Sorry folks if this direct Wiki quote has already been posted up. If you Wiki loperamide HCL, you'll find links to BBB potentiators - which, BTW, I've yet to try myself, having xref'd my PDR, and found that the most promising of these, such as Ritonavir/Quercetin are indicated for HIV therapy - and I'm not quite that desperate, since my refill's up in a day or 2 anyway. Yet one is an OTC. Do your own homework, because I am not a health care professional.
Just a word re my background - I've been on a CII Rx for at least 15 years now. And, if you are reading this, I'll leave it to your imagination as to how many WDs I've successfully endured. This particular cup of cold duck, which has followed a slight taper of a week or so, has been the easiest by a long shot: in addition to roughly 8mgs loperamide HCL 4x/day. we have diphenhydramine HCL 50mg 2 or 3x/day (generic Benadryl). Naturally, my alprazolam Rx (xanax) plays a mighty role, even as I'm really trying to taper off that stuff for good. Since the only thing that I can think of which is worse than an opioid cold kick is a benzo kick...or, better, both at the same time.
On a parting note, before the Wiki import, I have successful utilized a Vet Admin "cure" for very heavy habits - like up to 500mg OC/day. Since this one is not exactly a walk in the park, I'll spare everyone unless requested...
"Ability to cross the blood–brain barrier
Concurrent administration of P-glycoprotein inhibitors such as quinidine and its other isomer quinine (although much higher doses must be used), PPIs like omeprazole (Prilosec OTC) and even black pepper (piperine as the active ingredient) could potentially allow loperamide to cross the blood–brain barrier. It should however be noted that only quinidine with loperamide was found to produce respiratory depression, indicative of central opioid action.[8]
It is a misconception that loperamide does not cross the blood–brain barrier. Loperamide does cross this barrier, although it is immediately pumped back out into non–central nervous system (CNS) circulation by P-glycoprotein. While this mechanism effectively shields the CNS from exposure (and thus risk of CNS tolerance/dependence) to loperamide, many drugs are known to inhibit P-glycoprotein and may thus render the CNS vulnerable to opiate agonism by loperamide.[9]
Loperamide has been shown to cause a mild physical dependence during preclinical studies, specifically in mice, rats, and rhesus monkeys. Symptoms of mild opiate withdrawal have been observed following abrupt discontinuation of long-term therapy with loperamide.[10][11]"
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