PolyPhasic Sleep-Part Deux
If you missed part one, here ya go.
SLEEP 101 (probably more like 102)
“If sleep does not serve an absolutely vital function, then it is the biggest mistake the evolutionary process has ever made”
University of Chicago Sleep Laboratory
Smithsonian, November 1978
Why do we sleep? The answer to this question still remains a mystery, yet scientific advances have revealed many functions taking place at night to restore the brain and body for the next day. All of us recognize the need for sleep grows stronger the longer we stay awake. We also intuitively grasp its importance because even one night of either good or bad sleep affects our performance, mood, and wellbeing the next day. But what is taking place after you close your eyes that determines the version of You that is shared with the world the following day? This article will explore some of these mysteries and will hopefully deepen your understanding for this indispensible function of a healthy life.
Once asleep, we cycle through a sequence of stages that repeat several times over the night. The pattern of this cyclical sequence is referred to as ‘sleep architecture.’ The primary stages are named rapid eye movement (REM) sleep and non-REM sleep, which is then further subdivided into stage 1 non-REM, stage 2 non-REM and Slow Wave Sleep. From all the stages, the deepest is Slow Wave Sleep and it is in this stage that it is hardest to arouse a person. If you wake from Slow Wave Sleep, you will likely feel disoriented and confused. Not unlike those who attend Phish concerts.
As the night progresses the proportion of these stages change in each cycle. At the beginning of the night you have more non-REM sleep, and at the end of the night you have more REM sleep, per cycle. The sequence of these stages appears to have importance. A highly fragmented sleep sequence – as seen in those suffering from sleep apnea, which produces disruptive micro-arousals during sleep – has been associated with many maladies including inadequate restoration (i.e., next day sleepiness) and weight gain! This holds true even when the total amount of time in each sleep stage is not significantly different from a normal night of non-fragmented sleep. Sequence matters.
Many things differ between these stages including brain cell activity, hormone release, heart rate, blood pressure, breathing rate, etc. Interestingly, we’ve recently learned that brain activity is regionally specific and dependent on usage prior to the sleep period. Did you use your dorsal-lateral prefrontal cortex much today? If you did, the activity pattern in that specific part of the brain would be indicative of prior usage during sleep recordings. This type of local activity speaks to the dynamic interrelationship between these two states of consciousness, and also whispers hints suggesting how the deprivation of sleep is not likely a wise strategy for optimal performance.
How is your natural sleep wake cycle determined?
In the early 20th century, a Professor of Psychiatry and Neurology from Vienna named Constantin von Economo began to see patients with a mysterious brain virus that would make them either sleep 20 hours a day, or have severe insomnia. Further exploration by von Economo found these patients had brain lesions in locations he then determined important in the control of human sleep and wake states. More than a half a century later, scientists would discover the remarkable accuracy of von Economo’s interpretations.
Only in the last 20 years have we begun to unravel the circuits and signals in the brain that regulate sleep and wake states. We now understand that the wakefulness you’re experiencing at the current moment is dependent on a network of cell groups that coordinate to provide the signals to wake you up. Cells within the wake network produces a variety of neurotrasmitters to communicate their wake signal to the rest of the brain, including dopamine, acetylcholine, histamine, serotonin, and norepinephrine (or noradrenalin). These signals activate the thalamus and cortex to produce consciousness.
We’re also now aware of a specialized group of cells that facilitate sleep. Yep, these cells become more active during sleep and are located in an area of the brain called the VLPO (ventral lateral preoptic area) which is located in the anterior hypothalamus. Once activated, the VLPO shuts off the wake network actively suppressing wakefulness. It should therefore be no surprise that animals with lesions in this area have real bad insomnia.
So, during the night the sleep center suppresses the wake network, and reciprocally, during the day, the wake network suppresses the sleep center. In addition, it is important to mention a collection of cells in the posterior hypothalamus called hypocretin neurons. These neurons stabilize both states so that wake can be maintained throughout the day and so sleep can be maintained over the night. Notably, the absence of a functioning hypocretin system produces the neurological condition of narcolepsy, which in case you live under a rock or simply haven’t seen the movie My Own Private Idaho, is a condition most recognized for the pathological sleepiness it induces. Patients with narcolepsy don’t need more or less sleep than you or I. Rather, their sleep and wake schedule is highly fragmented. Because they don’t have functioning hypocretin neurons to stabilize the sleep-wake system, a narcoleptic can only maintain wakefulness for a few hours before falling asleep, and then once asleep, they can’t sleep very long. The end result is that these patients will transition between sleep and wake states many times over a 24 hour period instead of having one solid block of wakefulness and one solid block of sleep like you or I have the luxury to experience regularly.
Transitioning between sleep and wake: Why and when?
In 1982, sleep researcher Alexander Borbely (pronounces ‘Borbay’), currently a Professor of Pharmacology at the University of Zurich in Switzerland, published a paper in a small journal in which he proposed a model referred to as the “two-process model for sleep and wake.” Since that time, Borbely’s model has influenced entire sub-fields of research and has become a bedrock of human understanding of sleep, in general. In fact, this seminal article has been cited over 1000 times and is still widely cited today, 30 years after it was first published. What does this model propose, and why is it so important?
