Be careful with reboxetine and PEA + selegiline; apparently reboxetine is anticholinergic which combined with the above could result in severe (and I mean severe) psychosis. Ever heard of amphetamine psychosis? Yup. Generally when increasing dopamine, you need to also boost the function of the neurotransmitter acetylcholine to retain cognition, memory, intelligence, etc. There are a number of ways to achieve this, including acetylcholinesterase inhibitors (used for Alzheimer's), choline, Alpha-GPC, lecithin, etc. These would be especially important if using reboxetine.Regardless of the psy-doc's diagnosis (or lack thereof), I re-started taking Selegiline / Deprenyl (citrate) initially 5mg / day then taper back to 1-2mg / day for mao-b. I have also started to take 4mg Reboxetine 1 in the morning, 1 in the afternoon. I will start a new PEA regimin today, while keeping the Xanax XR nearby. I will report back on the results.
So much dopamine is probably giving you horrible nausea (and definitely if you add a cholinergic), so maybe the peripheral (not entering the brain) receptor-selective dopamine antagonist domperidone could be used. The drugs I'll mention below, memantine and mirtazapine, would also stop nausea (probably).
The glycine NMDA site also may need to be considered if you had any pre-existing paranoia/psychotic symptoms indicative of potential for schizophrenia-like illness. Info is scarce on methods to reach this receptor site, but some new antipsychotic medication being developed I predict will almost entirely eradicate schizo-like mental disorders without many side-effects, all via this mechanism. The zombies on dopamine antagonists will awake from the emotional coma of the pathetic current treatment methods.
Other things that might be worth researching are opioids (could replace benzos for anxiety), cannabinoids (in cannabis, for appetite etc.), and even psychedelics... We can't discuss illegals on this board though, even if it's for non-recreational purposes. If you're self-medicating, might as well go the whole way in my opinion. Then again most of my ideas aren't realistic. Have I mentioned this is all very dangerous unless you're medically trained, have proper monitoring equipment, etc.?
Atomoxetine is probably better than reboxetine, but has a shorter half-life (I'm not sure about the exact differences though). You should always have at least some potent benzos ready in case you get a hypertensive episode (if it wears off, etc.), or carvedilol.My past experience was that Selegiline + PEA is effective for focus, creativity, communication, and study if it is consistently and timed right in dosing to avoid the highs and lows. It was the first time almost a spiritual experience similiar to what some have described near to MDMA experience.
There seem to be some quite intelligent people on this forum which is why I'm posting. Rocknroll714 and Euphoria wrote some great posts including this quote by Euphoria:
"The obvious answer to the PEA problem is to take reboxetine/atomoxetine + selegiline + PEA, along with tyrosine etc. for the crash, magnesium for tolerance and benzos for whenever necessary.
Magnesium may not be enough to protect from tolerance, especially if not taken in the best forms (i.e. chelated such as glycinate, taurinate). Zinc can also help, but I'm not sure it's wise to over-do either (particularly zinc). Currently the best option appears to be memantine, which seems like a miracle for tolerance and neuroprotection:
It also has a very long half-life, while magnesium in pharmacological doses loses effects within hours.Wikipedia said:Memantine is a low-affinity voltage-dependent uncompetitive antagonist at glutamatergic NMDA receptors. By binding to the NMDA receptor with a higher affinity than Mg2+ ions, memantine is able to inhibit the prolonged influx of Ca2+ ions which forms the basis of neuronal excitotoxicity. The low affinity and rapid off-rate kinetics of memantine at the level of the NMDA receptor-channel, however, preserves the physiological function of the receptor as it can still be activated by the relatively high concentrations of glutamate released following depolarization of the presynaptic neuron.
All should be done slowly added individually with a blood-pressure monitor, of course, and with benzos/carvedilol nearby. I'm not gonna recommend doses because I'm unsure and also don't want to encourage potentially lethal cocktails. To anyone reading this though, the PEA dose on selegiline is much lower than without selegiline, and reboxetine/atomoxetine would have to be active in your system before any PEA dose if you wanted to prevent (nor)adrenaline release. Using 5-10mg of selegiline and low amounts of PEA would probably be better than the other way round.
Personally I think you're neglecting serotonin, which could help a great deal with anxiety and mood (instead of crappy benzos). All that dopamine and noradrenaline must be alienating some people around you, no? I'm a big proponent of taking both an SSRI + mirtazapine at night, but am not sure how mirtazapine's weak noradrenaline (also dopamine indirectly) action would interact with the rest. This is dangerous territory.
That sounds like it'd give an absolutely horrible (and possibly deadly) hypertensive crisis, or at least a very high cardiovascular load. Moclobemide has far too great an effect on (nor)adrenaline and too weak on dopamine to combine with Ritalin without serious problems. Moclobemide is complicated to understand in its effect on various neurotransmitters, but there certainly is a high possibility of severe problems. Do not try this!Well it's my first post as well. Your situation caught my eye because I have started on Manerix(moclobemide) recently and am about to add Ritalin to the diet. I don't think it's available to you in the states. Do you have other MAOI experience, other than Selegiline? Moclobemide is fast acting and almost as effective as Klonopin in my experience.
Selegiline on the other hand I've heard being used successfully with Ritalin, although dose would probably need to be majorly adjusted.
That's a big contradiction. If it only remained peripherally, it would not produce insomnia, agitation and irritability. These all result from central nervous system activation, whether from the levo-(meth)amphetamine metabolites or selegiline's MAOI-B action.AURORIX has the advantages over MAOI type-B, DEPRENYL (Selegiline)- which only inhibits the breakdown of DOPAMINE and PEA, furthermore, Selegiline is partly metabolised into amphetamine- but acting only peripherally, not in the Central Nervous System, and thus giving side effect such as insomnia, agitation, and irritability. The metabolite, amphetamine does not have any effect on the brain, thus, it does not give the same effect as amphetamine-salts ( such as, ADDERALL,etc)
Again he just contradicted himself, saying earlier that the vast majority of effects were on serotonin and (nor)adrenaline, not dopamine. PEA is metabolised by MAO-B, so wouldn't be increased much by a [relatively] selective MAOI-A.In conclusion, AURORIX works much better than DEPRENYL, as it increases the amount of SEROTONIN, NORADRENALINE, DOPAMINE, PEA, in the synaptic clefts, thus, improving mood and feeling of well-being. It also, according to some research papers, increases the total sleep-time and the quality of life.
The author also didn't acknowledge octopamine and its relevance with inhibitors of MAO-A.
My conclusion is that moclobemide is a pretty ****ty drug in relation to the possibilities of selegiline, but they are both different and used for different purposes so really no comparison should be made.