Thread: Naltrexone Reset

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    Naltrexone Reset 
    Has anybody used Naltrexone (normal dose, like 50mg) to reset their tolerance?

    For some reason, I can't really use opiods. I think it might have something to do with being on Lyrica, but I can wait months, and my tolerance does not go down.

    i.e. after 3 months of nothing, I would need at least 10g of strong kratom, or 40mg of Oxy.

    So I have been prescribed Naltrexone by my doc, the theory is that by blocking the opiate receptors, they'll upregulate.

    - Has anybody done this before, and if so, how long did they need to be on the stuff in order to reap the benefits?

    My game plan is to hopefully get my tolerance back to minimum, so say, 50mg of tianeptine will work again.

    Can then use V/ULDN to keep my tolerance low, and then basically use tia to get off lyrica, as that shit has destroyed my brain, and I ain't getting off it without assistance.

    Can always go for Ibogaine treatment down the line to get off the opes.. but I can't do it while on lyrica, and there isn't a wonder-cure for getting off the stuff either :/

    Stupid plan? Perhaps. But yeah..
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    Other Drugs
    Jekyl Anhydride's Avatar
    Join Date
    Jul 2016
    While I don't have any reference sources in my bookmarks pertaining to this atm, I have heard far more than a few anecdotal cases about inverse agonists/ antagonists doing wonders for bring tolerances down much faster than agonist abstinence alone. I used to converse with a BL'er that would go through a cycle of 3+ weeks opioid use followed by 3+ weeks of Naltrexone. While he highly recommended a week to WD off opioids before beginning with the Naltrexone, he mentioned he would never return to abstinence only tolerance reduction ever again.

    He was also quick to suggest how strange it was when going back to opioids, as the smallest doses would leave him wrecked. I would consider this important as most understand how deadly going back to things like H after coming out of rehab can be, and it would appear this method speeds things up.

    The ULDN has plenty of science behind it as it works to change how the receptors conform to opioids and stops the Gs-coupled protein/ adenyl cyclase/ excitatory issue that affects long term users, while increasing efficacy during coadministration of agonists.

    Electrophysiologic studies of opioid effects on nociceptive types of dorsal root ganglion (DRG) neurons in organotypic cultures have shown that morphine and most mu, delta, and kappa opioid agonists can elicit bimodal excitatory as well as inhibitory modulation of the action potential duration (APD) of these cells. Excitatory opioid effects have been shown to be mediated by opioid receptors that are coupled via Gs to cyclic AMP-dependent ionic conductances that prolong the APD, whereas inhibitory opioid effects are mediated by opioid receptors coupled via Gi/Go to ionic conductances that shorten the APD. Selective blockade of excitatory opioid receptor functions by low (ca. pM) concentrations of naloxone, naltrexone, etorphine and other specific agents markedly increases the inhibitory potency of morphine or other bimodally acting agonists and attenuates development of tolerance/dependence. These in vitro studies have been confirmed by tail-flick assays showing that acute co-treatment of mice with morphine plus ultra-low-dose naltrexone or etorphine remarkably enhances the antinociceptive (pain relieving) potency of morphine whereas chronic co-treatment attenuates development of tolerance and naloxone-precipitated withdrawal-jumping symptoms.

    The present study provides a cellular mechanism to account for previous reports that low doses of NLX and NTX paradoxically enhance, instead of attenuate, the analgesic effects of morphine and other opioid agonists. Furthermore, chronic cotreatment of DRG neurons with micromolar morphine plus picomolar NLX or NTX prevents the development of (i) tolerance to the inhibitory APD-shortening effects of high concentrations of morphine and (ii) supersensitivity to the excitatory APD-prolonging effects of nanomolar NLX as well as of ultra-low (femtomolar-picomolar) concentrations of morphine and other opioid agonists.

    These in vitro studies suggested that ultra-low doses of NLX or NTX that selectively block the excitatory effects of morphine may not only enhance the analgesic potency of morphine and other bimodally acting opioid agonists but also markedly attenuate their dependence liability.

    Something that reads better than a PubMed abstract:
    ~Ultra-low-dose opioid antagonists enhance opioid analgesia while reducing tolerance, dependence and addictive properties

    NMDAr Antagonists also have benefits that might be worth looking into. Better for keeping tolerance down vs speedily reducing it but still:

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