In the two-process model,1 alertness (i.e., how sleepy you feel or how awake you feel) is affected primarily by two, mutually exclusive processes: 1) sleep pressure, which builds up during wakefulness and dissipates during sleep and 2) by a wake-promoting circadian rhythm that oscillates in intensity over a 24 period, and in rhythm with the light and dark cycle of our environment.2 Across the day and night, at any moment in time, your sleepiness / wakefulness will be primarily determined by the combined effects of these two processes working somewhat independently of each other.
When conducting research, Borbely noticed sleep would be altered depending on how long the subject was previously awake. In fact, extending wakefulness changed sleep architecture in a dose-dependent fashion; more time awake, more sleep pressure builds, more changes to sleep occur. This led Borberly to hypothesize the existence of a substance that accumulates with wakefulness and subsides during sleep. As the brain continues to work at a high rate during wakefulness, the energy metabolite adenosine is released in the space outside the cell. While questions still remain, there is evidence that the accumulation of extracellular adenosine could be the molecule behind sleep pressure. Here are three pieces of evidence to support this: First, if you inject adenosine into the basal forebrain, sleep ensues rapidly. Second, Starbucks has achieved ubiquity born from the needs of a sleep deprived society. Caffeine blocks adenosine from binding to its receptor, thereby temporarily masking sleepiness. Third, adenosine stimulates Slow Wave Sleep. As Slow Wave Sleep occurs, adenosine rapidly reduces in concentration in a proportional manner.
Importantly, sleep pressure is relieved in a decreasing exponential fashion. In less nerd-like terms, per hour, you dissipate more sleep pressure in the beginning of the night than you do in the later half of the night. The additional sleep pressure that builds (after say, your sound decision to stay up late to watch reruns of Battlestar Galactica) then facilitates longer sleep times. Here’s an example: Let’s say you typically need around 8 hours of sleep per night to feel fully rested but this last week you averaged only 6 hours per night. Then, on the weekend, you were able to sleep 10 hours both on Saturday and Sunday. The elongated sleep was facilitated by the increased sleep pressure that had accumulated during the week – accruing day after day of insufficient nightly sleep. As you can see in this example, despite the fact that sleep pressure wears off faster in the beginning of the night, there was enough “pressure” remaining in the morning to elongate both nights of weekend rest. As mentioned earlier, just how long one can continue to accumulate sleep pressure, and just how long it takes to fully relieve prolonged, accumulated sleep are matters of ongoing investigation.
24 hour Wake Rhythm
The other component of Borbely’s 2-process sleep model is the rhythmic, 24 hour repeating process we’ll refer to as “wake drive.” This drive for wakefulness is independent of sleep pressure and dependent on the light and dark cycle of the environment. So, how does this process work? Environmental light enters the eye and stimulates specialized, light sensitive cells that produce a pigment called ‘melanopsin.’ These cells carry the light signal to a not-yet-mentioned area of the hypothalamus called the suprachiasmatic nucleus (SCN). (Side note: Are you seeing the dominance of the hypothalamus as a critical anatomical site for our sleep wake cycle yet?).
The SCN serves as the brain’s ‘central clock.’ On a daily basis, the “rhythm” of the SCN is reset by light in both direct and indirect ways. First, by light’s direct stimulation of the SCN through the process just described. Second, in a natural environment, when light dims at sundown, the pineal gland begins to release the hormone melatonin (aka: dim-light melatonin onset). Both light and melatonin affect the transcriptional-translational mechanisms that control output signals originating from the SCN. Thus, you can see here how the light / dark signal helps keep the 24 hour rhythm of the body in coordination with the 24 pattern of one complete day. Seasonal adaptions are also likely mediated through similar mechanisms but are beyond the scope of this article.
We now see how the brain synchronizes with the 24 hour cycle of the environment. From here, our central clock synchronizes with internal clocks in tissue throughout the body. It is in this way that our body forms a melody of hormones and behaviors. The timing of these rhythms form functional phase relationships between hormones, cellular activity, gene expression, and behavioral state. For example, as we enter sleep at night, our body temperature drops, melatonin levels are high, and cortisol levels are low. Perhaps the ultimate function of our tissues is dependent upon the entirety of these elements working together? What other process do you think are dependent on the synchronicity of these hormonal-gene-behavioral phase relationships? Everything.
When we sleep, if our body is attuned to our environmental signals, the phasic patterns of temperature, hormones, and other physiological processes come into a sort of balance. If, for example, you go to sleep many hours later than normal for you, you will be sleeping in a different hormonal pool than you would be if you went to bed at a normal time. This is one reason we can’t assume we can grab a few power naps over the day and have the same beneficial effects of nighttime sleep. A nap may relieve some sleep pressure but you may not experience other beneficial functions provided by circadian-aligned sleep episodes. Certainly, we have the ability withstand occasional perturbations of an off-balance night. I also think we have the capacity to withstand the adoption of a polyphasic schedule on a temporary basis. The most available example is new parents. With the birth of a child, all of a sudden a monophasic sleep is no longer an option. In this case, napping when possible seems to be a great temporary option for both the mother and father to achieve (or get closer to) total sleep need. However, chronic misalignment of the multitude of rhythms throughout our body is likely to have consequences. Indeed, shift workers who exist years at a time with an ever-changing schedule, suffer increased risk for many mortal conditions, like cardiovascular disease and cancer. We are, truly, one with nature and I believe it is useful for all of us to personally acknowledge that fact. This information helps us make that connection more tangible.
