I tried to use melatonin as a reversed-effect stimulant (the same principle could be used with other downers, like memantine, alcohol, naltrexone). The idea is to use downer for down-regulating its receptors, that is, in the case of melatonin, to lower production of the endogenous melatonin and down-regulate the receptors to it.
The protocol I tried is using 3 mg of the melatonin oral spray every 3 days before sleep. The dose is rather large and I often have some grogginess the next morning, but the next couple of days I have much less sleepiness in evenings and tiredness during the day. The same trick with memantine cured my depression, for which agomelatine was a complete failure and which effect was more similar to weak SSRI, which may be its actual mechanism of action.
One may also try larger doses of the melatonin recreationally, which induce nice relaxation, and, as some claim even stimulation on higher doses. The obvious risk is suppressing endogenous melatonin too much and get insomnia.
The science is solid for naltrexon low dose therapy which is used to up-regulate opiate receptors. The idea is to use small doses of antagonist to make the exiting receptors more sensible after some period of time. The same principle could be applied to other depressants, including melatonin, which start to simulate because of withdrawal effects.
I tried to use melatonin as a reversed-effect stimulant (the same principle could be used with other downers, like memantine, alcohol, naltrexone). The idea is to use downer for down-regulating its receptors, that is, in the case of melatonin, to lower production of the endogenous melatonin and down-regulate the receptors to it.
The protocol I tried is using 3 mg of the melatonin oral spray every 3 days before sleep. The dose is rather large and I often have some grogginess the next morning, but the next couple of days I have much less sleepiness in evenings and tiredness during the day. The same trick with memantine cured my depression, for which agomelatine was a complete failure and which effect was more similar to weak SSRI, which may be its actual mechanism of action.
One may also try larger doses of the melatonin recreationally, which induce nice relaxation, and, as some claim even stimulation on higher doses. The obvious risk is suppressing endogenous melatonin too much and get insomnia.
Not medical advise.
I am unfamiliar with the science here—what is the difference between a “reversed-effect stimulant” and a depressant?
The science is solid for naltrexon low dose therapy which is used to up-regulate opiate receptors. The idea is to use small doses of antagonist to make the exiting receptors more sensible after some period of time. The same principle could be applied to other depressants, including melatonin, which start to simulate because of withdrawal effects.