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It's interesting because I just started taking Qelbree\Viloxazine (a selective norepinephrine reuptake inhibitor), and even though I feel great I have a ton of trouble staying asleep. It seems to be a common complaint among folks talking it.

Before this, I took Strattera\Atomoxetine (which has the same method of action) for at least five years. And while falling asleep has long been difficult for me, staying asleep hasn't been.

Not quite sure how my experience relates, but makes me wonder if either too much norepinephrine also adversely impacts sleep or if I'm sleeping more "efficiently," so to speak, which is why I wake up feeling rested.

I don't remember any sort of similar experience when taking Effexor about a year ago, but I don't believe I ever reached a high enough dosage for the norepinephrine reuptake to take effect.




One of the primary roles of norepinephrine is literally mediating alertness, including stress/fight-or-flight responses more specifically.


“Mediating alertness”, as in more available norepinephrine increases or deceases how alert you are?

From my experience while awake, I would assume decreases. While it’s yet to have a huge impact on my ADHD, it’s has had a noticeable impact on reducing my self-doubt and hesitance to speak up. But I’m not sure how to unify that with it reducing the quality of my sleep.

Maybe, since I’m taking it in the AM it’s wearing off at night, and thus my level of alertness in the middle of the night is being heightened. That would line up with antidotal reports I’ve read of people saying they had less sleep disruptions when they took it at night. Something I’m planning to try moving to.

It’s also possible it takes take to reach a steady state (I’ve only been taking it two weeks)


Norepinephrine increases alertness, especially when it's targeted towards the prefrontal cortex (like straterra is)


Maybe a receptor resistance build up? Seems to be a common pattern that medication needs to be dosed up to work- and blunts the receptors for the "normal" amount the body produces, if it does not cease to produce it at all.


I'm not quite sure I'm smart enough to follow.

Don't sNRIs increase the availability of norepinephrine rather than decrease it? Which is effectively the equivalent of producing more, not less?


In that case, the body would theoretically adjust to down regulate the production of norepinephrine, since there’s already reuptake has been reduced.

But… I’m not sure it really works that simply in a real brain.




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