Wait, why specifically are we referring to this as the wake rhythm?
Good question. One of the many processes that are influenced by the SCN is the activation of our neural wake network. When it’s time to be awake, the SCN will indirectly activate the state-stability hypocretin neurons, which then signal the entire wake network to activate the cortex to produce consciousness. When it’s time for sleep, through some sort of “metabolic voodoo” (read: we ain’t quite sure how this happens), sleep pressure activates of the VLPO, which sends signals to directly inhibit the wake networks and the flip is switched from wakefulness to sleep. As discussed previously, once asleep, as the night progresses, the brain and body go through different stages associated with different restorative functions. Amongst those functions, is a reduction in sleep pressure and – if you’ve been getting good, consistent sleep – you’ll begin the next day with very low sleep pressure, feeling alert and vigilant. Indeed, healthy sleep results in a large variety of cognitive benefits: you are mentally fast and accurate; you have stable mood and stable attention, which allows you to focus on the task at hand; you have good working memory (holding new information in your mind, like digits of a telephone number) and good memory recall, where you’re able to retrieve learned memories stored in neural networks; your decision making is fully functional as executive functions counteract impulsive signals from the limbic system (e.g., yum, I’m going to eat a whole gallon of ice cream! Wait, maybe I shouldn’t. Impulse meets executive control); creativity is heightened; and your economic preferences for risk and reward are optimized. For the last point, when you are sleep deprived you tend to devalue losses and overvalue potential gains. Let’s consider this in the context of gambling. At 4 am at the craps table, you’re more likely to focus on the possibility of winning large sums of money and less likely to consider the consequences of losing your hard earned savings; Casinos make a lot of money during the hours of 3 and 6 am.
Conversely, inadequate sleep causes impairments in all the systems mentioned. However, here is one major problem: We don’t always recognize our own impairment. That’s right, despite significant objective impairments in cognitive performance, a sleep deprived person will tend to underestimate their impairment and overestimate their readiness to perform tasks. Therefore, we should be highly weary of self-reports that claim great performance despite little sleep. Who knows how well this person would have performed with normal sleep. Maybe they would have completed the job twice as fast.
Final judgement and recommendations
Here are my recommendations. Instead of trying to get more for less, try to get the optimal amount of sleep so that you allow yourself the best physical and cognitive performance during the time you are awake. Truly, 16 hours of full cognitive function is preferable to 20 hours of suboptimal performance. Having said that, I think that polyphasic sleep schedules can help those who are having difficulty achieving a full nights rest, and this includes new parents and (other) extreme situations. To these people, I recommend napping when the opportunity presents itself. Prioritize sleep so that you can be the most present, optimistic, and functional parent for your child. Other scenarios likely benefit from different napping schedules, but these benefits come not from reducing sleep need, but from recovering or preventing lost sleep, particularly if you need to adopt this polyphasic sleep schedule for more than a few days. Can a polyphasic sleep schedule reduce total sleep need (or, maintain wake performance) over a few day period? I think it’s possible, but I wouldn’t adopt this approach as a long term strategy for either performance or health. Know the facts and make the right decision for you.
To conclude, I thought I would offer a few alternative chapter titles for Ferris’ book for those who do want to attempt to use polyphasic sleep to sleep less (not more).
|Current Chapter Title||Alternative Chapter Title for Sleep Restrictors|
|Subtracting fat||Adding fat, heart disease, and cancer.|
|Adding muscle||Getting comfortable with sand kicked in your face.|
|Improving sex||Not tonight dear. I’m…..(pause….snore).|
|Perfecting sleep||How to be a version of yourself you don’t like, day after day.|
|Reversing injuries||Crutches: Get some!|
|Running faster and farther||Sitting and dozing.|
|On longer and better life||Just jump stupid. Life sucks anyway.|
Lastly, I’m glad biohackers exist to evaluate new concepts for an improved life. My default, however, is not to try to beat my nature, but to understand it, respect it, and make life decision that prioritize it so I can thrive with health, good performance, and longevity.
Dan Pardi is the CEO of Dan’s Plan, a ‘Quantified-Paleo’ company helping you pursue optimal health in our modern world. We help fix the core problem for poor health – a broken lifestyle. Dan’s Plan focuses on food, movement, and sleep, and provides tools to track personal health data and create feedback loops that “nudge” healthy behaviors. @dansplanonline1.
1. Borbély A. A two process model of sleep regulation. Human neurobiology 1982 1 195.
2. Van Dongen H & Dinges D. Sleep, circadian rhythms, and psychomotor vigilance. Clin Sports Med 2005 24 237-249.