The brain simulates actions and their consequences during REM sleep

During REM sleep our brains make up and work though simulated scenarios, while putting our bodies into paralysis so we don't thrash about dangerously....  Senzai and Scanziani show what in going on in mouse brains. Here is the first paragraph (abstract) of their open source text:

Vivid dreams mostly occur during a phase of sleep called REM1–5. During REM sleep, the brain’s internal representation of direction keeps shifting like that of an awake animal moving through its environment6–8. What causes these shifts, given the immobility of the sleeping animal? Here we show that the superior colliculus of the mouse, a motor command center involved in orienting movements9–15, issues motor commands during REM sleep, e.g. turn left, that are similar to those issued in the awake behaving animal. Strikingly, these motor commands, despite not being executed, shift the internal representation of direction as if the animal had turned. Thus, during REM sleep, the brain simulates actions by issuing motor commands that, while not executed, have consequences as if they had been. This study suggests that the sleeping brain, while disengaged from the external world, uses its internal model of the world to simulate interactions with it.

Neurons help flush waste out of our brains during sleep

More information (summarized here) on what is happening in our brains while we sleep is provided by Jiang-Xie et al.,, who show that active neurons can stimulate the clearance of their own metabolic waste by driving changes to ion gradients in the surrounding fluid and by promoting the pulsation of nearby blood vessels.  Here is the Jiang-Xie et al.abstract:

The accumulation of metabolic waste is a leading cause of numerous neurological disorders, yet we still have only limited knowledge of how the brain performs self-cleansing. Here we demonstrate that neural networks synchronize individual action potentials to create large-amplitude, rhythmic and self-perpetuating ionic waves in the interstitial fluid of the brain. These waves are a plausible mechanism to explain the correlated potentiation of the glymphatic flow through the brain parenchyma. Chemogenetic flattening of these high-energy ionic waves largely impeded cerebrospinal fluid infiltration into and clearance of molecules from the brain parenchyma. Notably, synthesized waves generated through transcranial optogenetic stimulation substantially potentiated cerebrospinal fluid-to-interstitial fluid perfusion. Our study demonstrates that neurons serve as master organizers for brain clearance. This fundamental principle introduces a new theoretical framework for the functioning of macroscopic brain waves.

When memories get complex, sleep comes to their rescue

Here I point to a PNAS article by Lutz et al. and a commentary on the work by Schechtman. Here is the Lutz. et al. abstract:

Significance

Real-life events usually consist of multiple elements such as a location, people, and objects that become associated during the event. Such associations can differ in their strength, and some elements may be associated only indirectly (e.g., via a third element). Here, we show that sleep compared with nocturnal wakefulness selectively strengthens associations between elements of events that were only weakly encoded and of such that were not encoded together, thus fostering new associations. Importantly, these sleep effects were associated with an improved recall of the complete event after presentation of only a single cue. These findings uncover a fundamental role of sleep in the completion of partial information and are critical for understanding how real-life events are processed during sleep.

Abstract

Sleep supports the consolidation of episodic memory. It is, however, a matter of ongoing debate how this effect is established, because, so far, it has been demonstrated almost exclusively for simple associations, which lack the complex associative structure of real-life events, typically comprising multiple elements with different association strengths. Because of this associative structure interlinking the individual elements, a partial cue (e.g., a single element) can recover an entire multielement event. This process, referred to as pattern completion, is a fundamental property of episodic memory. Yet, it is currently unknown how sleep affects the associative structure within multielement events and subsequent processes of pattern completion. Here, we investigated the effects of post-encoding sleep, compared with a period of nocturnal wakefulness (followed by a recovery night), on multielement associative structures in healthy humans using a verbal associative learning task including strongly, weakly, and not directly encoded associations. We demonstrate that sleep selectively benefits memory for weakly associated elements as well as for associations that were not directly encoded but not for strongly associated elements within a multielement event structure. Crucially, these effects were accompanied by a beneficial effect of sleep on the ability to recall multiple elements of an event based on a single common cue. In addition, retrieval performance was predicted by sleep spindle activity during post-encoding sleep. Together, these results indicate that sleep plays a fundamental role in shaping associative structures, thereby supporting pattern completion in complex multielement events.

