I don't think 120mg of dxm is overkill is it?
My apologies. I again spoke too soon, drawing upon my feeble, drug-addled memory to suit needs better served by a cursory review of the literature. 120 milligrams is indeed an optimal dosage that would likely marginalize side effects and subjective properties while maximizing therapeutic gain. The only concern of apparent verisimilitude relates less to the drug's debatable physical toxicity and more to its frequently bizarre effects upon the human psyche, and the subsequent behavioral toxicity that might ensue. However, I sincerely doubt that doses under 150mg will produce any long- or short-term complications - but
caveat emptor: the endless tide of tachyphylactic progression remains of constant concern when even the most well-minded user stacks one ameliorative compound upon another. Each problem solved often leads by extension to yet another dilemma in need of another problematic solvent, and so on, ad infinitum.
Not to be a total buzzkill, but tolerance to the
NMDA antagonists themselves via the classic [and apparently poorly reversible once instated] phenomenon of progressive ionophore upregulation and sensitization in response to the continued presence of the antagonist. Withdrawal of the anesthetic following chronic use can be far more injurious than most other drugs with less obtrusive actions upon such fundamental mediators of neurochemical homeostasis; it can be permanently incapacitating and assuredly life-threatening. Of course, this is highly dependent upon dosage, duration of use, and the individual in question. The dosages that you intend to take would very likely cause few serious issues, but given their gravity, the concerns are hard to dismiss.
While I understand that your ambitious goals may preclude a more conservative strategy, I strongly advise the adoption of a 5-on/2-off cycling schedule, wherein weekdays are populated by perpetual drug use, followed by total weekend abstinence (and perhaps with full weeks off every 35 days, just "to be safe"). This will hopefully stifle any potential adaptation to the methorphan (the tolerance to which is rather rapidly reversible) and further compensate for any heavy weekday amphetamine use.
Also, I forgot to mention last post: I'm sure you've come across posts on this site (among others) recommending the supplementation of magnesium as part of a tolerance-reducing regimen. Though a first glance at the literature makes it sound like little more than pseudoscientific absorption of silly marketing ploys, I'm beginning to wonder whether the idea truly does have merit when taken to the extreme. The divalent magnesium cation plays a crucial role in the inhibitory regulation of glutamatergic transmission at the NMDA complex. By 'stopping up' the ionophore in an entirely voltage-dependent manner, Mg++ ions act as a handy sort of atomic plug that is 'uncorked' following action potential allowing influx of calcium ions following the binding of an agonistic ligand (typically glutamate and its co-agonist, glycine). Magnesium is thus often referred to as an 'NMDA antagonist,' even though it bears little pharmacodynamic similarity to the class of powerful dissociative anesthetics, of which DXM is a member. These drugs bind at an entirely separate location within the pore itself, the 'PCP site,' uncompetitively blocking influx of Ca++ ions into the postsynaptic neuron, an effect that is fully independent of voltage. On the other hand, the adamantane drugs appear to have surprisingly similar actions as magnesium, allowing for their contrastingly side-effect-free profile.
As magnesium is an essential dietary nutrient whose supplemental administration has little noticeable impact upon vital biomarkers (let alone conscious mental state) in non-deficient individuals, conventional wisdom suggests that the animal studies in which clinically relevant effects were observed are merely representative of the many artifacts present in rodent research into the mammalian nervous system, and were likely obtained by unrealistic routes of administration (intraventricular injection, for instance) or insane dosing protocols (3424732894655739790 mg/kg). I quickly dismissed the 'magnesium is a functional NMDA antagonist' hype for these reasons. However, after reading that massive doses of magnesium salts have been efficaciously used as anesthetics and that the often life-threatening effects of such treatment were consistent with those of other centrally numbing agents (and bore some similarity to the reported effects of memantine overdose), I was forced to reconsider whether highly bioavailable salts of magnesium could indeed provide additive benefit when taken concomitantly with a sensible dose of methorphan. As it appears that memantine is essentially nothing more than a molecularly fancier and pharmacologically dirtier version of magnesium on steroids, you could probably save quite a bit of cash by just ordering some magnesium malate (or some comparable form) online. This could, of course, be administered consistently, and fully without regard to concerns of tolerance. Just a thought. Some links for verification/interesting info/relevant reading:
Magnesium deficiency increases ketamine sensitivity in rats
http://www.springerlink.com/content/064612695h4130l4/fulltext.pdf
http://jama.ama-assn.org/cgi/content/summary/LXVII/16/1131
![:\](https://bluelight.org/xf/BL_Images/Orig_Emoji/wrygrin.gif "wry grin :\")