Georgia Hunter said...
Psilociraptor said...
GH that's certainly an interesting perspective. That would certainly be part of it, but a herxheimer in theory at least should encompass all aspects of immunity that the endotoxin (or endotoxins) would engender including adaptive immunity. Hence why things like autoimmune arthritis and CIDP can worsen as well. Though oxidative stress clearly goes hand in hand
Mustard seed - i agree. in buhners defense though i think people expect too much out of him so he just makes up answers as a best guess. as for herxing, whether immunological mechanisms or direct lysis by the antimicrobial is involved the end result is similar. dead spirochetes. the sorts of autoantibodies produced that contribute to symptoms are also bacteriocidal. The issue is simply that an equilibrium has been established between the death of spirochetes through antibody secretion and their persistence through immunosuppression. so a raise in immune function would essentially accomplish the same thing as a herx. either the direct secretion of more antibody and immune effectors, better recognition of the bacteria and secretion of antibody and immune effectors, or the lysis of bacteria followed by enhanced recognition and secretion of antibody and effectors. I think why people don't stop herxing often has to do with how much they're taking. I've found that at some of the recommended doses herxing can become catalytic whereas if i stay just above the threshold it goes away in about 3 days. Think of it this way... you kill the bacteria at a high dose. This relieves immune suppression and leads to release of antigens, which leads to recognition and secretion of antibody. This is your herx (the things GH stated also apply of course). But the release of effector molecules leads to more dead borrelia which leads to more antigen which leads to more detection which leads to more secretion of antibody ad nauseum. Herxes might become cyclical if the dose is sufficient that the herx itself kills more bacteria and stimulates more herxing. Just a thought on why low doses might be better in theory. It's certainly made a world of difference to me.
Studies have shown that endotoxins are not responsible for all herxes. They are present in most herxes, but it is believed that tumor necrosis factor is responsible for herxes. I described the process of how herxes happen but I just didn't name endotoxins, tnf, or IL-1B. What comes first, the chicken or the egg? I say the cytokines cause the problems and the endotoxins make it worse. I say this because studies have been able to prevent herxes by giving anti-tnf and blocking cytokines like IL-1B. There have also been experiments where herxes occurred and no endotoxin was present. My feelings are that herxes are bad for us and the oxidative stress they cause is harmful long term. I think more herxes come from cell wall deficient bacteria than anything else. They live in the extracellular matrix, in leukocytes, and in other phagocytic cells. The sicker you are, the more bacteria you have to deal with, both in numbers and variety.
Borrelia is pretty easy clear from the blood stream. A low grade temperature for a few days will do it. They are just so adaptable that they'll be back because reducing them in the blood and eliminating them are two entirely different things. So to have a herx, we must hit many more pathogens than normal to overload our pathways. I can herx from crying, flying, running, abstaining from fats, or if I wanted to literally kill myself, take 20 drops of cryptolepis. This tells me that I am
opening up a compartment where these pathogens live and by gaining access to them, I can kill them.Cytokines come downstream of endotoxins. If a study says no endotoxins are present they are probably strictly referring to LPS and not the greater range of PAMPs that are necessary to stimulate inflammation. Spirochetes are generally void of true endotoxin so this wouldn't be a shock. I've never been a fan of limiting the term "endotoxin" to one particular immunogen but it is what it is. It isn't so much chicken or egg but quite linear as far as things can be in biology. PAMP->PRR activation->cytokine release->innate immunity->adaptive immunity. Endotoxins and PAMPs are toxic quite literally for their effects on causing inflammation. The two are not separate issues. My only point was to say that in addition to all that ROS you have to include everything downstream as well which includes autoantibodies. I have autoimmune neuropathy which gets profoundly worse with treatment. Sure that's anecdotal but it's consistent. The reason biologics work is because they block everything downstream of cytokine activation. That doesn't mean cytokines are the source of the chain of events. They have to be activated by something and there are numerous "pathogen-associated molecular patterns" analogous to endotoxins to do it.
Post Edited (Psilociraptor) : 7/2/2017 11:15:35 AM (GMT-6)