie our research back to this contention that was previously discussed in lecture 13. Within the lecture context, the assertion was made that GABA inhibits certain awake structures, stimulating them to sleep. Further, the course author discussed how lesions to this area discouraged sleep and encouraged wakefulness. Investigating this notion, the author reviewed a study considering left dorsomedial frontal brain damage and its association with insomnia (Koenigs, Holliday, Solomon, & Grafman, 2010).
Within this study, researchers selected a group of 192 patients suffering from insomnia to investigate its pathophysiological origins. Patients in the study group possessed focal brain lesions. They demonstrated sleep impairment to the degree classified as insomnia proximate to damage sustained during penetrating head injuries during the Vietnam War. They registered within the Vietnam Head Injury Study (VHIS) Registry. Relevant to the study and beneficial from a conceptual standpoint, insomnia is defined as a sleep disorder involving difficulty initiating and maintaining sleep (Ohayon MM, 2009) and having cognitive and mood impairments during wakefulness, (MM, 2009). It has been known to impair one in three adults and is strongly correlated with anxiety and depression (Koenigs et al, 2010).
CTs were acquired, with and without contrast, and analyzed for location and volume using specific brain lesion software. Lesion volume was calculated by tracing relevant slices, then summing the traced areas and multiplying by slice thickness. The procedure was performed by a neuropsychiatrist and confirmed by a neutral.
Further qualifying the participant pool, researchers administered an insomnia self-report according to the Hamilton Anxiety Rating Scale (HAM-A) (Hamilton, 1959) [2], which contains an item specifically loaded to insomnia. Participants ranked their responses on a scale of 0-4. Those having scores of two or greater were included in the study.
Findings support that moderate-to-severe insomnia, as determined by patients’ self-reports on the HAM-A, is strongly correlated to left dorsomedial prefrontal cortex damage within the context of this study. Koenigs et al demonstrate the struggle of this analysis however, in the assertion that insomnia is a common symptom of mood and anxiety disorders. Koening further asserts that the potentiality exists that damage to the left dorsomedial PFC is secondary to the role of this area in the management of mood and anxiety. Essentially, the researchers explain that selection may have been due to self-reported depression and anxiety symptoms rather than the selection of the primary criterion, insomnia. To this end, researchers attempted to isolate a subset of subjects from the no insomnia group, having anxiety and depression symptomology scores equal or greater to that of the insomnia group.
Their findings in this regard contend that the concentration of lesions observed in the insomnia group support left dorsomedial PFC damage and its association specifically with the sleep disturbance classified as insomnia. To this end, our course author and lecturer are supportive also of the notion that inhibition of certain awake structures of the basal forebrain by GABA can encourage sleep. This contention is further supported by the research on patients having left dorsomedial frontal brain damage.
Reflections
It seems that napping in the afternoon has positive health benefits, especially somatic, behavioral, and emotional. While researching and writing this paper, the notion that naps can have adverse health implications was revealed on more than one occasion. While it seems there isn’t enough time in the day to study each slice of this subject to the degree it deserves, the health detractions do deserve some attention. Napping was classified through a highly engaging table by the authors of the primary research for this paper (Mantua) and is now relevant when we consider the types of naps commonly undertaken.
Table 1
|
Nap Type |
Definition |
|
Recovery |
Due to sleep loss |
|
Prophylactic |
In preparation for sleep loss |
|
Appetitive |
For enjoyment |
|
Fulfillment |
Due to increased sleep need (during development) |
|
Essential |
Due to sickness or inflammatory burden |
(Mantura & Spencer, 2017)
Certain nap types do come at a cost. Frequent napping can predict negative health outcomes, especially when naps are considered essential. Essential naps are frequent and habitual and have been associated with microvascular disease, depression, diabetes, osteoporosis, functional limitations, general medical morbidity, and cognitive decline. It seems that these associations are predominately found in older populations, however, some do exist in middle age and younger adults, (Mantura & Spencer, 2017).