Breath - Some basic facts and instructions

I’ve enjoyed reading through James Nestor’s book “Breath - The new science of a lost art,”  and I tried out some of the exercises he points to, such as Tummo, which increases breathing to deliver a brief shock therapy to the sympathetic and parasympathetic systems that regulate breathing, thus temporarily resetting to a more appropriate balance between the two.  He describes numerous useful breathing therapies that have been discovered, forgotten, and then rediscovered over the past 3000 years by different cultural and religious traditions, and in the past 300 years by more modern medical and scientific insights.  Nestor: “Breathing is a key input. From what I’ve learned in the past decade, that 30 pounds of air that passes through our lungs every day and that 1.7 pounds of oxygen our cells consume is as important as what we eat or how much we exercise. Breathing is a missing pillar of health.”

The epilogue to his book provides a very concise list of breathing instructions that can serve as preventative maintenance to assist in maintaining balance in the body so that milder problems don’t blossom into more serious health issues and might restore balance when it is lost.  Here is Nestor’s list, with an assist from ChatGPT 4 condensations of the book’s text that I have tweaked where appropriate.  The condensations are amazing.  They cut through the folksy personal reader-friendly stuff to give the basic facts presented.

In a nutshell, this is what we’ve learned:

SHUT YOUR MOUTH    

A 20-day study found that chronic mouth breathing has significant negative effects on health, including increased stress hormones, risk of sinus infections, high blood pressure, and reduced heart rate variability. Participants experienced persistent nocturnal suffocation, snoring, and sleep apnea, potentially leading to hypertension, metabolic and cognitive problems. Although some measurements remained unchanged, the overall impact was negative, with participants experiencing fatigue, irritation, anxiety, and other discomforts. The human body has evolved to breathe through both the nose and mouth for a reason, and chronic mouth breathing is not a normal or healthy behavior.

BREATHE THROUGH YOUR NOSE

Upon switching back to nasal breathing, participants experienced improved health, with normalized blood pressure, carbon dioxide levels, and heart rates. Snoring reduced dramatically and nasal infections cleared up. Nasal breathing also enhanced physical performance on a stationary bike. The positive outcomes of nasal breathing inspired further research into the effects of sleep tape on snoring and sleep apnea. The experience emphasized the importance of nasal breathing for overall well-being and debunked misconceptions about chronic allergies, congestion, and sleep issues being natural parts of life.

EXHALE

Carl Stough spent a half century reminding his students of how to get all the air out of our bodies so that we could take more in. He emphasized the importance of proper exhalation to improve various aspects of health and performance. By training individuals to exhale longer and more fully, he enabled emphysema patients to recover significantly, opera singers to improve their voices, asthmatics to prevent attacks, and Olympic sprinters to win gold medals. Practicing full exhalations and engaging more of the lung capacity can enhance breathing efficiency, leading to better overall performance and well-being.

CHEW

Ancient skeletons and pre-Industrial Age skulls exhibit large sinus cavities, strong jaws, and straight teeth, attributed to extensive chewing. Unlike other bones, facial bones can continue to grow and remodel throughout life, allowing for improvements in breathing ability at any age. To achieve this, incorporate rougher, raw, and heartier foods into your diet, similar to what our ancestors consumed, which require more chewing effort. Practicing proper mouth posture with lips together, teeth slightly touching, and tongue on the roof of the mouth is also important.

BREATHE MORE, ON OCCASION

While over breathing can be harmful, practicing controlled, heavy breathing for short, intense periods, such as in Tummo, Sudarshan Kriya, and vigorous pranayamas, can be therapeutic. These techniques intentionally stress the body to reset its normal functions and improve overall well-being. Conscious heavy breathing helps us gain control over our autonomic nervous systems and bodies, transforming us from passive passengers to active pilots of our own health.

