Why you come to me

... FarmBoy language for country hicks and city slicks

Jul 08, 2023

This is the second in the Frenemy series evaluating just what the hell Naltrexone might do to the human body.

I'm not a doctor. I can't give medical advice. But it seems that they can't either.

https://www.sciencedirect.com/science/article/abs/pii/S0028390811003625

Chronic treatment with the opioid antagonist naltrexone favours the coupling of spinal cord μ-opioid receptors to Gαz protein subunits

Abstract

Sustained administration of opioid antagonists to rodents results in an enhanced antinociceptive response to agonists. We investigated the changes in spinal μ-opioid receptor signalling underlying this phenomenon. Rats received naltrexone (120 μg/h; 7 days) via osmotic minipumps. The antinociceptive response to the μ-agonist sufentanil was tested 24 h after naltrexone withdrawal. In spinal cord samples, we determined the interaction of μ-receptors with Gα proteins (agonist-stimulated [35S]GTPγS binding and immunoprecipitation of [35S]GTPγS-labelled Gα subunits) as well as μ-opioid receptor-dependent inhibition of the adenylyl cyclase (AC) activity. Chronic naltrexone treatment augmented DAMGO-stimulated [35S]GTPγS binding, potentiated the inhibitory effect of DAMGO on the AC/cAMP pathway, and increased the inverse agonist effect of naltrexone on cAMP accumulation. In control rats, the inhibitory effect of DAMGO on cAMP production was antagonized by pertussis toxin (PTX) whereas, after chronic naltrexone, the effect became resistant to the toxin, suggesting a coupling of μ-receptors to PTX-insensitive Gαz subunits. Immunoprecipitation assays confirmed the transduction switch from Gαi/o to Gαz proteins. The consequence was an enhancement of the antinociceptive response to sufentanil that, in consonance with the neurochemical data, was prevented by Gαz-antisense oligodeoxyribonucleotides but not by PTX. Such changes in opioid receptor signalling can be a double-edged sword. On the one hand, they may have potential applicability to the optimisation of the analgesic effects of opioid drugs for the control of pain. On the other hand, they represent an important homeostatic dysregulation of the endogenous opioid system that might account for undesirable effects in patients chronically treated with opioid antagonists.

Now the reason why I make y’all suffer through stuff like that is because this is an example when they use PRECISE language in science, however, unless you are a specialist or, like me, have a medical dictionary at your feet at all times, then you, like Fran Zetta (and often me these days) will have your eyes glaze over and be thinking of that hawaiian vacation that you took in ‘63 before you fade back into the bulk of this Stack after having experience Lost Time that had nothing to to with an alien abduction.

You have to respect the precision in language, but at some point it just seems that they’re showing their ass.

Not being a specialist in their lingo I will attempt to cover their bottoms and bring this down to a level that we can all get a handle on, because all sarcasm aside this stuff has a direct impact on people’s health and their lives.

“Sustained administration of opioid antagonists to rodents results in an enhanced antinociceptive response to agonists.”

No, these are not religious denominations. As we have established in my Calling All Hens Stack an antagonist is something that fits into the recpetor site that would otherwise allow an opioid to slip into in order to block the opioid from filling that space but it also fills the role of not turning on that receptor’s function.

Nociceptive = stimulus causing pain.
Aunty Nociceptive = a pain in your Aunt…. no; strike that. Anti-nociceptive is something that works against a stimulus that causes pain.

Agonist = something that causes agony just like this shitty science papers that need a priest, a rabbi, a farmboy and a dictionary to sort out…. no; strike that…

an Agonist is something that makes something work the way it was intended. So an opioid receptor Agonist is an opioid, an opioid analog, or a substance natural to the body like an endorphin or enkephalin that turns that switch on.

Lettuce now try to wrap our pitiful little minds around the Pita Sanwich of the word-salad that we were given as just the FIRST SENTENCE of this absurd abstract.

FARM BOY VERSION:
When you give a LOT of drugs that block opioid receptors to micey-things, it boosts the pain-blocking effects of … what? OK, they’ve got me by the short hairs.

So far so good and why the hell didn’t they just say that in the first place? but it’s the last word that got me hung up. Agonist to PAIN RECEPTORS? which would be the noisy scepters… or agonist to the opioid receptors? Huge fucking difference. You would think with all of this ass-showing specific language for a minority class of people that have a snowball’s chance in hell of GETTING what you were saying that you might have been more specific about your specifics.

Now because I brag that I’m the Smartest Man That Ever Existed, I don’t want to tarnish that well-polished reputation (that I gave to myself), by looking stupid, but Homey don’t Do Stupid. The Agonist of my Agonist is not my friend. I’m not sure that I BELIEVE in this undefined Agonist. With the ambiguity of which Agonist they are referring to, I can’t be held responsible for knowing what they were thinking, vs. what they actually wrote.

