How To Induce Sleep Paralysis - The Definitive Guide
Everyone has heard stories about how terrifying and bizarre sleep paralysis can be. There’s quite a bit folk lore about possession by demons causing sleep paralysis.
It’s an experience that mixes aspects of the alert, conscious mind with a surreal, dream-like state. During an episode of sleep paralysis, you’re fully conscious but unable to move, and are in limbo between sleep and wake.
Here’s a personal anecdote. In every sleep paralysis episode I’ve had, I’m desperately trying to jerk myself awake (despite knowing full well that I’m temporarily paralyzed), and I’m also screaming my SO’s name for help, but unable to utter a peep.
What makes sleep paralysis so strange is that you can intellectually appreciate that you’re having a sleep paralysis episode and out of harm’s way, yet somehow this knowledge doesn’t translate. It’s like watching The Shinning, you’re afraid and the fear is both real and unreal simultaneously.
- How To Induce Sleep Paralysis
- Method #1
- Method #2: Drugs
- What The Hell Is Going On During An Episode of Sleep Paralysis
- Why would someone enter REM sleep prematurely?
- No REM Sleep? That Sounds Dangerous
How To Induce Sleep Paralysis
- Lay down in bed prior to your normal bedtime. If you’re exhausted you will fall asleep too quickly for SP to occur.
- Make sure to lay down on your back and not your side. Relax your entire body and make sure no muscles are tensed.
- Close your eyes and breath deeply and slowly.
- Stay relaxed, but don’t move.
- Your nervous system “checks” every couple of minutes whether you’re awake by giving you the impulse to move. If you resist the urge to move for long enough, you’ll “trick” your nervous system that you’re asleep.
- Completely relax your body without falling asleep.
- If you give into the temptation to move, start the process from the beginning.
- After an interval of time, you’ll begin to feel detached from your body and you’ll have a sleep paralysis episode, where you’re conscious but in an altered mental state and your limbs are paralyzed.
Method #2: Drugs
- Drugs that increase acetylcholine or activate cholinergic receptors
- Galantamine, acetylcholinesterases like Donepzil, nutraceuticals like CDP-Choline or Alpha GPC, nootropics like coluracetam
- Withdrawal from drugs that increase serotonin
- SSRIs, tricyclics antidepressants, MAOIs, etc. Drugs that decrease serotonin
- Tianeptine sodium (hypothetical; may not be clinically meaningful)
What The Hell Is Going On During An Episode of Sleep Paralysis
Put simply, sleep paralysis occurs when the brain enters rapid eye movement (REM) sleep before the “switch” to unconsciousness has occurred.
Under normal circumstances, sleep is coordinated such that your brain enters REM sleep AFTER you’ve become unconscious. When REM begins, you’re body is paralyzed to prevent you from acting at your dreams or interacting with the world during sleep. Hence, sleep paralysis has both features of REM sleep (which causes the paralysis) and wakefulness that coincide temporally.
Brief aside: REM sleep is juxtaposed against non-REM (NREM) sleep, which is considered “deep” sleep and is considered more restorative and indispensable.
Why would someone enter REM sleep prematurely?
The answer lurks somewhere within the concept of “neurotransmitter homeostasis.” REM sleep is regulated directly or indirectly by acetylcholine, serotonin and norepinephrine.
Acetylcholine plays a role in promoting REM sleep. Specifically, it has been noted that drugs that activate acetylcholine receptors in the brain facilitate REM sleep, whereas receptor blockers (antagonists) have the opposite effect. Here’s a cogent summary of the situation:
There is a great deal of evidence that acetylcholine is associated with REM sleep. For example, release of ACh in the cortex is highest during waking and REM sleep, and lowest during delta sleep. Further, drugs that act as ACh agonists increase REM, and antagonists decrease REM. In terms of brain structure, it appears that REM sleep initiation begins in the ACh neurons located in the pons, in one particular area called the Peribrachial Area. In one sense, the ACh neurons in this area of the brain are “REM headquarters”.
Excess serotonin, by contrast, appears to markedly suppress REM sleep.
For example, most classes of antidepressants globally increase serotonin in the brain. E.g., SSRIs like Zoloft increase serotonin by inhibiting the reuptake (removal) of serotonin. Tricyclic antidepressants also inhibit serotonin reuptake, albeit less strongly and less specifically. Monoamine oxidase inhibitors (MAOIs) globally elevate serotonin (and other monoamines) by inhibiting the metabolism of serotonin.
All of these classes of antidepressants markedly suppress or even abolish REM sleep in humans. For example, a patient taking Parnate (a potent and irreversible MAOI) may have little to no REM sleep during the night.
No REM Sleep? That Sounds Dangerous
That’s what all the neuroscientists and MD-PhD’s thought too! It turns out that REM sleep is relatively dispensable, compared to NREM or deep sleep). A prolonged lack of REM sleep does not cause any obvious deficits or impairments. By contrast, one night of skipped deep sleep reliably impairs cognition in healthy subjects.
How Is This Relevant To Inducing Sleep Paralysis?
As it turns out, while REM sleep was suppressed for patients taking conventional antidepressants, as soon as patients discontinued antidepressants they experienced a REM rebound. In the absence of the REM-suppressing antidepressant, the pendulum swings the other way and the subject spends copious amounts of time in REM sleep.
This “REM rebound”, where REM sleep has been suppressed and then suddenly the breaks are removed, is when sleep paralysis is most likely to occur.