HOLD YOUR BREATH

Dr. Donald Klein's research on chemoreceptor flexibility, carbon dioxide, and anxieties inspired further investigation into the connections between the amygdalae, breathing, and anxiety. The amygdalae, which govern perceptions of fear and emotions, also control aspects of breathing, and communication between chemoreceptors and the amygdalae is crucial. People with anxiety may suffer from connection issues between these areas, causing them to unintentionally hold their breath and ultimately panic. As a result, their bodies may adapt by over breathing to maintain low carbon dioxide levels. This suggests that anxiety might not be a psychological problem, but rather a natural reaction to an emergency in the body. Further research is needed to test this theory, which could explain why slow and steady breathing therapy is effective for panic, anxiety, and other fear-based conditions.

HOW WE BREATHE MATTERS

The perfect breath, according to the author, involves inhaling for 5.5 seconds and exhaling for 5.5 seconds, resulting in 5.5 breaths per minute and a total of about 5.5 liters of air. Practicing this perfect breathing promotes peak efficiency in the body. Many devices and apps are being developed to help people breathe at this optimal rate. However, the simplest approach requires no technology or equipment and can be practiced anywhere, anytime. This technique has been used by our ancestors for thousands of years, and the author uses it as a way to return to normalcy after periods of stress or inactivity.

 

An appendix to Nestor's book describes several different breathing techniques (such as alternative nostril breathing) and an extended bibliography available at James Nestor's website offers video and audio tutorial for numerous breathing techniques.

How sleep shapes what we remember and forget.

I have found monitoring the quality of my sleep to be a fascinating and useful activity. I use both the Oura ring and Apple watch to monitor body temperature, body movement, heart rate, and heart rate variability, and then compare their different (but broadly similar) algorithmic estimates of deep sleep, REM sleep, non-REM sleep, and wake periods. I'm on the lookout for articles on sleep during my scans of journals' tables of contents, and have come upon this review by Sakai of what is happening in our sleep to be concise and useful. Below is a more general overview from edited and rearranged clips (The article goes into more electrophysiological and cellular details):

 

(image credit Dave Cutler)

...memory at the beginning of the consolidation process is very much anchored in hippocampal networks, and in the end of this process, it primarily resides in neocortical networks...New memories are rich with contextual clues such as the time, place, and sensory details of an experience...as memories get encoded in the cortex, many of those spatial and temporal details fade...forgetting—through weakening or loss of synapses—seems to play a key role in the process of memory consolidation, especially during sleep... What remains are the elements representing the essential core of the memory. When learning how to drive, for example, the movements needed to steer and brake are critical; the details of avoiding a specific car on a particular outing are not...sleep’s role in memory is not simply about passive storage. Rather..a more active process of consolidation that extracts key information and forms a generalized version of the overall memory that can later be accessed and applied to relevant situations.

Sleep in mammals has distinct phases as characterized by specific EEG patterns. These include brain-wide slow oscillations (less than 1 Hz in frequency), sharp-wave ripples (100-300 Hz) in the hippocampus, and spindles (10-15 Hz), which are related to the firing of neurons in the circuits connecting the thalamus and the cortex. Upon onset of sleep, the brain enters a non-rapid eye movement (non-REM) phase. During non-REM sleep, slow oscillations sweep across large regions of the brain, punctuated by swells of spindles and bursts of sharp wave-ripples. A period of rapid eye movement (REM) sleep follows, with characteristic bursts of its namesake eye movements and low-amplitude theta oscillations around 4-8 Hz. The brain cycles through these phases throughout the sleep period, with slow-wave, non-REM sleep dominating the early hours and REM sleep the late hours.

There are...

...distinct roles of different stages of sleep in memory formation. Non-REM sleep has been shown to be very important for consolidation of declarative memories—those based on recall of information—while REM sleep seems to play a larger part in procedural or task-based memories...this may relate to the degree of synaptic change required. For declarative memories, most of the foundational learning has already taken place; remembering a new fact likely requires only small changes in synaptic strengths. By contrast, procedural memories require a massive amount of synaptic change...If you want to learn how to ride a bike, or how to play capoeira … it's not like learning a new name...I’s weeks, months, years of work. And so it seems like REM sleep is really, really necessary to do this long-term persistent synaptic change.”

