Lauea-
I began having blood pressure problems which I finally realized were seemingly coming from several natural MAOIs that I was unwittingly taking (green tea, turmeric, etc). I also had realized that I was a slow metabolizer and getting mild (but pleasant) hallucinations as a result. With other things to deal with. it went on the shelf for a while.

There is an interesting paper at http://www.braintechllc.com/Dextromethorphan.aspx

"What makes DXM so interesting is that the behavioral changes caused by varying doses of the drug can be traced directly to proportional amounts of receptor occupation. In this way, effects of DXM can be separated into three different behavioral and experiential “plateaus”. These plateaus directly correlate with various dosages at which certain receptors become saturated. In this way, DXM offers a unique glimpse at how neuropharmacological action is directly related to drug experience and behavioral changes (White, 2001, Section 9). Throughout the following sections, please refer to figure 1 for a graph approximating the receptor binding (and saturation) as a function of DXM dose.

At a low dose (1.5 to 2.5 mg/kg), or “level 1”, the effects of DXM are mainly determined by its PCP2 receptor binding profile (see figure 1). When DXM binds to the PCP2 binding site (which is located in the dopamine reuptake complex), dopamine reuptake is inhibited (Akunne et al., 1992). This has the effect of raising synaptic dopamine levels, which has a similar end-effect (but of different magnitude) as the antidepressant Bupropion or the recreational drug cocaine (Witkin et al, 1993). The PCP2-related increase in dopamine levels may be related to the reports of euphoria at this first “dose level.” These reports often link a feeling of euphoria to auditory stimulation (music) and motor stimulation (motion). Prolonged use of DXM can lead to addiction in some individuals because of its dopaminergic activity (especially in the nucleus accumbens). Although there are no dangerous physical withdrawal symptoms, psychological dependency (and withdrawal-related depression) can occur with regular use (McElwee, 1990). Fortunately, it is reported (but has not yet been scientifically verified) that many users find significant negative effects also accompany the DXM experience. These negative side effects may explain why so few people choose to use DXM regularly. Acting counter to this dopamine increase, activation of sigma1 receptors, located on dopaminergic nerve terminals, reduces normal NMDA-stimulated dopamine release (Gonzales et al., 1995). At low doses, binding to sigma1 is relatively low. However, at higher doses, PCP2 receptors become saturated and sigma1 activity continues to increase. For this reason, synaptic dopamine increase is most dramatic at this low dose level and diminishes at higher doses. This dopamine regulation at higher doses may also help explain why DXM is not more commonly abused."