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Many people are unaware that both enhanced effectiveness of narcotic analgesics AND prevention or reversal of tolerance is readily achievable through the oral use of up to 200-250 mg of Proglumide [(DL)-4-Benzamido-N,N-dipropylglutaramic acid]. [See Ott 1999; Watkins et al. 1984] The work of Watkins suggests there may be a therapeutic dosage window with diminished results above it but more detailed work to define this is apparently lacking. Rather than simply augment the action of the opiates, proglumide actually interferes with the anti-opioid activity of the neuropeptide CCK. The chronic administration of opiates, or spinal cord and other CNS injuries, elevates the level of Cholecystokinin (CCK) that is present. Such elevated levels exert an antagonistic effect on opioid activity resulting in significantly diminished analgesic effects. (Watkins et al. 1984; Xu et al. 1993 & 1994) It is this rise in CCK levels that directly leads to the condition known as drug tolerance and the corresponding increase in its anti-opioid activity that requires the opiate user to use increasingly larger amounts to achieve the same effects. This anti-opiate effect can be prevented or even reversed through the administration of CCK inhibitors such as proglumide. (Watkins et al. 1984) Besides just interfering with the adverse action of CCK on opiate activity, proglumide is also known to augment the analgesic effect of opiates. Often this can provide a higher quality of analgesia for those patients who suffer from an incomplete response to pain medications. Watkins & coworkers reported that proglumide reversed morphine tolerance and also 1) hastened the onset of analgesia, 2) increased the peak levels, and 3) prolonged the duration. They suggested that not simply did this indicate that effective narcotic doses could be decreased but it also indicated that proglumide might be able to enhance the effects of other procedures, such as acupuncture, which involve endogenous opiates. (Watkins et al. 1984) Proglumide is a nonselective CCK inhibitor that was formerly employed as an anti-ulcer medication (Hahne et al. 1981). It shows NO analgesic effects of its own. Although proglumide is now considered to be an obsolete pharmaceutical due to changes in our understandings of ulcer etiology, it has already seen extensive pharmacological and toxicological testing proving its safety and has been approved for use in humans. It has largely fallen into disuse but is still available in bulk via chemical houses or as a pharmaceutical in Europe and Africa sold under the trade name Milid and Milide. Other CCK inhibitors show similar properties (Idänpään-Heikkilä et al. 1997; Xu et al. 1993). However, beyond simply having seen previous use in humans, proglumide is both inexpensive and nontoxic. (Ott 1999) Proglumide is not some sort of magic bullet for completely eliminating the risk of tolerance development and addiction as its effects are only effective for a limited duration before tolerance to IT begins to develop. (After 8 days its effectiveness begins to wane) The work of Kellstein & Mayer 1990 suggests that successful therapeutic/maintenance applications will probably require its discontinuation for a week after each week of use. More work is needed to better define the precise parameters of its effective use for this purpose. Despite this, proglumide has already demonstrated itself to be of value both in pain management and as an adjunct to maintaining a narcotic addiction within a larger program of harm reduction (Anonymous 2000; Ott 1999). What is fascinating is how few drug educators, drug treatment facilities or even drug users are aware of this despite it being readily available information for nearly 20 years. If development of tolerance and the high price of a sustained addiction are truly as serious of a problem as we all agree that they are, one can only wonder how it is that, despite the tools existing to remove or at least reduce this problem, there seems to be no interest or research except on a limited scale related to specific small areas of chronic pain management and understanding. The current misguided approach of substituting methadone is commonly reported to actually cause MORE perceptual and thinking problems than the opiates it replaces PLUS methadone is known to cause physical damage to internal organs that are not encountered with opiate use itself. Harm reduction approaches would benefit greatly by using proglumide as a cornerstone and making it readily available to both narcotic users and abusers. Those who will most certainly object include organized crime and drug dealers who enjoy the obscene profits reaped from escalating drug tolerances, and possibly also the so-called “drug educators” that sadly often seem to be the ones most in need of some factual education. There are many problems associated with opiate use and abuse. While the majority of these are legal in origin, the most sensible approach would be to ameliorate [or mitigate] those that aren’t. Increased analgesic effectiveness and prevention of tolerance are two obvious areas where harm reduction is readily possible TODAY. Both sufferers of chronic pain and narcotic addicts stand to benefit from having their needs met and their health risks simultaneously decreased. As this is first and foremost a health problem, the current approach of harm maximization is both counterproductive and unacceptable. To a rationale or caring mind it might even be perceived of as unethical and amoral. Not only do sufferers of chronic pain and narcotic addicts stand to benefit from such harm reduction approaches but, by decreasing drug-associated crimes, a significant area of the true “drug problem” can be directly addressed, thereby benefiting society as a whole.