Sleep preferentially consolidates negative aspects of human emotional memory

The Nov. 1, 2022 issue of PNAS has a special feature on Sleep, Brain, and Cognition. A large body of research suggests that sleep benefits memory, and I want to point in particular to an article by Denis et al. showing that sleep preferentially consolidates negative aspect of emotional memory. They also found that while research participants demonstrated better memory for positive objects compared to their neutral backgrounds, sleep did not modulate this effect.  

Significance

Recent research has called into question whether sleep improves memory, especially for emotional information. However, many of these studies used a relatively small number of participants and focused only on college student samples, limiting both the power of these findings and their generalizability to the wider population. Here, using the well-established emotional memory trade-off task, we investigated sleep’s impact on memory for emotional components of scenes in a large online sample of adults ranging in age from 18 to 59 y. Despite the limitations inherent in using online samples, this well-powered study provides strong evidence that sleep selectively consolidates negative emotional aspects of memory and that this effect generalizes to participants across young adulthood and middle age.

Abstract

Research suggests that sleep benefits memory. Moreover, it is often claimed that sleep selectively benefits memory for emotionally salient information over neutral information. However, not all scientists are convinced by this relationship [e.g., J. M. Siegel. Curr. Sleep Med. Rep., 7, 15–18 (2021)]. One criticism of the overall sleep and memory literature—like other literature—is that many studies are underpowered and lacking in generalizability [M. J. Cordi, B. Rasch. Curr. Opin. Neurobiol., 67, 1–7 (2021)], thus leaving the evidence mixed and confusing to interpret. Because large replication studies are sorely needed, we recruited over 250 participants spanning various age ranges and backgrounds in an effort to confirm sleep’s preferential emotional memory consolidation benefit using a well-established task. We found that sleep selectively benefits memory for negative emotional objects at the expense of their paired neutral backgrounds, confirming our prior work and clearly demonstrating a role for sleep in emotional memory formation. In a second experiment also using a large sample, we examined whether this effect generalized to positive emotional memory. We found that while participants demonstrated better memory for positive objects compared to their neutral backgrounds, sleep did not modulate this effect. This research provides strong support for a sleep-specific benefit on memory consolidation for specifically negative information and more broadly affirms the benefit of sleep for cognition.

Eye movements are related to the contents of consciousness in REM (rapid eye movment) sleep

Senzai and Scanziani have recorded head direction cells in the anterior dorsal nucleus of the thalamus in mice during wake and sleep. The direction and amplitude of eye movements encoded the direction and amplitude of the heading of mice in their virtual environment during REM sleep. It was possible to predict the actual heading in the real and virtual world of the mice during wake and REM sleep, respectively, using saccadic eye movements. Their abstract:

Since the discovery of rapid eye movement (REM) sleep, the nature of the eye movements that characterize this sleep phase has remained elusive. Do they reveal gaze shifts in the virtual environment of dreams or simply reflect random brainstem activity? We harnessed the head direction (HD) system of the mouse thalamus, a neuronal population whose activity reports, in awake mice, their actual HD as they explore their environment and, in sleeping mice, their virtual HD. We discovered that the direction and amplitude of rapid eye movements during REM sleep reveal the direction and amplitude of the ongoing changes in virtual HD. Thus, rapid eye movements disclose gaze shifts in the virtual world of REM sleep, thereby providing a window into the cognitive processes of the sleeping brain.

Widespread ripples synchronize human cortical activity during sleep, waking, and memory recall

I pass on the summaries of work by Dickey et al.:  

Significance

Different elements of a memory, or any mental event, are encoded in locations distributed across the cortex. A prominent hypothesis proposes that widespread networks are integrated with bursts of synchronized high-frequency oscillations called “ripples,” but evidence is limited. Here, using recordings inside the human brain, we show that ripples occur simultaneously in multiple lobes in both cortical hemispheres and the hippocampus, generally during sleep and waking, and especially during memory recall. Ripples phase-lock local cell firing and phase-synchronize with little decay between locations separated by up to 25 cm, enabling long-distance integration. Indeed, corippling sites have increased correlation of very-high-frequency activity which reflects cell firing. Thus, ripples may help bind information across the cortex in memory and other mental events.

