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Fluoroquinolone antibioitics, including Cipro (ciprofloxacin)

Is getting "floxed" (potentially life-ruining side effects from Cipro or other fluoroquinolone antibiotics) simply another version of Poison/"Vitamin A" toxicity?  There is the distinct possibility of that.

First, it has been shown that Cipro decreases the rate of ethanol (aka alcohol) elimination/detoxification/metabolism by 10% specifically by reducing the number of specific types of bacteria in the gut that contain aldehyde dehydrogenase (aka retinaldehyde dehydrogenase) and alcohol dehydrogenase (aka retinol dehydrogenase)...this would mean that it also decreases the rate of Poison/"Vitamin A" breakdown in an extremely similar way:

Ciprofloxacin decreases the rate of ethanol elimination in humans

BACKGROUND—Extrahepatic ethanol metabolism is postulated to take place via microbial oxidation in the colon, mediated by aerobic and facultative anaerobic bacteria. 
AIMS—To evaluate the role of microbial ethanol oxidation in the total elimination rate of ethanol in humans by reducing gut flora with ciprofloxacin. 
METHODS—Ethanol was administered intravenously at the beginning and end of a one week period to eight male volunteers. Between ethanol doses volunteers received 750 mg ciprofloxacin twice daily.
RESULTS—A highly significant (p=0.001) reduction in the ethanol elimination rate (EER) was detected after ciprofloxacin medication. Mean (SEM) EER was 107.0 (5.3) and 96.9 (4.8) mg/kg/h before and after ciprofloxacin, respectively. Faecal Enterobacteriaceae and Enterococcus sp. were totally absent after medication, and faecal acetaldehyde production capacity was significantly (p<0.05) decreased from 0.91 (0.15) to 0.39 (0.08) nmol/min/mg protein. Mean faecal alcohol dehydrogenase (ADH) activity was significantly (p<0.05) decreased after medication, but ciprofloxacin did not inhibit human hepatic ADH activity in vitro. 
CONCLUSIONS—Ciprofloxacin treatment decreased the ethanol elimination rate by 9.4%, with a concomitant decrease in intestinal aerobic and facultative anaerobic bacteria, faecal ADH activity, and acetaldehyde production. As ciprofloxacin has no effect on liver blood flow, hepatic ADH activity, or cytochrome CYP2E1 activity, these effects are probably caused by the reduction in intestinal flora. 

A gigantic article connecting the fluoroquinolone side effects as being suspiciously similar to Poison/"Vitamin A" toxicity (there are no coincidences), unfortunately the author is still sold on the idea that Poison/"Vitamin A" being needed biologically:

Vitamin A (Retinoid) Toxicity and Deficiency: A Role in Thyroid Disorders, Fluoroquinolone Toxicity, ME/CFS, Sjogren’s Syndrome, and More?

Review of Similarities of Accutane/Isotretinoin and FQ [FluoroQuinolone] ADRs

Both classes of drugs appear to cause or trigger a similar set of systemic “side effects” involving musculoskeletal, neurological, CNS, ocular, and in particular, sicca (severe dryness) symptoms.   These possible side effects are well described by the drug manufacturers, the FDA, and the patients themselves.

Both classes of drugs are anti-neoplastic (anti-cancer) drugs, especially in higher concentrations.

Both classes of drugs are given to millions of people of all ages every day without cancer.

Both classes of drugs have one or more Black Box Warnings on them to warn of these severe side effects.

Most people appear to take both classes of drugs without incident, but for an unknown percentage of people, severe side effects can occur.

For both classes of drugs, the actual number of people who experience severe side effects is actually unknown, due to poor recognition, acknowledgement, and reporting by the medical profession and the FDA.

For both classes of drugs, side effects can start immediately, or be delayed weeks, months, and possibly years.

For both classes of drugs, there appears to be a “cumulative threshold” level which, once crossed, can result in severe systemic side effects.

For both classes of drugs, these “side effects” can be permanent.

For both classes of drugs, these permanent side effects can be devastating and catastrophic for quality of life.

For both classes of drugs, FDA hearings on the safety of these drugs occurred due to consumer/patient complaints about the side effects.

For both classes of drugs, some brands/versions of the drugs have been either discontinued voluntarily or were forced to be pulled from the market due to the side effects.

