Of Mice and Men and Wee Men and Frenemies

OK. I’m on techobabble burn out. This will be the last review of the material that the Hens have sent until i recover my sanity. Strike that - that would take too long.

A motivating factor behind getting to the bottom of naltrexone being used as a coverup for pain is that almost 20-years ago when my mother was on dialysis she had a debilitating headache. The nephrologist wanted to prescribe Darvon. She was opposed to drugs including narcotics that would just make you loopy but not do anything for the pain or the underlying cause. So she refused. She ended up in the hospital where she was diagnosed with SEPSIS.

The lesson of this story is: that if you cover up pain you will never get to the root cause and that cause might KILL YOU.

Paradoxical effects of the opioid antagonist naltrexone on morphine analgesia, tolerance, and reward in rats; J Pharmacol Exp Ther; 2002 Feb;300(2):588-96. doi: 10.1124/jpet.300.2.588.

Abstract

Opioid agonists such as morphine have been found to exert excitatory and inhibitory receptor-mediated effects at low and high doses, respectively. Ultra-low doses of opioid antagonists (naloxone and naltrexone), which selectively inhibit the excitatory effects, have been reported to augment systemic morphine analgesia and inhibit the development of tolerance/physical dependence. This study investigated the site of action of the paradoxical effects of naltrexone and the generality of this effect. The potential of ultra-low doses of naltrexone to influence morphine-induced analgesia was investigated in tests of nociception. Administration of intrathecal (0.05 and 0.1 ng) or systemic (10 ng/kg i.p.) naltrexone augmented the antinociception produced by an acute submaximal dose of intrathecal (5 microg) or systemic (7.5 mg/kg i.p.) morphine in the tail-flick test. Chronic intrathecal (0.005 and 0.05 ng) or systemic (10 ng/kg) naltrexone combined with morphine (15 microg i.t.; 15 mg/kg i.p.) over a 7-day period inhibited the decline in morphine antinociception and prevented the loss of morphine potency. In animals rendered tolerant to intrathecal (15 microg) or systemic (15 mg/kg) morphine, administration of naltrexone (0.05 ng i.t.; 10 and 50 ng/kg i.p.) significantly restored the antinociceptive effect and potency of morphine. Thus, in ultra-low doses, naltrexone paradoxically enhances morphine analgesia and inhibits or reverses tolerance through a spinal action. The potential of naltrexone to influence morphine-induced reward was also investigated using a place preference paradigm. Systemic administration of ultra-low doses of naltrexone (16.7, 20.0, and 25.0 ng/kg) with morphine (1.0 mg/kg) extended the duration of the morphine-induced conditioned place preference. These effects of naltrexone on morphine-induced reward may have implications for chronic treatment with agonist-antagonist combinations.

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Rybacki’s Essential Guide to Prescription Drugs, 2000, says that the line between the therapeutic and toxic dose of naltrexone is very thin. This abstract above indicates something that they discovered in drugging the water in NATOs Biology of Aggression text: high dose had a polar opposite effect to low dose drugging.

Thanks to the mice that were drugged and tortured we know that ultra low doses of naltrexone make morphine feel gooder and that it is less addictive. Hmmm….

I forgot to stuff this odd definition in the earlier Stacks:

Inverse Agonist - An inverse agonist is a drug which acts at the same receptor as that of an agonist, yet produces an opposite effect.

From: Annual Reports in Medicinal Chemistry, 1998

Pretty much that is what I was looking for the entire time that I started this roll down the Alcohol slide of razor blades. Thanks Harriet the Harrier.

Yet I’m still left with corn fusion and doubt with what it means to ANYONE with Lyme disease, Cancer, or any of the Herpes infections.

IF you use a drug that still allows Opioids to bind, but those opioids don’t make you a Jonsin’ Nutjob needing more, then could that be a sign that it was the Viruses that were granted permission into the cell by AGONISTS that started the whole cascade of allowing the Alien Into The Airlock leading to the spiral of addiction as found in my write up in

Calling all Hens

- When opioids contact the receptors on nerve cells it opens them up so that herpes viruses can enter.
- Herpes viruses cause pain in nerves.
- Pain causes the host to seek more opioids.
- More opioids creates more cell permissivity to viruses that lets in more Herpes.
- More Herpes causes more pain.
- More pain causes the host to seek MORE OPIOIDS.
- Lather, Rinse, Repeat.

It’s a tough call because the abstract above indicates that the morphine acts more efficiently as a pain killer, the host does not build up tolerance or addiction. The addiction part was where I suspected the virus had so taken over the host that it was the little mouse with the wire in it’s head hitting the paddle for stimulation until it died.

We still don’t know if the naltrexone allows the morphine to work but not open the cells to the virus. From the definition of Inverse Agonist we can presume (very expensive gambit) that the naltrexone itself does not let the Alien Inside The Airlock which was the primary concern during this Foray Into Madness. But we have to cover all angles since naltrexone POTENTIATES the action of morphine.

Another major hold-back for me is that these studies are in mice. Mice are not humans. Each animal has a unique physiology thus reaction to whatever pathway is being studied and although you can make generalizations, I’ll repeat it like on our Fran Zetta Faux Comic cover: Mice are not Men.

https://politicalartfranzetta.com/of-mice-and-men/

So for now I will leaf it as:

?