Through the CCR5 pain mu-opiod receptor, Kratom is shown to have potential to inhibit CCR5 pathway

December 18th, 2023

Awake Goy

We have been infected with the CCR5 gene, which has given the Transhumanists an open door to shove any poison they want into our bodies. ¹ CCR5 also enhances our addictions, our fears, our emotional distress, ven effects how we respond to electromagnetic frequencies. CCR5 is even required to infect us with the Clathrin GQD neural interface. ²

We’ve discovered a plant named Kratom, which might hold the answer to shutting the door on this GQD Transhumanists Agenda assault against us.

According to the National Institute on Drug Abuse (NIDA) ³, Kratom is an herbal substance that can produce opioid and stimulant-like effects in users. Kratom comes from the leaves of an evergreen tree (Mitragyna speciosa) grown in Southeast Asia and is generally sold in liquid or powder form—think capsules, infused in beverages, and eaten raw.

The Food and Drug Administration (FDA) has yet to release approved medical uses for kratom, but some Americans have reported using the supplement as energy booster, mood enhancer, pain reliever and sedative.

Several US States have banned this herbal supplement called Kratom: ⁴

Current research, Sepetember 2023, indicates that Kratom is a powerful antioxidant and anti-inflammatory and natural antibiotic. ⁵

“fermented kratoms showed significant antibacterial activity against the tested pathogens and antibiofilm formation by S. aureus and MRSA. Furthermore, the eradication of established biofilms of fermented kratoms was observed in S. aureus (day 2, 50 mg/mL) and E. coli (day 2, 100 mg/mL and day 4, 50 mg/mL). To the best of our knowledge, this study is the first to report that fermented and non-fermented kratoms could be nutraceutical sources of antibacterial, antibiofilm, antioxidant, and anti-inflammatory substances against related diseases.”

It also has a protective effect against Metabolic Syndrome, a condition: Metabolic syndrome is a cluster of conditions that occur together, increasing your risk of heart disease, stroke and type 2 diabetes. These conditions include increased blood pressure, high blood sugar, excess body fat around the waist, and abnormal cholesterol or triglyceride levels. Similar conditions are associated with exposure to high EMFs. ⁶ ⁷

The Kratom plant produces indole and oxindole alkaloids. ⁸

“Dry leaves of kratom (mitragyna speciosa) are anecdotally consumed as pain relievers and antidotes against opioid withdrawal and alcohol use disorders. There are at least 54 alkaloids in kratom; however, investigations to date have focused around mitragynine, 7-hydroxy mitragynine (7OH), and mitragynine pseudoindoxyl (MP).” ⁹ ¹⁰

It’s a MU OPIOD receptor. ¹¹

“Pain accompanies rheumatoid arthritis and other chronic inflammatory conditions and is difficult to manage. Although opioids provide potent analgesia, chronic opioid use can cause tolerance and addiction. Recent studies have demonstrated functional interactions between chemokine and opioid receptor signaling pathways. Reported heterodimerization of chemokine and opioid receptors led our group to develop bivalent compounds that bind both types of receptors, with the goal of targeting opioids to sites of inflammation. MCC22 is a novel bivalent compound containing a CCR5 antagonist and mu opioid receptor (MOR) agonist pharmacophores linked through a 22-atom spacer. We evaluated the efficacy of MCC22 in the K/B.g7 T-cell receptor transgenic mouse model of spontaneous inflammatory arthritis.” ¹² ¹³ ¹⁴

Indole acts to inhibit Quorum Sensing signal in bacteria. ¹⁵

Kratom’s major alkaloid, mitragynine. ¹⁶ ¹⁷ ¹⁸

BINGO.

“Drug abuse has major implications on the prevention and treatment of human immunodeficiency virus (HIV). Use of the opioid morphine has been observed to accelerate the onset of HIV infection through the up[1]regulation of chemokine receptor CCR5, used by the HIV virus to infect host cells. Recent studies have shown the mu opioid receptor (MOR), which is bound by morphine, forms a putative MOR/CCR5 heterodimer. This could revolutionize treatment options for opioid addicted HIV patients. Current treatments involve simultaneous opioid substitution therapy and HIV antiretroviral agents, but this treatment regime has been observed to have an adverse drug-drug interaction. Further characterization of the MOR/CCR5 heterodimer should be performed to explore the possibilities of the simultaneous treatment of opioid dependence and HIV infection.

