I came across this very interesting Korean paper that very much scores points for the toxic stress hypothesis of misnamed and misnomered HIV/AIDS.
Expression of exosomal and cellular microRNAs: as biomarkers for toluene, ethylbenzene, xylene (TEX) exposure
What's interesting about the VOCs that they mention is that toluene is heavily implicated in the gay fastlane lifestyle behavior straight out of Stonewall and into the the 1980s. People like John Lauritsen and Mark Conlan talk about this toxic factor.
This paper is showing how exosomes biomark these toxicants. Essentially these toxins(not an exoviral agent) are what induce Gallo positivity and eventually what is called aids. My own view is that what is called HIV/AIDS is really a bioenergetic morphostatic breakdown triggered by oxidation as well as thymus/thyroid breakdown. These VOCs are part of an overall oxidation process as the Perth Group correctly predicts.
When you combine the ideas of The Perth Group, Jamie Cunliffe and Ray Peat with assists from papers such as the above you begin to see a much clearer picture of what this actual infection and disease is. I think Gallo and Montangier did discover something but it was likely an endogenous derivative of exosomal processes. There probably is some kind of infection(of toxic disease vesicles) but it is what I would call a broad quantitative infection not a singular acute qualitative one.
Any thoughts?
Expression of exosomal and cellular microRNAs: as biomarkers for toluene, ethylbenzene, xylene (TEX) exposure
What's interesting about the VOCs that they mention is that toluene is heavily implicated in the gay fastlane lifestyle behavior straight out of Stonewall and into the the 1980s. People like John Lauritsen and Mark Conlan talk about this toxic factor.
This paper is showing how exosomes biomark these toxicants. Essentially these toxins(not an exoviral agent) are what induce Gallo positivity and eventually what is called aids. My own view is that what is called HIV/AIDS is really a bioenergetic morphostatic breakdown triggered by oxidation as well as thymus/thyroid breakdown. These VOCs are part of an overall oxidation process as the Perth Group correctly predicts.
When you combine the ideas of The Perth Group, Jamie Cunliffe and Ray Peat with assists from papers such as the above you begin to see a much clearer picture of what this actual infection and disease is. I think Gallo and Montangier did discover something but it was likely an endogenous derivative of exosomal processes. There probably is some kind of infection(of toxic disease vesicles) but it is what I would call a broad quantitative infection not a singular acute qualitative one.
Any thoughts?