Revelation? Further testing may be required...
after being on gabapentin for 3 days now i can say with slight confidence that the two drugs are not the same. the effects of both vary wildly. the molecular structures are different as well. the fact that there is no cross tolerance tops it off. i really was under the impression that pg was an evergreened version of gp. it is not. they are very closley related but they are different drugs.
In response to this, I am going to throw something wild out there that I have been thinking about recently.
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I personally believe you can say with
complete confidence that the two drugs are
not the same!
Pregabalin was designed to be a
successor to gabapentin,
not a more potent
analogue of gabapentin. The two compounds share the properties of being GABAergic anticonvulsants with nocioception-blocking properties, but I believe this is less likely due to the
inhibition of glutamate release via the blockage of voltage-gated N-calcium channels, but rather the
inhibition of substance P release via the blockage of voltage-gated N-calcium channels. The degree to which each drug accomplishes its inhibition of neurotransmitter release is obviously different based on the variances in potency, and more or less neurotransmitters of other types may still be released despite the presence of one drug or the other.
Thus, GP & PG's
mechanisms of action (although not known precisely)
are the same. The obvious difference lies in the
efficacy of the mechanism; PG is obviously more efficient and effective at blocking the release of substance P, which accounts for why a lower milligram dose is required. In my mind, the less obvious difference between GP & PG lies in their respective
side effects profiles*. I think that GP's side effects profile is more haphazard and uncontrolled than that of PG; its side effects are
more weakly expressed in a
wider range of physiological and psychological areas in the human body. By contrast, PG's side effects manifest
more strongly throughout a
narrower range of the human body's physiology and psyche.
*When I use the term
side effects profile here for each of the two compounds, I am referring to their primary effects (for instance, "mood stabilization") that are
not related to nocioception in any way. I do not mean "side effects" in the traditional sense of the term, such as "dry mouth" or "constipation."
The article that I dredged up established that
there is no cross-tolerance between GP & PG. Given that their
mechanisms of action are the same (which ought to imply cross-tolerance), one hypothesis of mine for explaining the paradoxical lack of cross-tolerance is that
the differences between the side effects profiles (as I have defined them here)
may be implicated in either
negating, preventing, re-routing or
rendering physiologically impossible the development of the type of cross-tolerance one would expect to see between two compounds with nearly identical modes of action.
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*whew*
It took me so very long to put into hopefully comprehensible terms what I believe may lie at the root of the disparity between scientific logic and what we are observing in reality with regard to these fascinating chemical compounds. I shall leave it open to scrutiny now.
~ vaya