Porcine Stress Syndrome and Excited Delirium Syndrome

My focus is on helping Law Enforcement and First Responders. There has been a ton of negativity directed at Law Enforcement even before the BLM movement. I believe it is a direct result of their training involving TASER use. They are trained to believe the TASER works 100% of the time. They even have a video of it dropping a large bovine bull. This has led to the TASER being used as a tool of compliance instead of a tool of incapacitation. When a subject does not comply, they simply apply it again and again. Now there is such negativity directed towards TASER use they are using lethal force, another publicly perceived negative. I would like to implore Law Enforcement to have another look at how they deal with non-compliant subjects. 

I have done significant research into Excited Delirium Syndrome (EDS) and have found what I believe to be a direct link between Porcine Stress Syndrome (PSS) and EDS.

 I have studied and researched Excited Delirium Syndrome (EDS), Porcine Stress Syndrome, Capture Myopathy and PTSD. It has been asserted by Dr. Deborah Mash of the University of Miami that Excited Delirium is a brain disease and possibly linked to one gene. My theory is that all of the above listed conditions are either related or similar enough in presentation to warrant a change in negative practices that are in place to deal with agitated and/or violent behavior with unknown etiology. The signs and symptoms of EDS, Capture Myopathy and Porcine Stress Syndrome (PSS) are strikingly similar: easily excitable, hyperthermia, abnormal breathing, skin discoloration, muscle tremors, abnormal vocalization and death in the presence of “rough handling” and stressors. Based on what I have been able to look up, those individuals afflicted with extreme cases of PTSD have what is termed psychotic events. I am currently researching through an acquaintance with a background in neurological sciences in the military if these extreme cases of PTSD also have other physical manifestations that are similar to the other models I have found that are representative of humans, domesticated livestock and wild animal populations.

In swine they have isolated one gene, known as a stress gene (officially trademarked as Hal-1843 by* **University of Toronto Innovations Foundation* due to Halothane sensitivity), that has historically been a high frequency finding in non ambulatory and/or DOA swine post transport to slaughter. Dueto aggressive identification and eradication practices, the occurrence of this gene is on a decline. It still makes up a major percentage of non-ambulatory and DOA swine on arrival at the slaughter facility and was found in roughly 11% of swine producing farms that participated in a 2006 study. Not only is there similarities in how EDS and PSS physiologically manifest as a response to stress, there is also a possible link with Halothane sensitivity. A small percentage of human test subjects presented with hyperthermia after being anesthetized with halothane. Though I was not able to determine any other side effects  that were observed during this particular study, it deserves further research. Halothane anesthesia in stress gene identified swine also present with signs and symptoms of PSS (hence, the naming of that gene).

  In wild animal populations, it has been discovered that in certain geographic locales that there is a much higher incidence of death when attempting to relocate the animals. Efforts to reduce death have included changing relocation attempts to cooler seasons, nutrient and vitamin supplements and the aggressive use of sedatives post capture.

   All of this brings reason to ponder:   

1.  Is it possible that the stress gene in found humans and swine interferes or is triggered by dopamine and excess epinephrine causing the massive breakdown at the cellular level that is similar to the cascade of events caused by sepsis in the fatal stages.  

 2.   With this line of reasoning, could CNS stimulants be simply be facilitating an “animal” response in humans, i.e.; super strength, animal noises, reaction to reflections…?   

3. Could this same gene impact the uptake and use of selenium and vitamin D which help protect cell wall integrity?   

4. Has there been any finding of accelerated rigor in subjects dying from EDS or PTSD? This has been one of the observations of death in PSS.   

5. What if the two genes are one and the same?