Ricah pisze:

DXM to aptekowy Acodin, kosztuje chyba z dyszke, a dawki sa rzedu 15-45mg, z tym raczej dasz rade.

Jezeli faktycznie chcesz sprobowac odstawki, to pomysl moze o 'zamienniku'? Stymulanty tutaj raczej odpadaja, ale tianeptyna ma profil dopaminergiczny, wiec moze by zadzialala jako "łatka", a czesc efektow zauwazysz juz od 1 tabletki. Ciezko mi powiedziec wiecej w ciemno.

In spite of what those studies say, lobeline doesn't stimulate dopamine release because it blocks the dopamine neuron from being able to release dopamine. It prevents the neuron from firing by blocking VMAT, and it prevents the reversal of the transporter by blocking the transporter itself. This means dopamine neurons do not release any dopamine through either the transporter or the vesicle firing.It also does this for norepinephrine and serotonin neurons.
When this wears off you have an upregulated dopamine transport and loading system. Each time your dopamine neuron fires it will release more dopamine.
Amphetamine kind of does the opposite, but with a non-opposite mechanism. Amp inhibits the VMAT, like lobelia, but reverses the transporter instead of blocking it, which makes dopamine flood the synapse out of the transporter instead of the vesicles. Amp. tolerance results in less dopamine functioning. Lobeline will reverse this by upregulating both the reuptake transporters and VMAT at the same time.
Antagonizing dopamine receptors isn't going to really fix the amphetamine tolerance because the effect of a dopamine agonist is different than the effect of amphetamine. A dopamine releasing agent feels different from a dopamine agonist. Dopamine administered into the blood feels different from a dopamine releasing agent too, because dopamine releasing agents only release them in certain areas that are meant to be released in. Dopamine agonists and dopamine itself suck because they turn on a lot of pain and discomfort sensing neurons. Serotonin administered as an agonist really sucks because it turns on all the fever and flu systems, and the 5-HTfour receptor controlling anxiety, and the 5-HT3 nausea receptor... But release serotonin via the transporter reversal and you're fine up to a certain point.
Meaning, by taking a dopamine antagonist the effect that you will be creating in your body once the upregulation occurs is that of a dopamine agonist. This is because you will be upregulating the dopamine receptors instead of reversing the mechanisms of amphetamine tolerance, which aren't dopamine receptor downregulation. You will not be recreating the same feeling you had before you took amphetamine, nor will you be setting yourself back at baseline. You'll be creating a different effect: that of dopamine agonism [upregulating the dopamine receptors by antagonizing them gives you the effect of that receptor long term]. Amphetamines work differently, not really causing receptor downregulation but instead working through the TAAR and VMAT systems. This is why lobelia is better at reversing amphetamine tolerance: it's geared towards dealing with the systems that amphetamine uses. When lobelia wears off you create a natural amphetamine effect in your body, the feeling of increased dopamine release upon neuron firing.
Lobeline also upregulates opiate receptors and acetylcholine receptors. It also blocks the acetylcholine receptor responsible for managing addiction: the one nicotine turns on.
Lobeline administered on its own produces mild dopamine release [I have speculations on why this happens in other people, but in me it doesn't release any dopamine and just feels really sucky because of its antagonist effect] but when administered with methamphetamine it blocks the release of dopamine induced by meth. This is because it blocks the dopamine transporter.
Cocaine is known to block the effects of meth because it blocks the dopamine transporter, not allowing the transporter to reverse itself and release dopamine into the synapse. Studies show this.
NMDA antagonists don't work long term. There is no long term pharmacological solution for anything other than daily taking a substance that induces the opposite effect you're trying to achieve. This is why cycling is recommended, to give you a break from the substance. You can't take it forever and expect it to work. However, a single dose of heroin taken at the same time as a strong NMDA antagonist results in no tolerance to the heroin at all: meaning no crash due to opiate receptor downregulation. NMDA receptors are what the body uses to track the activity of a synapse, to which it responds by changing the level of receptors on the surface of the cell. By blocking the NMDA receptors you can prevent the body from telling itself to downregulate the opiate receptors when heroin activates them. After a long time of taking NMDA antagonists the NMDA receptors will upregulate to a point where they start to signal again, meaning you can't cheat the downregulating system forever.
Magnesium has some tolerance with it, but I would venture to say because it is a natural component of the body that it doesn't cause the same level of upregulation that an external compound would.

Hash_Oil pisze:

Amfetaminy downregulują DAT. Najlepsza jest PEA w miksie z selegiliną.

Ricah pisze:

Musialyby byc wtedy duze dawki (>600mg), ale musialbys wtedy juz uwazac na diete.

Hash_Oil pisze:

Lepiej, żeby uważał, ale przy iMAO-B ryzyko jest bardzo małe.
To przestrzeganie przed dietą bogatą w tyraminę w trakcie zażywania iMAO jest jak odradzanie łączenia SSRI z MDMA, czyli głupota.

nie nazwalbym glupota odradzanie laczenia SSRI z MDMA. O ZS nie jest az tak latwo, ale laczenie tak silnych dwoch srodkow o roznych mechanizmach dzialania jest po prostu nieodpowiedzialne.