Rapamycin and improved sleep quality

Before starting rapamycin, I had disrupted sleep patterns. Sometimes I would wake up 4 times a night. After rapamycin, I now wake up almost only once a night. Has anyone experienced this? What is the reason?


Probably more efficient mitochondria


That is interesting. When do you take rapamycin? dose and frequency?

2mg/week since a month

1 Like

Do you take it in the morning or in the evening?

I have much, much better (much deeper, more restful) sleeps after starting rapamycin. The sort of wonderful deep sleeps I used to have when I was in my teens. I have no idea on the reason for this, I’ve not come across any research that touches upon this. And this is when I take my rapamycin in the morning. If I take rapamycin in the late afternoon or early evening I’ve found (the one time I did this) that I couldn’t go to sleep until 4 or 5 in the morning…


l take in the afternoon

I definitely agree with you. Like a sleep in your early 20s age

1 Like

Unfortunately I do not have that same effect (yet?:crossed_fingers:). I take 4mg once a week for the moment.

Thank you for sharing. Timing as well as dosing is important. I have tried 6 mg right before going to bed. But with no improved sleep.


Rapa has always made me feel tired. I now take it before bed for a good night of sleep.


I have mentioned this before on the forum somewhere, but sleep is regulated by a circadian process(which is responsible for the timing of your sleep, along with typically regulating when you experience NREM and REM throughout the night), and homeostatic process(which is regulates your need for sleep, it is termed as sleep pressure or sleep drive, it also is what is driving someone to have deeper sleep/better sleep quality).
We have the circadian biology mostly mapped out in scientific literature, yet in the field of sleep, we have no idea what regulates our homeostatic process. We still have little idea about the substrates/genes/mechanisms regulating our homeostatic process.

Sleep occurs in organisms ranging from fruit flies to humans and is found in all mammals studied to date(even seems to occur in c.elegans, and organisms that lack a cephalized nervous system like the upside down jellyfish). In these organisms sleep deprivation leads to increased durations of sleep and, if prolonged, severe deficits in performance . The predominant form of sleep, non-rapid eye movement sleep (NREM), is defined by dramatic changes in neuronal activity within the cerebral cortex. Cortical neurons synchronize into an alternating pattern of rapid firing and silence. This pattern of firing during NREM sleep appears to fulfill the brain’s “need” for sleep; it alleviates the negative effects of sleep loss on the brain and is regulated by a homeostatic process. Multiple roles are proposed for NREM sleep in the brain; however, none explain the wide array of negative effects caused by lost sleep . It is unclear why synchronous firing among cortical neurons during sleep is required for the cortex to efficiently function. Again, the homeostatic mechanism regulating NREM-sleep remains to be identified. Also, who is to say that sleep is mainly regulated in the brain, as much evidence indicates that the whole brainI(local sleep or unihemispheric sleep) or the brain in general is not necessary for sleep to occur( upside down jellyfish, BMAL1 in skeletal muscle,etc)!

When it comes to the variation of responses people have on the forum in regards to sleep and rapamycin, many factors come into play(Age, sleep hygeine, health, secondary issues that may alter their sleep such as neuropsychiatric disorders, sleep apnea, insomnia, pain, etc).
My thoughts is rapamycin is probably changing genes/functions invovled in various processes(whether direct or indirect) that allow for some individuals to experience better sleep, while for others it causes increase in energy or disrupts their normal sleep pattern.
This could include the circadian process, where maybe someone has a chronotype(controlled by genes and is responsible for the preference of when you go to bed/wake up) that drives them to go to bed early/wake up early and rapamycin dirsupts genes/processes driving this chronotype and shift them into some sort of circadian disruption that affects their sleep. The opposite might be seen in others who sleep better.

My gut feeling is rapamycin is altering other processes that influence sleep, like production of various hormones /neurotransmitters, metabolism/metabolic health, mitchondria(as @John_Hemming is a proponent of) that depending on the individual alters their sleep response. Whether it has something to do with energy production that it might give some people more energy or more fatigue, or some other process, it’s hard to say and I wish more research would be conducted in this area.


Transcription of non-coding DNA also requires effective mitochondria.

1 Like

Are you meaning Non-Coding RNA?

Same difference really

1 Like

Ah, I have only read about non-coding RNAs during my literature searches in epigenetics, so I never knew they were the same thing. Thanks

1 Like