Dr Michael Levin Dr Mark Bailey connecting cellular ionic bonds to the "emergent" ionic performance of ivermectin and fenbendazole

Not medical advice.

I connect several intriguing concepts: the potential ionic interactions of fenbendazole and ivermectin, the role of bioelectricity in disease as proposed by Michael Levin, and the critique of viruses as primary disease agents posited by Dr. Mark Bailey https://youtu.be/9vl-mAIhGx0?si=bNBFNueAnL5raIWN. These connections suggest that both drugs and bioelectric interventions might address fundamental ionic imbalances or disruptions in cellular signaling, rather than targeting "viruses" or "cancers" directly as traditionally understood.

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Key Ideas and Connections:

1. Fenbendazole and Ivermectin’s Ionic Interactions

Both fenbendazole and ivermectin are antiparasitic drugs with noted off-label uses, particularly in experimental cancer treatment and, controversially, in viral infections:

Fenbendazole disrupts microtubule dynamics by binding to tubulin, affecting cellular structure and potentially ionic flow within cells. This could influence cancer cells by restoring normal signaling or inducing apoptosis (programmed cell death).

Ivermectin binds to glutamate-gated chloride ion channels in parasites, causing paralysis. In mammalian systems, it has been proposed to alter ionic channels and disrupt viral replication, possibly by interfering with cellular ion homeostasis.

2. Bioelectricity and Cellular Signaling

Michael Levin’s research highlights that ionic gradients—flows of charged particles across cell membranes—are crucial for maintaining cellular identity and behavior. Disruptions in these gradients can cause diseases like cancer or result in cellular "miscommunication".

If fenbendazole or ivermectin restores ionic balance in stressed or cancerous cells, this aligns with Levin’s findings that correcting bioelectric signaling can reverse pathological states.

3. Challenges to Viral Theory

Dr. Bailey’s argument questions whether "viruses" are the root cause of disease, suggesting that cellular stress or ionic imbalance might explain observed effects attributed to viruses. If true, the actions of fenbendazole and ivermectin might reflect ionic rebalancing rather than antiviral activity.

For instance, symptoms labeled as "viral" could result from systemic ionic disruptions that these drugs alleviate.

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Unified Hypothesis:

1. Diseases as Ionic Dysregulation:

Both cancers and "viral infections" might result from disrupted ionic environments in cells rather than specific pathogens or mutations.

Fenbendazole and ivermectin could function by interacting with cellular ion channels or microtubule structures to restore ionic homeostasis, leading to remission or resolution of symptoms.

2. Reframing Treatment:

Traditional views hold that fenbendazole and ivermectin target pathogens or tumor cells. However, their mechanism might instead involve correcting deeper bioelectric or ionic imbalances that underlie various diseases.

This ties to Levin's theory: if disease originates from cellular miscommunication due to ionic disruptions, targeted ionic interventions could have wide-ranging therapeutic effects.

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Potential Implications:

If these ideas hold, they could revolutionize medicine by shifting focus from targeting specific "pathogens" or genetic abnormalities to restoring fundamental cellular signaling. Bioelectric therapies, alongside drugs like fenbendazole and ivermectin, could represent a new frontier in addressing diseases ranging from cancer to chronic infections.

Further research would need to:

1. Establish how these drugs specifically affect ionic signaling in both healthy and diseased cells.

2. Demonstrate whether bioelectric and pharmacological interventions can universally address diseases attributed to "viruses" or "cancer."

I'm suggesting that the ionic mechanisms underpinning diseases and the effects of these treatments warrant DEEPER exploration.

Addendum:

Building on the discussion of ionic bonds and their role in cellular repair, it is worth exploring how glucagon-like peptide-1 (GLP-1) may indirectly influence these processes. While GLP-1 primarily acts through receptor-mediated pathways to regulate metabolic functions, its ability to modulate ion channels and restore ionic pathways may be a crucial factor in its broader cellular effects. Activation of GLP-1 receptors triggers signaling cascades, such as the cAMP-PKA pathway, which regulate voltage-gated potassium and calcium channels, thereby stabilizing membrane potential and correcting disrupted ionic pathways. This stabilization could enhance cellular repair mechanisms, creating a more favorable environment for restoring ionic bonds within cells. I propose that this indirect correction of ionic pathways is the primary mechanism underlying GLP-1's therapeutic effects, offering new insights into how this drug supports cellular health and mitigates pathogenic behavior in damaged or stressed cells.

I further expand on potentially correcting depression permanently thru ionic therapy instead of SSRI.