LONGECITY

I saw somewhere that certain dose act on pre-synaptic receptors only. Thought it was about 50mcg. That's why I ask all the time if I choose the dose wise and is once daily enough.

Full-blown DA agonism could be fun probably, but I don't want to be dependent on drug, nor to risk to ruin such an important and frgile system as DA, nor to get all the not-so-fun sides..

"Full-blown" DA agonism is good for keeping prolactin on the low  side and therefore eliminating the refractory period - it's also good as augmentive "hormonal enhancement", but ONLY if you have forskolin on hand or at least albuterol or a beta agonist.

Dopamine agonists have in human studies failed to show consistent antidepressive effect but they MAY be effective as adjunct treatments.

 

Ketamine is an awful idea. Unless you can get medical grade stuff and it isn't actually any more effective than SSRI's with a 60% effectivness rate. Also oral trials haven't been performed and so far only intramuscular trials have been successful. The effects don't last for that long a month at most. More importantly there is hardly an research supporting it in human trials.

 

If you don't want SSRI antidepressant side effects, why don't you take a different type of antidepressant??? Mirtazapine, Trazadone, Tianeptine, Wellbutrin, Moclobremide, Reboxetine, Agomelatine and Viloxazine are all non-ssri options with reasonable side effects.

 

If you want to try some unevidence based supplemental treatment then you could always use CDP-Choline, L-Tryptophan, a multi-vitamine, Sulbutramine, Noopept, etc...

where does one get Viloxazine?  About 6 years ago I was able to order it online but then it was taken off the market in many countries and only available in France.

Has the status changed?  I would love to try it again because it was one of the few anti-deps that truly worked for anhedonia, low emotion, poor drive/motivation and lack of interest. 

I've been working on ways to increase and protect dopamine - https://mybiohack.co...amine-naturally

I saw somewhere that certain dose act on pre-synaptic receptors only. Thought it was about 50mcg. That's why I ask all the time if I choose the dose wise and is once daily enough.
Full-blown DA agonism could be fun probably, but I don't want to be dependent on drug, nor to risk to ruin such an important and frgile system as DA, nor to get all the not-so-fun sides..

"Full-blown" DA agonism is good for keeping prolactin on the low side and therefore eliminating the refractory period - it's also good as augmentive "hormonal enhancement", but ONLY if you have forskolin on hand or at least albuterol or a beta agonist.

I've been working on ways to increase and protect dopamine - https://mybiohack.co...amine-naturally

it's either to get a synergy or to balance out some negatives, i'm never really sure with Area.  he's banned anyways, so yeah.

it shouldn't really be necessary.  mono-therapy produces enough of an anti-anhedonic effect, e.g. dopamine agonist prampiprexole^[1] and ketamine^[2], the latter also being a unique NMDA antagonist

Dopamine–prolactin pathway potentially contributes to the schizophrenia and type 2 diabetes comorbidity
https://www.ncbi.nlm...les/PMC4872408/

Beta-adrenergic stimulation of prolactin release from superfused pituitary cell aggregates.
https://www.ncbi.nlm.../pubmed/6282573
l-Isoproterenol (l-ISO), a specific agonist of beta-adrenergic receptors, evoked a prompt rise of prolactin (PRL) release from superfused anterior pituitary cell aggregates established in culture for 5 days. The effect was concentration-dependent between 1 and 100 nM. d-Isoproterenol was more than 2 orders of magnitude weaker than the l-isomer. When dopamine receptors were blocked with domperidone, PRL secretion was also stimulated by l-epinephrine (E) and l-norepinephrine (NE), the rank order of potency being l-ISO greater than E much greater than NE. Under the latter conditions dopamine and the alpha-adrenergic agonists, clonidine and phenylephrine, had no stimulatory effect at 1 microM. Stimulation of PRL release by l-ISO and E was blocked by the beta-receptor antagonist, propranolol, but not by the alpha-receptor blocker, prazosin.

does anybody have experience with selective D4 agonists like low-dose apomorphine? D4 is theorized to be responsible for inattentive ADHD symptoms. both agonists and antagonists seem to have beneficial effects on cognition as far as i know.