Let’s try to go on to see if it gets any clearer than Loch Ness with the Beastie brushing up against us in the murk.

“We investigated the changes in spinal μ-opioid receptor signalling underlying this phenomenon.”

OK no help there so fart.

I find it curious that they are looking at the Mu-receptor in the spine. Most of my thoughts are always focused on the peripheral nerves so now I have another distraction of my attention to sort out. Mu binds with morphine, Delta and Kappa receptors bind with airplanes and sororities…. no; strike that. Delta binds with enkephalins and Kappa binds with ???

https://www.frontiersin.org/articles/10.3389/fphar.2022.837671 › full
Frontiers | The Kappa Opioid Receptor: A Promising Therapeutic Target ...
Jun 20, 2022 Kappa-opioid receptors (KOR) are widely expressed throughout the central nervous system [other sources include peripheral nerves], where they modulate a range of physiological processes depending on their location, including stress [bullshit non-science word], mood, reward [dopamine], pain, inflammation [cytokines?], and remyelination [cut off my legs and call me: Shorty. First time I’ve heard that one].

This is what happens when you’re a Data Dog digging down a rabbit hole and the ground collapses around you to reveal a Denver Airport complex of hidden bunkers that you had no idea existed.

I will issue a caveat here that since we’ve graduated to the SPINE that I have major concerns with clearing foreign substances like SYNTHETIC morphine once it gets implanted in the receptor sites. After we’re done here I’ll be issuing some cavair with some Ritz Crackers.

[Can I paws for a moment to have a Heart-to-Heart talk that I really hate doing this kind of work? I do it because I must, but I’d rather be talking about Flat Earth while having my back molars drilled without Anna Stezia.]

I’ll skip the techno-vomitus to get the point: They juiced Mickey and Minnie Mouse with naltrexone for a week, gave them a day off and then pulled their spines out like Predator taking a trophy to see what kind of changes happened.

Butt…. sorry kids, I can’t skip the “….increased the inverse agonist effect of naltrexone on cAMP accumulation.”

Yer gunna freak when you see this shit:
Adenylate Cyclase

Purified adenylate cyclase inhibits chemotaxis, chemiluminescence, and superoxide anion generation by monocytes and neutrophils in vitro, and in vivo it augments production of cyclic AMP from adenosine triphosphate in the phagocyte, resulting in an excessive accumulation of cyclic AMP and paralysis of the various phagocytic functions.

From: Plotkin's Vaccines (Seventh Edition), 2018

What they do is they hold out a promise:
This drug will help you with pain.
OK, doc, how does it work?
Well, it’s totally experimental but it decreases pain and inflammation.
Sounds great, doc, let’s give ‘er a try.

Butt Ewe Sea: One of the main contributions that Jordan gave to the world is the expose that the AlterNUTS claim that their gurujuice can dampen inflammation and boost immunity.

INFLAMMATION IS AN IMMUNE RESPONSE.

So what Plotkin of Vaccine Infamy showed was that instead of BOOSTING immunity the DRUG Naltrexone shut down the white blood cells. The ‘inflammation’ was not resolved because it had to have come from a source that provoked it. Like ALL allopathic abominations they MERELY SHUT OFF THE BODY’S REACTION TO A THREAT!

Let’s do this so that you can see it through Farm Boy eyes:

Purified adenylate cyclase inhibits chemotaxis,

Stops the cell signal for the firemen to come to the fire.

chemiluminescence,

How odd outside of a laboratory-created marker for them to study a biochemical reaction?

and superoxide anion generation by monocytes and neutrophils in vitro,

The religious hysteria over anti-oxidants ignores the fact that the ‘firemen’ show up to the ‘fire’ (infection) to fight FIRE WITH FIRE because the One Trick Pony of white blood cells uses super OXIDE to blast the invaders into the next dimension. Only AFTER the invaders have been disintegrated with phasers on KILL does the Super Oxide Dismutase break the still raging Peroxide fires down into things that can be changed into water by Glutathione. The firemens’ job ENDS with water - it does not start with water. What Plotkin against mankind is saying is that it shuts down the signal for white cells to show up, then it shuts down their ability to react.

and in vivo it augments production of cyclic AMP from adenosine triphosphate in the phagocyte, resulting in an excessive accumulation of cyclic AMP and paralysis of the various phagocytic functions.

FARM BOY VERSION:
Phage means eat. Cyte means cell. In the cells that would eat up all of the smoke and embers post-fire this same inhibitory process that took out the monocytes and neutrophils also takes out the phagocytes so that they just hang out like police during a smash and grab in a jewelry store in San Fran.

Farm Boy enough for yuh?

“In control rats, the inhibitory effect of DAMGO on cAMP production was antagonized by pertussis toxin (PTX) whereas, after chronic naltrexone, the effect became resistant to the toxin, suggesting a coupling of μ-receptors to PTX-insensitive Gαz subunits.”