Abstract

Declarative memory encoding, consolidation, and retrieval require the integration of elements encoded in widespread cortical locations. The mechanism whereby such “binding” of different components of mental events into unified representations occurs is unknown. The “binding-by-synchrony” theory proposes that distributed encoding areas are bound by synchronous oscillations enabling enhanced communication. However, evidence for such oscillations is sparse. Brief high-frequency oscillations (“ripples”) occur in the hippocampus and cortex and help organize memory recall and consolidation. Here, using intracranial recordings in humans, we report that these ∼70-ms-duration, 90-Hz ripples often couple (within ±500 ms), co-occur (≥ 25-ms overlap), and, crucially, phase-lock (have consistent phase lags) between widely distributed focal cortical locations during both sleep and waking, even between hemispheres. Cortical ripple co-occurrence is facilitated through activation across multiple sites, and phase locking increases with more cortical sites corippling. Ripples in all cortical areas co-occur with hippocampal ripples but do not phase-lock with them, further suggesting that cortico-cortical synchrony is mediated by cortico-cortical connections. Ripple phase lags vary across sleep nights, consistent with participation in different networks. During waking, we show that hippocampo-cortical and cortico-cortical coripples increase preceding successful delayed memory recall, when binding between the cue and response is essential. Ripples increase and phase-modulate unit firing, and coripples increase high-frequency correlations between areas, suggesting synchronized unit spiking facilitating information exchange. co-occurrence, phase synchrony, and high-frequency correlation are maintained with little decrement over very long distances (25 cm). Hippocampo-cortico-cortical coripples appear to possess the essential properties necessary to support binding by synchrony during memory retrieval and perhaps generally in cognition.

The Dance of Sleep

Sleep and wakefulness are characterized by unique intrinsic activity patterns and are usually thought to be two distinct global states, with the preoptic area of the hypothalamus being the regulator of brain state changes. Yamagata et al. find that this area also affects within-state changes of sleep and wake intensity.  

Significance

Our current understanding of how sleep is regulated is based upon the model of sleep homeostasis, which defines a variable called Process S as a measure of sleep need, and a so-called “flip-flop” model of state switching, which builds on a notion of a mutually antagonistic relationship between subcortical sleep-promoting and wake-promoting circuits. The neurobiological substrates of the interaction between the sleep switch and Process S are unknown. Our study identifies a previously unrecognized role of hypothalamic circuitry in tuning within-state brain activity or levels of arousal, which in turn determine the homeostatic drive for sleep.

Abstract

Sleep and wakefulness are not simple, homogenous all-or-none states but represent a spectrum of substates, distinguished by behavior, levels of arousal, and brain activity at the local and global levels. Until now, the role of the hypothalamic circuitry in sleep–wake control was studied primarily with respect to its contribution to rapid state transitions. In contrast, whether the hypothalamus modulates within-state dynamics (state “quality”) and the functional significance thereof remains unexplored. Here, we show that photoactivation of inhibitory neurons in the lateral preoptic area (LPO) of the hypothalamus of adult male and female laboratory mice does not merely trigger awakening from sleep, but the resulting awake state is also characterized by an activated electroencephalogram (EEG) pattern, suggesting increased levels of arousal. This was associated with a faster build-up of sleep pressure, as reflected in higher EEG slow-wave activity (SWA) during subsequent sleep. In contrast, photoinhibition of inhibitory LPO neurons did not result in changes in vigilance states but was associated with persistently increased EEG SWA during spontaneous sleep. These findings suggest a role of the LPO in regulating arousal levels, which we propose as a key variable shaping the daily architecture of sleep–wake states.

Losing sleep with age.

Jacobson and Hoyer summarize experiments of Li et al.:

Humans spend approximately one-third of their lives asleep, but this is not distributed equally across their life span. Sleep quantity and quality decline as age advances, and insomnia and sleep fractionation are common in older people. Sleep is essential for vitality and health. At any age, chronic sleep deprivation causes a range of issues, including disrupted cognition and memory. Correspondingly, sleep complaints in older people are associated with increased risks of impaired physical and mental health and with mortality. Beyond evidence of degenerating subcortical nuclei in age-associated sleep disturbances, the underlying mechanisms remain unclear despite decades of awareness of the problem and its consequences...Li et al.report the hyperexcitability of hypocretin neurons as a core mechanism underlying sleep disruption in aged mice, explaining why sleep is punctuated by intruding wakefulness despite the loss of wake-promoting neurons.

