Homeostasis and Tripping Forever

[MeDieViL]

I read on Longecity an interesting experiment suggested by Euphoricmind(user) to maintain euphoria as long as possible week-after-week:



Why would it/ wouldn't it work ?

ldopa with coke would accelerate tolerance, the dopaming agonist would mabe prevent downregulation of da receptors in soe way perhaps but onces that work would block coke
subutriamine to reverse da agonism? lol and te dxm after taking the drug? lol
3. piracetam accelerates tolerance and reversing nmda amtagonism doesnt make sense, it would have worn off and wouldnt prevent adderall tolerance and then youd accerlerate it with pir
again reversing adderalls noradrenaline agonism the day after? lol
ssris would inhibit lsd in a part maybe
again reversing the ssri antagonism?
maoi at day7? this shit is the most retarded ever, also on some days you wont be able to function with whatever drug the guy takes, hey this guy is alot on monday, starts getting tired thursdays because the alcohol, trips on friday and tried again on saterday

its like being a guy with soe sort of extree menstrual cycle if you saw him lol

 

[MeDieViL]

Agreed, but the dose makes the poison as does the peak plasma concentration and the AUC.

Adderall XR vs Insufflated Speed

Xanax XR vs a crushed bar

low dose phenethylamine is not only plausible but experimentally validated -- a test subject consumed approximately 10-15 mg /BID MDMA sublingual/oral DAILY for over a month without any tolerance or negative impact on the subjective experience of 120 mg

subject reported a general uplifted mildly euphoric mood with increased color saturation (especially blue and violet)

multiple GRAMS of mixed ascorbate salts taken daily

subject reported hyperhydrosis identical to that experienced when starting SSRI/SSNRI therapy that resolved after several days, initial sleep disturbance - resolved, anorexic action - resolved

Subject reported MDA did not provide same success - discontinued due to dysphoric reaction and tolerance

YMMV with tryptamines

ive allways said here that serotonin releasers in therapeutic dose would make excellent antidepressants with less side effects then ssris and better effectiveness.

pea is only said to work long term in a study where test subjects only took 2 doses a day with selegiline, im skeptical it would stay effective without memantine.

a

 

[MeDieViL]

You would think it is possible for neuronal damage or changes in neuronal expression of things like parvalbumin to cause a persistent ASC, I'm sure that this would take high doses of a drug and a vulnerable individual, but it seems like it should be possible.

I know a lot of people argue about "This drug isn't neurotoxic in humans" etc, but it seems to me that with a brain that is already degenerating due to early stage neurodegenerative disease, it might be possible for normally non-neurotoxic substances to induce some neuronal degeneration in small amounts,

Part of what I'm getting at is that maybe to some degree everybody has pathology.

You could entertain that idea with regards to beta blockers or whatever, this is negative gueswork, but anyway its allways a risk as chronic dosing can be unpredictable

abolishing hyperthermia abolishes mdma damage in rodents, HOWEVER with chronic dosing this is not the case

 

[serotonin2A]

#facepalm
Furthermore, this is an experiment. No one said it had to be practical or sociably acceptable.

I guess I should have said that it isn't a scientific experiment. One of the most important parts of the scientific method is falsifiability. In the sequence of drug intake posted above, there is no attempt to account for or control the multitude of factors that could influence the outcome.