Ameer, Barbara & Randy A. Weintraub (1997) Clinical Pharmacokinetics 33 (2): 103-121. “Drug Interactions with Grapefruit Juice.”Anonymous (2000 & 2001) Personal interviews with assorted opiate users & abusers. Caraco, Y. et al. (1996) Drug Metab. Dispos. 24(7): 761-764. “Microsomal codeine N-demethylation: cosegregation with cytochrome P4503A4 activity.” [Y. Caraco, T. Tateishi, F.P. Guengerich & A.J. Wood] [Abstract from PubMed] Crain & Shen 1996: See patent references farther below. Crain, Stanley M. & Ke-Fei Shen (2000) Pain 84: 121-131. “Antagonists of excitatory opioid receptor functions enhance morphine’s analgesic potency and attenuate opioid tolerance/dependence liability.” Dresser, G.K. et al. (2000) Clinical Pharmacokinetics 38(1): 41-57. “Pharmacokinetic-Pharmacodynamic Consequences and Clinical Relevance of Cytochrome P450 3A4 Inhibition.” [George K. Dresser, J. David Spence & David G. Bailey] Entheogen Review; POBox 19820, Sacramento, CA 95819-0820. [www.entheogenreview.com] Feierman DE, & J.M. Lasker (1996) Drug Metab. Dispos. 24(9):932-939. “Metabolism of fentanyl, a synthetic opioid analgesic, by human liver microsomes. Role of CYP3A4.” [Abstract from PubMed] Hahne, W.F. et al. (1981) Proceedings of the National Academy of Science (USA) 78 (10): 6304-6308. “Proglumide and benzotript: Members of a different class of cholecystokinin receptor antagonists.” [W.F. Hahne, R.T. Jensen, G.F. Lemp & J.D. Gardner] Idänpään-Heikkilä, J.J. et al. (1997) Journal of Pharmacology and Experimental Therapeutics 282 (3): 1366-1372. “Prevention of Tolerance to the Antinociceptive Effects of Systemic Morphine by a Selective Cholecystokinin-B Receptor Antagonist in a Rat Model of Peripheral Neuropathy.” [Juhana J. Idänpään-Heikkilä, Gisèle Guilbaud & Valérie Kayser] Jansen, Karl (2001) e-mail correspondence with Jon Hanna (Book reference is to Ketamine: Dreams & Realities by Karl Jansen; see www.maps.org) Kellstein, David E. & David J. Mayer (1990) Brain Research 516: 263-270. “Chronic administration of cholecystokinin antagonists reverses the enhancement of spinal morphine analgesia induced by acute pretreatment.” Ott, Jonathan (1999) Entheogen Review 7(2): 62-73. “Jonathan Ott Speaks…Part Two.” (Interviewed by Will Beifuss & Jon Hanna in 1998) (Proglumide comments are on p. 69) Pain Therapeutics, Inc., 250 E. Grand Avenue, STE 70, San Francisco, CA 94080 Peterson, F.J. et al. (1983) Gastroenterology 85(1): 122-129. “Prevention of acetaminophen and cocaine hepatotoxicity in mice by cimetidine treatment.” [F.J. Peterson, R.G. Knodell, N.J. Lindemann & N.M. Steele] [Abstract from PubMed] Pellinen, P. et al. (1994) Eur. J. Pharmacol. 270(1): 35-43. “Cocaine N-demethylation and the metabolism-related hepatotoxicity can be prevented by cytochrome P450 3A inhibitors.” [P. Pellinen, P. Honkakoski, F. Stenback, M. Niemitz, E. Alhava, O. Pelkonen, M.A. Lang & M. Pasanen] [Abstract from PubMed] R.A.H. (2000) Entheogen Review 9(3): 145-147. “Opiate Potentiation.” Watkins, L.R. et al. (1984) Science 224: 395-396. “Potentiation of Opiate Analgesia and Apparent Reversal of Morphine Tolerance by Proglumide.” [L.R. Watkins, I.B. Kinscheck & D.J. Mayer] Xu, X.-J., et al. (1993) Neuroscience Letters 152: 129-132. “Up-regulation of cholecystokinin in primary sensory neurons is associated with morphine insensitivity in experimental neuropathic pain in the rat.” [X.-J. Xu, M.J.C. Puke, V.M.K. Verge, Z. Wiesenfeld-Hallin, J. Hughes & T. Hökfelt] Xu, X.-J., et al. (1994) Pain 56: 271-277. “Chronic pain-related behaviors in spinally injured rats: evidence for functional alterations of the endogenous cholecystokinin and opioid systems.” [Xiao-Jun Xu, Jing-Xia Hao, Åke Seiger, John Hughes, Tomas Hökfelt & Zsuzsanna Wiesenfeld-Hallin] Additional information that was not used or referenced above: