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Cell danger response: EPM or PNE?

The cell danger response (CDR) is a universal response to environmental threat or injury. Once the CDR is triggered, healing can’t be completed until each stage is reset to the readiness baseline. The complicated pathway is a stepwise path to survival and ultimately healing. The CDR is regulated by mitochondria, the energy producing organelles in cells.

The CDR can change thoughts and behavior, childhood development, physical fitness and resilience, fertility, and even a populations susceptibility to disease. That means the tiny, powerful mitochondria connect cell health to environmental health. The result of overwhelming chemical pollutants is that 90% of adults over 65 live with chronic illness, 60% of adults, 50% of teens and 40% of children. And the pathways of the CDR affect your horses response to infectious diseases such as sarcocystosis, (S. neurona).

Mitochondria respond to chemical, physical, and infectious threats by changing their structure and function. The changes they make signal safety or danger in a cell. One cell signals nearby cells thereby transmitting responses throughout the organism. Changes in the mitochondria alter gene expression, trigger a healing response, and even adjust an organisms susceptibility to chronic illness. Once the CDR is triggered, an organism resets the cell to optimize survival and hopefully completes the cycle to a reset that allows healing.

Of the many stereotyped responses to danger, the most important to Pathogenes, is the activation of innate immunity. The only way to turn off or reset the CDR is sending an “all clear” signal; until then the CDR pathway is stuck in a repeating loop that blocks further healing as an attempt to eradicate perceived danger. This is one explanation for the by-stander mechanism.

Once treatments to reset the CDR are proven effective it is believed that the body can heal itself. The CDR guru is Dr. Robert Naviaux, you can listen to a presentation.

Our experiments with ALS support the idea that dysregulated ATP causes mitochondrial stress and result in a loop of pro-inflammatory responses. The good news is that these responses are targetable and reversible. The positive response to effective therapy is clinically apparent in days. These concepts underlie our approach to polyneuritis equi. Our idea is to target multiple pathways resetting the delicate responses back to safety. Sometimes the system is hypervigilant, even when the “all clear” is signaled the cells are ready for another danger signal. That means the animal with hypervigilant responses should be monitored and treated before serious damage is done.