For both classes of drugs, lawsuits abound as a result of their “side effects”.

Both classes of drugs remain on the market.   However, one major difference between Isotretinoin and FQs is that within the US, there are much stricter prescribing restrictions on Isotretinoin due to severe birth defects as one of the “side effects” of Isotretinoin.  This has resulted in the “iPledge” program for Isotretinoin in an attempt to prevent this particular side effect.

The following is worth reading as well, which is from the same site:

Additional Mechanisms to Consider

These started out as notes to myself to keep in mind. So the information here isn’t very organized. The information on this page and the next couple of pages is more for people interested in looking deeper into mechanisms to consider for research.

All of these are strong contenders on my list as unintentional targets of FQ’s. These listed areas of focus, with all their related cascade of mechanisms, probably encompass a million or more places to look for actual FQ binding and FQ induced damage, whether that’s genomically or metabolically. So I’m under no illusion that finding where the problem(s) are is simple. However, given the billions of places in the body for potential FQ induced damage to occur, this does narrow it down a bit, even if only to “ a million” places to look.
Steroid Super Family Receptors/ HRE’s (with a side of Neural Crest Cell Derivatives):  I believe the FQ’s are severe endocrine disrupters, and these receptors and hormone response elements, or their common pathways, may be unintentional targets.  I’ve discussed this concept several times throughout this document.  As one example, the retinoid X receptors (RXR) serve as a common important partner for many other nuclear receptors, including thyroid hormone, Vitamin D/Calcitriol, Retinoic Acid (Vitamin A), Pregnane X/Steroid and Xenobiotic Sensing, Peroxisome Proliferator transcription factors for metabolism of carbohydrates, lipids, and proteins, Liver X regulators of cholesterol, fatty acid, and glucose homeostasis, Bile Acid receptors, and more.   A quick look through Nuclear Receptors, RXR and the Big Bang shows how intertwined the thyroid and steroid hormones are with vitamins, amino acid, carbohydrate, fatty acid, glucose, and xenobiotic metabolism just via RXR alone.   Many of my symptoms seem to read like a road map of neural crest cell (NCC) derivatives (See Wiki Neural Crest, and scroll down to “Cell Lineages” [Cranial, Trunk, Vagal, Cardiac] and “Neural Crest Derivatives” [Mesectoderm, Endocrine, Peripheral Nerves, Melanocytes].  Note how NCCD’s make up the connective tissue of the head and neck glands [thyroid, pituitary, thymus, salivary, lacrimal], tendons of ocular and masticatory muscles, dental related cells, peripheral nerves including of the head and neck, the catecholamine releasing chromaffin cells of the adrenal medulla, calcium regulating parafollicular cells of the thyroid, oxygen/carbon dioxide and pH sensing glomus cells in the carotid and aortic bodies, etc.   Also note that paraganglioma-like symptoms are high on my differential list for my “flares”, either as a pathological process or as an appropriate compensatory response for problems elsewhere  [scroll to “Horrible Flare“; here I consider mitochondrial succinate and aKG area] ).   In Topoisomerases – The Obvious Targets, I ask the question, what underlying factors do these NCC’s continue to have in common in the adult despite being differentiated?  RXR genes (1) may be one such example.  Interestingly, one of the many adverse effects of Isotretinoin, which has a close molecular resemblance to retinoic acid, includes Achilles tendon pain and rupture (do a search on Accutane and tendonitis or tendon pain for descriptions by patients; also see transthyretin (TTR) down on this page under “Carrier Proteins”).   This could be due to some as of yet unknown connection (1), or possibly due to the RXR/VDR connection, affecting Vitamin D and Calcium homeostasis (see below).   Mefloquine, a quinoline, has a similar CNS adverse effect profile to the quinolones; an interesting hypothesis relating a retinoid (Vitamin A) toxicity to quinoline toxicity is presented here (Please note that in this paper, the word quinolone is a typo, and they should all be replaced with the word quinoline; I confirmed this with the author.)   An interesting study I would love to see repeated with quinolones is this one here.   For more Aldehyde/Thyroid related references, see here, scroll down to “Aldehyde Dehydrogenases”.

Dr. Garrett Smith, the "Nutrition Detective"
Licensed Naturopathic Physician (NMD) in Arizona
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