A few clips from the Li et al. article: 

RATIONALE

We hypothesized that the decline in sleep quality could be due to malfunction of the neural circuits associated with sleep/wake control. It has been established that hypocretin/orexin (Hcrt/OX) neuronal activity is tightly associated with wakefulness and initiates and maintains the wake state. In this study, we investigated whether the intrinsic excitability of Hcrt neurons is altered, leading to a destabilized control of sleep/wake states during aging.

RESULTS

Aged mice exhibited sleep fragmentation and a significant loss of Hcrt neurons. Hcrt neurons manifested a more frequent firing pattern, driving wake bouts and disrupting sleep continuity in aged mice. Aged Hcrt neurons were capable of eliciting more prolonged wake bouts upon optogenetic stimulations. These results suggested that hyperexcitability of Hcrt neurons emerges with age. Patch clamp recording in genetically identified Hcrt neurons revealed distinct intrinsic properties between the young and aged groups. Aged Hcrt neurons were hyperexcitable with depolarized membrane potentials (RMPs) and a smaller difference between RMP and the firing threshold.

CONCLUSION

Aged mice exhibited sleep fragmentation and a significant loss of Hcrt neurons. Hcrt neurons manifested a more frequent firing pattern, driving wake bouts and disrupting sleep continuity in aged mice. Aged Hcrt neurons were capable of eliciting more prolonged wake bouts upon optogenetic stimulations. These results suggested that hyperexcitability of Hcrt neurons emerges with age. Patch clamp recording in genetically identified Hcrt neurons revealed distinct intrinsic properties between the young and aged groups. Aged Hcrt neurons were hyperexcitable with depolarized membrane potentials (RMPs) and a smaller difference between RMP and the firing threshold.

Addicted to dreaming.

Dopamine (DA) is usually associated with pleasure and addiction. Now Hasegawa et al. show that release of DA in the basolateral amygdala (BLA), a brain structure associated with emotional processing, can trigger rapid eye movement (REM) dreaming sleep in mice.

The sleep cycle is characterized by alternating non–rapid eye movement (NREM) and rapid eye movement (REM) sleeps. The mechanisms by which this cycle is generated are incompletely understood. We found that a transient increase of dopamine (DA) in the basolateral amygdala (BLA) during NREM sleep terminates NREM sleep and initiates REM sleep. DA acts on dopamine receptor D2 (Drd2)–expressing neurons in the BLA to induce the NREM-to-REM transition. This mechanism also plays a role in cataplectic attacks—a pathological intrusion of REM sleep into wakefulness—in narcoleptics. These results show a critical role of DA signaling in the BLA in initiating REM sleep and provide a neuronal basis for sleep cycle generation.

Reconsolidation of a reactivated memory can be altered by stress hormone levels.

Stern's summary in Science Magazine of work by Antypa et al.:

Reactivation of a memory can make it malleable to subsequent change during reconsolidation. Targeted pharmacological and behavioral manipulations after memory reactivation can modulate reconsolidation and modify the memory. Antypa et al. investigated whether changes in stress hormone levels during sleep affected later memory of a reactivated episode. The authors recited a story accompanied by a slide show to a group of male and female subjects. If subjects were given treatment to block cortisol synthesis during early morning sleep, then their 3-day-old memory of the story was more precisely recalled than if the early morning cortisol spike was uncontrolled. However, this improvement only occurred if the subjects had been given a visual cue for the story just before anti-cortisol treatment.

