• Chugs 1984

    +Naloxone is Naloxone with Ibudilast.

    Hutchinson discovered that Ibudilast, a simple anti-inflammatory, reduces heroin withdrawals & tolerance whilst improving the analgesic affect of opiates.

    The root of all this is that he discovered that opiates induced glial activation,which participates in the mediation of pain including neuropathic pain, due to release of neuroexcitatory, proinflammatory products – it this process that causes opiate withdrawals.

    Basically the withdrawals have nothing to do with pleasure, conditioning or a failure of character to get off of heroin.

    Instead the individual is primed at birth to be a drug addict. Hutchinson proved this by purposely damaging rats in pre/post natal development and saw that these rats proved to be all the more addicted to heroin then rats that weren’t damaged.

    Furthermore he could reverse the withdrawals with the use of ibudilast . See previous Addiction Medicine orthodoxy thought that addiction and withdrawals were caused by the other. What is now being realised is that people are born with addictions.

    See tomorrows drug addict is right now feeling sick as the brain produces inflammatory molecules that target the glia. Not in huge amounts but enough to encourage the individual to engage in risky activities thus flooding the brain with dopamine, adrenaline and endorphins. Eventually the individual is exposed to opiates and the rest is history. Their forever tied into using this drugs in a sub-concious form of self-medication.

    Drug addiction is not a weakness of character but rather brain damage. What is amazing is that ibudilast has been found to work with Meth addicts and in theory should work with any drug that causes classical withdrawal symptoms that we see with opiate users.

    Hutchinson claims Naloxone is required to:

    “Additionally, this nonstereoselectivity provides a means of specifically blocking opioid-induced glial activation by using drugs such as (+)-naloxone. This would allow (-)-opioids to act neuronally to suppress pain via their actions on classical opioid receptors, while preventing (-)-opioids from simultaneously activating glial TLR4, which causes the release of pain-enhancing proinflammatory cytokines that oppose or counter-regulate the pain suppressive effects of opioids.”