Just so you know: A laboratory control is where you do NOTHING to the small cohort of test subjects set aside to gauge what happens when you do NOTHING instead of Something. So this is just shit science and even fraudulent reporting.

This is almost like high level Illuminutty-speak to get a point across to their initiates while leaving the rest of us in the dust.

Thanks God, for hyperlinks:
Enkephalin[2 Dextro Alanine 4 Methylphenylalanine 5 Glycine]
For example, DAMGO, an agonist, and CTOP, an antagonist, are selective for the μ-opioid receptors, whereas DPDPE, an agonist, is selective for the δ-opioid receptors.

From: Reference Module in Biomedical Sciences, 2014

FARM BOY VERSION:
So the Damn Go! slips into the opioid receptor site because it was MEANT to go in there and then you get an anti-pain effect.

So Damn Go! shuts down the formation of cAMP that we saw earlier would build up and paralyze the white blood cells. But PERTUSSIS TOXIN - you know: that poison they put in the DTP shot? - shuts down the shutting down of that process.

It’s like a double, double, double spy… So are they on your side? or the side of pain?

But then we get a double, double, double, double-agent when you juice someone with naltrexone so that even the poison used in vaccines to cause the diabetes epidemic worldwide doesn’t cause the immune system to attack its own host.

Interesting that they would use that poison. Interesting that they would tell us that. But the hyperlink for the word pertussis toxin brings us to:

Pertussis Toxin
Pertussis toxin (PT) helps organism evade host defenses and causes systemic manifestations;

From: Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases (Eighth Edition), 2015

Evade Host Defenses? How? Did I miss something in the double-double-double-double spy thing? Funny that the adenylyl cyclase thing was referenced by Plotkin in his Vaccine book and then the poison of the day is something that appears in vaccines as well while they are studying the effects of opioid pain killers?

Gettng a sense that Project Paperclip is bigger than you could have ever imagined that you are the Mouse inside the experiment and that their vaccine hollow cost was the Medical Manhattan Project that set off a bomb inside your Nuclear DNA?

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

“In control rats, the inhibitory effect of DAMGO on cAMP production was antagonized by pertussis toxin (PTX) whereas, after chronic naltrexone, the effect became resistant to the toxin, suggesting a coupling of μ-receptors to PTX-insensitive Gαz subunits.”

We’re trying to beat this tent peg into a nice tufted top since it really doesn’t want to go too deep into the ground. So much technical language precisely framed to give possible double-meaning so that only those who are in on the topic can possibly discern what was meant of it. All of that vaccine and Paperclip expose I posted above? They never expected anyone other than THEM to read past the:
…interaction of μ-receptors with Gα proteins (agonist-stimulated [³⁵S]GTPγS binding and immunoprecipitation of [³⁵S]GTPγS-labelled Gα subunits)…

so who cares if they gave away the Keys To The Kingdom? Nobody but us is reading this shit and nobody including us is qualified to even TRY to decipher this shit. But lets try to at least slay this one dragonian sentence:

FARM BOY VERSION:
After a week of naltrexone the opioid receptor site no longer triggered from the Pertussis toxin because the Mu opioid receptor got shorted to the some Agatha Christie bit thrown into the murder mystery novel at the last minute that we never heard of before!
whatinthehell is a Gαz subunit? If I can do my counter-counter-counter-spy thing again.

FARM BOY VERSION:
The natural process that was antagonized by the pertussis toxin was itself antagonized by the naltrexone. Or said another way the inhibition that the pertussis toxin incited was inhibited by the drug in question.

Is this accurate? I don’t know.
Does it matter? You’re damned skippy as you will see if you follow me and Mengele to the end.

“Such changes in opioid receptor signalling can be a double-edged sword. On the one hand, they may have potential applicability to the optimisation of the analgesic effects of opioid drugs for the control of pain. On the other hand, they represent an important homeostatic dysregulation of the endogenous opioid system that might account for undesirable effects in patients chronically treated with opioid antagonists.”

Here’s the part that I can’t rectify (rectum fried?):

They are saying that the use of a synthetic opioid that shuts down the addiction/craving for opioids might/possibly/kinda make the pain relief from OPIOIDS work better. Unless I’m just suffering from high falutin’ word fatigue.

Butt on your other hand (should have wiped) if you do that then it will FUCK UP YOUR ENDOGENOUS = normal natural to your body Opioid system = endorphins and enkephalins in people who are ADDICTED TO (say it like it is then there is no debate) the PHARMACEUTICAL drugs that are supposedly helping them get off their addiction to Pharmaceutical and/or Street drugs?

We can only close with what the Profit Ms. MaGoo told me a Decade Hence:
“You can’t Doctor and Do Natural at the same time.”
Meaning that pharmaceuticals and natural therapies don’t mix.
We can expand that meaning to be that allopathy and the natural functions of the human body don’t mix neither.

VACCINEFRAUD 1

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