It seems there is further supporting evidence that frequent napping and long overnight sleep habits do increase the risk for metabolic syndrome and cardiovascular events, (Wu J, 2015). Further research supports to some degree essential napping and its association with certain cognitive declines, (Hayashi & Motoyoshi, 2005). Some research supports the notion that age-related changes in brain integrity lead to cognitive declines and may increase sleep drive and subsequent daytime napping. Moreover, astonishingly, the notion that older adults who report daytime sleepiness are twice as likely to be diagnosed with dementia within three years, (Foley D, 2001), seems alarming.
From our research, there are several health benefits to napping and detractors for napping as we age. Once again, the author has found himself in an exciting entanglement: are my naps to be considered essential? Are they a function of my environment, which is not conducive to rest, and have become a necessary component of my biopsychology? As a middle-aged male, with low-risk factors for dementia, it seems that my daily task of a nap in the afternoon may be more of a recovery-style nap and less of an essential-style nap. Either way, from a highly objective opinion, I do feel rested and more focused following a nap and better able to perform as a father (emotional processing), student (memory formation, subsequent learning), and risk manager and consultant (executive functions, memory formation, learning). To this degree, I think I’ll continue my family legacy of the afternoon nap. After all, we just function better when rested.
References
Borbely, A. (2982). A Two Process Model of Sleep Regulation. Human Neurobiology, 1:195-204.
Brooks, A., & Leon, L. (2006). A Brief Afternoon Nap Following Nocturnal Sleep Restriction: Which Nap Duration is Most Recuperative? Sleep.
CDC. (2023, 04 21). NIOSH Training for Nurses on Shift Work and Long Work Hours. Retrieved from cdc.gov: https://www.cdc.gov/niosh/work-hour-training-for-nurses/longhours/mod2/11.html
Fernandez-Chiappe, F. H.-L.-F. (2020). Dopamine Signaling in Wake-Promoting Clock Neurons Is Not Required for the Normal Regulation of Sleep in Drosophila. The Journal of neuroscience : the official journal of the Society for Neuroscience, 40,9617-9633. doi:10.1523/JNEUROSCI.1488-20.2020
Foley D, M. A. (2001). Daytime sleepiness is associated with 3-year incident dementia and cognitive decline in older Japanese-American men. J Am Geriatr Soc., 49:1628–32. doi:10.1046/j.1532-5415.2001.t01-1-49271.x.
Freberg, L. (2018). Discovering Behavioral Neuroscience: An Introduction to Biological Psychology (4th ed.).
Hayashi, M., & Motoyoshi, N. (2005). Recuperative power of a short daytime nap with or without stage 2 sleep. Sleep, 28:829-36.
Holst, S. C., & Landolt, H. P. (2015). Sleep Homeostasis, Metabolism, and Adenosine. Curr Sleep Med Reports, 1:27-37.
Koenigs, M., Holliday, J., Solomon, J., & Grafman, J. (2010). Left Dorsomedial Frontal Brain Damage is Associated with Insomnia. Journal of Neuroscience, 16041-16043.
Mantura, J., & Spencer, R. M. (2017). Exploring the nap paradox: are mid-day sleep bouts a friend or foe? Sleep medicine, 37,88-97.
MM, O. (2009). Observation of the natural evolution of insomnia in the American general population cohort. Sleep Med, 4:87-92.
Ohayon MM, R. C. (2009). 3rd Epidemiological and clinical relevance of insomnia diagnosis algorithms according to the DSM-IV and the International Classification of Sleep Disorders (ICSD) . Sleep Med., 10:952-960.
The Pennsylvania State University. (2023a, 03 04). Discovering Biological Psychology [Lecture Notes]. The Pennsylvania State University.
The Pennsylvania State University. (2023b). Lesson 13: Sleep and Waking [Lecture Notes]. The Pennsylvania State University.
Wu J, X. G. (2015). Daily sleep duration and risk of metabolic syndrome among middle-aged and older Chinese adults: cross-sectional evidence from the Dongfeng-Tongji cohort study. BMC Public Health., 15:178. doi:10.1186/s12889-015-1521-z
Yokoi, R. O. (2018). Impact of Sleep–Wake-Associated Neuromodulators and Repetitive Low-Frequency Stimulation on Human iPSC-Derived Neurons. Retrieved from National Library of Medicine: https://doi.org/10.3389/fnins.2019.00554