Real-time talking with dreamers during REM sleep

A fascinating new window for reserach on dreaming has been opened by four collaborating but independent laboratory groups. The summary of the open source article from Konkoly et al.:

Dreams take us to a different reality, a hallucinatory world that feels as real as any waking experience. These often-bizarre episodes are emblematic of human sleep but have yet to be adequately explained. Retrospective dream reports are subject to distortion and forgetting, presenting a fundamental challenge for neuroscientific studies of dreaming. Here we show that individuals who are asleep and in the midst of a lucid dream (aware of the fact that they are currently dreaming) can perceive questions from an experimenter and provide answers using electrophysiological signals. We implemented our procedures for two-way communication during polysomnographically verified rapid-eye-movement (REM) sleep in 36 individuals. Some had minimal prior experience with lucid dreaming, others were frequent lucid dreamers, and one was a patient with narcolepsy who had frequent lucid dreams. During REM sleep, these individuals exhibited various capabilities, including performing veridical perceptual analysis of novel information, maintaining information in working memory, computing simple answers, and expressing volitional replies. Their responses included distinctive eye movements and selective facial muscle contractions, constituting correctly answered questions on 29 occasions across 6 of the individuals tested. These repeated observations of interactive dreaming, documented by four independent laboratory groups, demonstrate that phenomenological and cognitive characteristics of dreaming can be interrogated in real time. This relatively unexplored communication channel can enable a variety of practical applications and a new strategy for the empirical exploration of dreams.

Moonstruck sleep: Synchronization of human sleep with the moon cycle

From Casiraghi et al.:

Before the availability of artificial light, moonlight was the only source of light sufficient to stimulate nighttime activity; still, evidence for the modulation of sleep timing by lunar phases is controversial. Here, we use wrist actimetry to show a clear synchronization of nocturnal sleep timing with the lunar cycle in participants living in environments that range from a rural setting with and without access to electricity in indigenous Toba/Qom communities in Argentina to a highly urbanized postindustrial setting in the United States. Our results show that sleep starts later and is shorter on the nights before the full moon when moonlight is available during the hours following dusk. Our data suggest that moonlight likely stimulated nocturnal activity and inhibited sleep in preindustrial communities and that access to artificial light may emulate the ancestral effect of early-night moonlight.

A brief afternoon nap is probably good for your brain.

On some days I feel midafternoon drowsyness that makes it difficult for me to think or write. I lie down and do "a 10 minute naplet." After zonking out, I then suddenly awaken to find my watch reading exactly 10 min later. Over the next 30 seconds or so I completely awaken and feel mentally fresh, like a brain scrub has happened. There is debate, however, on whether brief day time napping is beneficial or detrimental to our health, especially as we age. Rich Harrity now points to a study of 2014 elderly Chinese suggesting that an afternoon nap of more than 5 min and less than 2 hours duration correlates with better overall cognitive function including orientation, language, and memory. Other studies have shown that more than 2 hours of napping during the day is detrimental to cognitive function. One speculation is that brief sleep during the day might lower the level of brain inflammatory markers know to compromise cognitive function.

Why do our brains dream?

I want to point to a review by Nick Romeo of Zadra and Stickgold's new book "When Brains Dream". The review summarizes important theories about dreams and gives the authors' own model:

...Though they tour a broad range of contemporary research and theorizing, they ultimately propose that a primary function of dreaming is to detect and dramatize the possible meanings of information latent in memories and associations that we rarely access while awake...Their own theory proposes that dreaming extracts new information from memories by discovering and strengthening previously unexplored associations (they brand their model with the acronym NEXTUP: network exploration to understand possibilities). For this capacity to be a target of natural selection, however, the new information that dreaming discovers must provide at least some periodic survival benefit. They could be clearer in asserting this directly. They could also distinguish more precisely at points between the benefits of sleeping and the benefits of dreaming per se.

Effects of lockdown on human sleep and chronotype during the COVID-19 pandemic

An open source article in Current Biology from Leone et al., the summary:

The COVID-19 pandemic resulted in many countries imposing a lockdown, which in turn reduces sunlight exposure and alters daily social schedules. Since these are the main entrainment factors for biological rhythms, we hypothesized that the lockdown may have affected sleep and circadian rhythms. We indeed show that participants slept longer and later during lockdown weekdays, and exhibited lower levels of social jetlag. While this may seem to be an overall improvement of sleep conditions, chronotype was also delayed under the lockdown. This signature of a weaker light–dark cycle should be monitored attentively since it may progressively cause disruptive effects on sleep and circadian rhythms, affecting human performance and health.