“Opioid substitution and antiretroviral therapies have steadily increased the life spans of AIDS patients with opioid addiction, while the adverse drug–drug interactions and persistence of HIV-associated neurocognitive disorders still require new strategies to target opioid abuse and HIV-1 comorbidities. A bivalent ligand 1 with a 21-atom spacer was thus synthesized and explicitly characterized as a novel pharmacological probe to study the underlying mechanism of opioid-enhanced NeuroAIDS. The steric hindrance generated from the spacer affected the binding affinity and Ca²⁺ flux inhibition functional activity of bivalent ligand 1 at the chemokine receptor CCR5 more profoundly than it did at the mu opioid receptor (MOR). However, the CCR5 radioligand binding affinity and the Ca²⁺ flux inhibition function of the ligand seemed not necessarily to correlate with its antiviral activity given that it was at least two times more potent than maraviroc alone in reducing Tat expression upon HIV-1 infection in human astrocytes. Furthermore, the ligand was also about two times more potent than the simple mixture of maraviroc and naltrexone in the same viral entry inhibition assay. Therefore bivalent ligand 1 seemed to function more effectively by targeting specifically the putative MOR–CCR5 heterodimer in the viral invasion process. The results reported here suggest that a properly designed bivalent ligand may serve as a useful chemical probe to study the potential MOR–CCR5 interaction during the progression of NeuroAIDS.” ¹⁹ ²⁰

“Toxicities typically occur when the ingested dose exceeds 8 grams. Multiple organ systems are at risk for injuries related to kratom use, with hepatotoxicity, seizure and coma, lung injury, kidney injury, and cardiotoxicity being reported.” ²¹ ²² ²³

“Among the symptoms of COVID-19 fever, general malaise, pain and aches, myalgia, fatigue, and headache can affect the quality of life of patients, even after the end of the acute phase of the infection and can be long lasting. The current treatment of these symptoms, also because COVID-19 patients have been asked not to use non-steroidal anti-inflammatory drugs (NSAIDs), in particular ibuprofen are often unsatisfactory. Among the above mentioned symptoms malaise and fatigue seem the most difficult to treat. In this case report we describe the use of kratom (Mitragyna speciosa) by a patient with confirmed COVID-19 infection. What we observed was a fast and sustained relieve of the above mentioned symptoms.” ²⁴ ²⁵

It contains Chloroquine. ²⁶

“Kratom contains a special compound known as chloroquine or Cq, that research shows is powerfully combative against the coronavirus. There are many viruses that can be harmful to humans and Cq could be a type of master key that protects against all of them.” “In addition, he said it was reported from researchers in Wuhan that Chloroquine (Cq) can be used for the treatment of patients with Covid 19.”

“Recent studies have suggested that C-C chemokine receptor (CCR) 5 interacts with μ-opioid receptor and modifies a nociceptive reaction. We examined effects of CCR5 deficiency on pain responses by employing CCR5 knockout (KO) mice. We found that pain responses of CCR5 KO mice to chemical or inflammation stimuli were milder than those of CCR5 wild type (WT) mice.” ²⁷

CCR5 is linked to pain!

When Kratom derived chemicals bind to mu-opioid receptor the opioid receptor binds to CCR5. It creates a dimer (two proteins bound together on the membrane).

You see, when Kratom binds to the mu-opioid receptor on the cell membrane it causes a change in shape on the CCR5 receptor (separate receptor/protein). This is called a conformational change (the CCR5 receptor is still there it just morphed into another shape). When a protein receptor changes shape its original function may also change and although Kratom may or may not inhibit the CCR5 function it did something? There is nothing in the literature about what happens to the CCR5; was it blocked or not? What they do know is that the binding of Kratom causes pain and inflammation to diminish, the opposite of what CCR5 (if activated) would do.

So, is this statement correct: ; “Through the CCR5 pain mu-opioid receptor, Kratom is shown to have potential to inhibit CCR5 pathway”… Possibly?