My favorite theory about the pathology/cause of floxing (of course, fluoroquinolone use is the CAUSE of floxing, but not all people who use fluoroquinolones get floxed – something goes horribly wrong in the bodies of the people who do), is that a neurotoxin is produced by the damaged bacteria within the body and that neurotoxin is the actual cause of the health problems that Floxies experience. More information on this theory can be found on https://floxiehope.com/2013/06/20/test-post/ and at the bottom of this page.
This theory, that neurotoxins are produced when fluoroquinolones mess up the bacteria, makes me think about a lot of things. One of these things is our meat.
Fluoroquinolones are used rampantly in agriculture, even though there has been some regulation limiting their use. If fluoroquinolones cause the production of neurotoxins, could it be possible that these neurotoxins are in the flesh of the animals that are exposed to fluoroquinolones – the meat that we eat? If so, what are the health consequences of this to the humans who eat that meat?
I believe that meat is tested for antibiotics and other agriculturally utilized pharmaceuticals before it goes to market, but if the meat is actually contaminated with a neurotoxic byproduct of the pharmaceutical, as opposed to the pharmaceutical itself, then maybe the wrong thing is being tested for. Is our meat contaminated with neurotoxic byproducts of fluorquinolone antibiotics? I don’t know, but it’s something that is definitely worth looking into.
Admittedly, this line of thinking involves a lot of unproven jumps and assumptions, but I don’t think that I’m being completely unreasonable. The theories described below seem more than reasonable, they seem right, and I think that looking into the health consequences of eating meat that is from animals that have been floxed is something that we should do. Question everything. It’ll keep you safer and make you smarter.
There are many good reasons not to use fluoroquinolone antibiotics on livestock animals. Antibiotic resistance is becoming a bigger and bigger problem and the thought that we may be breeding antibiotic resistant bacteria in our feedlots is appalling. This problem, though not without controversy, is generally acknowledged and some regulation is being put into place to try to prevent an atrocity from happening. However, humans are slow to change the status quo unless there is an emergency and I doubt that real, meaningful regulation will come about until an antibiotic resistant bacteria is bred in feedlots and that bacteria infects people. Antibiotic use in livestock also enables ranchers to keep their animals in dirty, unsanitary, inhumane conditions – something that is also appalling. Even though I haven’t done a whole lot of research into the topic, I think that with the research that has been done, we can add potential contamination with neurotoxic byproducts to the list of reasons that antibiotics generally, and fluoroquinolones specifically, should not be used in livestock.
I like meat and I eat it, but I’ve tried to exclusively consume organic meat since I got floxed. I’m going to try harder now. I suggest that you do the same.
Is a neurotoxin produced by the damaged/bad bacteria after exposure to fluoroquinolones (or the die-off of the “good” bacteria that keep the bad ones in check)? There are several interesting things noted in Beyond Antibiotics by Michael Schmidt. Dr. Schmidt points out that both tartaric acid and tricarbalyte are noxious compounds produced by bad gut bacteria when good gut bacteria in the gut are not available to keep them in check. Tartaric acid “is a known poison of the energy system of mitochondria,” and tricarbalyte “binds to magnesium and may reduce the availability of dietary magnesium.” (pages 28-29) Dr. Schmidt also says that antibiotics cause the production of clostridiam which is a known neurotoxin producing organism (p. 44). And, on page 47 he says, “Whever a CPY enzyme is blocked or slowed, its ability to detoxify other drugs can be impaired.” My thought on this is that the fluoroquinolones slowed our CPY enzymes then the NSAIDs, steroids, other toxins in our system, did other damage – and maybe that’s why each of us have so many different symptoms.
Also, John Travis reported in Science News (July 2003;164) that research performed by John F. Prescott found that certain antibiotics, such as the fluoroquinolones, the class of antibiotics that includes the name-brands and generic brands of Levaquin[R], Cipro[R], Tequin[R], and Avelox[R], actually are known to trigger a type of virus called bacteriophages (viruses that can infect bacteria) to change the genetic sequencing of the bacteria, causing the bacterium they have infected to start producing toxins. These viruses can act as genetic delivery vans, invading bacteria, such as spirochetes, often lying dormant, until activated by a change in the host (your body’s) environment. Once activated, these viruses insert their toxin-generating genes into the bacterial chromosomes. These viruses can turn basically harmless bacterium into killers through this genetic sequencing of toxins (Travis 2003). Not only are these toxins released through bacteria die-off and not only can antibiotics actually increase the production of the toxins, but these viruses can cause the bacteria to rupture, spilling their toxins into the body (Waldor 2004). http://www.benbrew.com/lb/lyme5.pdf
* I haven’t had the time to do a whole lot of research into this theory, so if anyone has any articles about it, please forward them on to me.