The perils of nighttime dining

Kelly et al. show that lipids in late evening snacks are less likely to be oxidized and most likely to be stored as fats than lipids in morning meals. Circadian control of metabolism appears to control whether ingested food is oxidized or stored.:

Circadian (daily) regulation of metabolic pathways implies that food may be metabolized differentially over the daily cycle. To test that hypothesis, we monitored the metabolism of older subjects in a whole-room respiratory chamber over two separate 56-h sessions in a random crossover design. In one session, one of the 3 daily meals was presented as breakfast, whereas in the other session, a nutritionally equivalent meal was presented as a late-evening snack. The duration of the overnight fast was the same for both sessions. Whereas the two sessions did not differ in overall energy expenditure, the respiratory exchange ratio (RER) was different during sleep between the two sessions. Unexpectedly, this difference in RER due to daily meal timing was not due to daily differences in physical activity, sleep disruption, or core body temperature (CBT). Rather, we found that the daily timing of nutrient availability coupled with daily/circadian control of metabolism drives a switch in substrate preference such that the late-evening Snack Session resulted in significantly lower lipid oxidation (LO) compared to the Breakfast Session. Therefore, the timing of meals during the day/night cycle affects how ingested food is oxidized or stored in humans, with important implications for optimal eating habits.

Evidence for premature aging caused by insufficient sleep.

I have come to realize in the past year or so that my physical and mental robustness require getting at least seven, and preferably eight, hours of sleep every night. Thus I was intrigued by finding an extensive and well documented study by Teo et al. (open source) showing that telomeres, sequences of DNA on the end of chromosomes taken as a marker of biological aging, are, on average, 356 base pairs shorter in study participants who slept for fewer than five hours per night than in those who slept for seven hours. They found that sleep metrics were reported more accurately by wearable fitness trackers than by self report. Here is the abstract of their article, titled "Digital phenotyping by consumer wearables identifies sleep-associated markers of cardiovascular disease risk and biological aging."

Sleep is associated with various health outcomes. Despite their growing adoption, the potential for consumer wearables to contribute sleep metrics to sleep-related biomedical research remains largely uncharacterized. Here we analyzed sleep tracking data, along with questionnaire responses and multi-modal phenotypic data generated from 482 normal volunteers. First, we compared wearable-derived and self-reported sleep metrics, particularly total sleep time (TST) and sleep efficiency (SE). We then identified demographic, socioeconomic and lifestyle factors associated with wearable-derived TST; they included age, gender, occupation and alcohol consumption. Multi-modal phenotypic data analysis showed that wearable-derived TST and SE were associated with cardiovascular disease risk markers such as body mass index and waist circumference, whereas self-reported measures were not. Using wearable-derived TST, we showed that insufficient sleep was associated with premature telomere attrition. Our study highlights the potential for sleep metrics from consumer wearables to provide novel insights into data generated from population cohort studies.

New work on how and why we sleep.

The fact that I'm finding the quality of my sleep to be central to my robustness and well-being makes me want to pass on descriptions of four pieces of work described in recent issues of Science Magazine, work showing housekeeping changes in our brains happening while we sleep, changes whose disruption by sleep deprivation has debilitating consequences. Fultz et al. show that deep sleep drives brain fluid oscillations that may facilitate communication between fluid compartments and clearance of waste products. Todorova and Zugaro show that spikes during delta waves of sleep (widespread cortical silence) support memory consolidation. Brüning et al. find in the mouse brain that half of the 2000 synaptic phosphoproteins quantified show changes with daily activity-rest cycles. Sleep deprivation abolishes nearly all (98%) of these phosphorylation cycles at synapses. Noya et al. find a sleep-wake cycle in which transcripts and proteins associated with synaptic signaling accumulate before the active phase (dusk for nocturnal mice), whereas messenger RNAs and proteins associated with metabolism and translation accumulate before the resting phase.