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Fluoroquinolones, Beta Glucuronidase and Oxalosis: New Connections

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Fluoroquinolones, Beta Glucuronidase and Oxalosis

Have you ever taken antibiotics and felt they had possibly both beneficial and detrimental effects on your health? There are plenty of scientific journals that debate just this (here, here). In the functional medicine world, we hear many stories from people about moderate to severe adverse reactions to fluoroquinolones and other antibiotics. This website has many such stories about the fluoroquinolone reactions and has published several articles on the mechanisms. One way fluoroquinolones wreak havoc on health that has not be discussed here is their role in oxalosis. There are several straightforward ways that antibiotics may increase oxalate, but I would like to share some new ideas about what changes they may make that might impact oxalate and inflammation.

What Are Fluoroquinolones?

Fluoroquinolones are a family of antibiotics that have a powerful bactericidal effect by inhibiting bacterial type II DNA topoisomerase. Due to their potent antibacterial effect, fluoroquinolones are most commonly used to assist with a wide variety of infectious conditions. This class of drug contains a black box warning from the FDA, indicating that it can cause serious issues like tendinitis, tendon rupture, peripheral neuropathy, myasthenia gravis and central nervous system effects. The negative effects of these drugs have become so widespread that a nickname has been coined for those who have endured fluoroquinolone injuries, called Floxies.

In our functional medicine circle we have heard many of their stories. In some instances, the original problem for which the antibiotic was prescribed becomes worse after treatment. In other cases, Floxies seem to experience major hormonal shifts with changes to their skin, collagen, hair, and connective tissues. In the worst cases, patients experience tendon ruptures, often of the Achilles, which is one of the more likely areas to be affected. Additionally, some patients develop sudden onset of allergic reactions to things in their environment or diet that they were not previously allergic too. Angioedema, skin rashes, peripheral neuropathy, and air hunger are some of the many other common symptoms that develop after using fluoroquinolone antibiotics. Many of these may be related to newly developing oxalate issues driven by these antibiotics.

What Is Oxalate?

Oxalic acid is an organic acid that is highly corrosive and elevated levels in the body correlate to having high inflammation. Oxalic acid binds to minerals in the body forming insoluble oxalate crystals that can deposit in organs, tissues, joints and the vascular system.

We can ingest exogenous sources of oxalate in the foods we eat, with certain plant foods like spinach having the highest level of oxalate. The liver can produce oxalate endogenously if one has certain SNPs in oxalate metabolism or nutrient deficiencies. There are many other ways to increase oxalate, including certain antibiotics, like fluoroquinolones.

The Antibiotic-Oxalate Connection

Research shows that antibiotics are not selective for only the bad bacteria. They kill off good bacteria as well. Humans cannot metabolize oxalate. We need help from our microbiota, particularly the oxalate degraders. Antibiotics will kill off many beneficial oxalate degrading flora, like oxalobacter formigenes, allowing oxalate levels to increase.

The bacteria in the gut also absorb and produce many B vitamins. Most of the vitamins synthesized endogenously are used by the bacteria themselves, but a small percentage is released into circulation. Both poor absorption and reduced synthesis of B vitamins will have many deleterious effects on health. Among them, increased oxalate synthesis and decreased metabolism and elimination.

Thiamine (B1) and pyridoxine (B6), for example, in addition to all of their other functions in human health, are instrumental in preventing endogenous production of oxalate. The bacteria that produce these vitamins are affected negatively by antibiotics.

Menaquinone or vitamin K producing bacteria also take a hit when antibiotics are used. Reduced vitamin K impacts calcium handling. Calcium homeostasis is critical for cell function in general and oxalate management in particular. It is also important for something called matrix Gla protein expression. Matrix Gla is a protein produced in the bone that inhibits vascular calcification. In other words, matrix Gla prevents the accumulation of oxalate, when expressed. When it is not expressed sufficiently, because vitamin K concentrations are diminished either by diet, antibiotic use, or both, oxalate will accumulate (here, here). Vitamin K is also critical in balancing hormones by multiple mechanisms. It is important to androgen/estrogen balance as seen in this study about PCOS. Hormonal balance plays a significant role in oxalate metabolism, which will be discussed later. These are just a few of the ways in which antibiotics contribute to an increase in oxalate and oxalate-driven inflammation

Beta Glucuronidase: A New Player in Oxalosis

In addition to the antibiotic-induced changes to oxalate-degrading and vitamin-synthesizing flora, antibiotics also alter carbohydrate metabolism. Antibiotics inhibit an enzyme called beta-glucuronidase (BG). BG is a lysosomal enzyme needed for the breakdown of complex carbohydrates and for the proper degradation of other small molecules like glycosaminoglycans (GAGs) such as hyaluronic acid, heparin/heparin sulfate, chondroitin sulfate/dermatan sulfate, and keratin sulfate and glucuronides such as bilirubin.

We have both human (encoded by the GUSB gene) and bacterially produced BG enzymes. Some main bacterial producers of BG are Escherichia coli, Clostridium species, Bacteroides species and Staphylococcus species. As men age, BG will increase. For women though, BG declines over time.

In disease states, certain enzymes become elevated and can therefore reliably indicate various pathological conditions. Beta glucuronidase is one of those enzymes. With metabolic disease and diabetes, for example, BG is elevated and the mix of gut bacteria shifts considerably.

Elevated BG also interrupts an important part of phase II liver detoxification called glucuronidation. This is where a glucuronic acid molecule is added onto toxic substances to inactivate and make them water soluble and easier to excrete. Beta glucuronidase can break the glycosylic bonds freeing the carcinogen and allowing its reabsorption and enterohepatic recirculation, rather than the proper clearance. Elevated BG, because of its impact on glucuronidation/phase II liver detoxification, will decrease the clearance of sex steroid hormones, xenobiotics, pesticides, herbicides, and insecticides, BPA, mycotoxins, pharmaceutical medicines, and more.

Elevated BG can be a marker for, and can contribute to, various issues. The recirculation of these carcinogens can contribute to colon cancer. The poor clearance of estrogens is associated with hormonal cancers like breast and ovarian cancer and endometriosis. In prostate cancer, upregulated BG is related to disease progression. It is not just cancers where BG is problematic, in chronic periodontitis, an 8-fold increase in BG activity has been recorded along with 33-fold increase in BG in bacterial peritonitis. This study details some of these observations.

This is where the fluoroquinolones and other antibiotics enter. A key job that they perform is to inhibit BG enzyme activity and the BG producing bacteria, pushing these levels back down into range. BG inhibition helps limit the recirculation of toxins that contribute to a vast number of diseases. A quick look at studies shows that fluoroquinolones like ciprofloxacin significantly inhibit BG. This study reveals that a combination of other antibiotics such as penicillin and metronidazole can have an inhibitory effect of up to 50% on enzyme activity.

What Happens When Beta Glucuronidase Is Too Low?

While it is clear that elevated levels of BG contribute to serious disease states, there are many substrates in the body that have to be at just the right concentration; where either too much or too little can be harmful to health. BG is one of these substrates. If fluoroquinolones and other antibiotics inhibit BG, and BG manages oxalate accumulation, could repeated use of these drugs over-inhibit BG such that oxalosis develops? I believe so. Below are a few of the pathways that may lead to high oxalate.

Beta-Glucuronidase Effect on Flavonoids

There is a strong relationship between inflammation and deconjugation. Conjugation and deconjugation are terms used to describe the addition or separation of molecules during liver detoxification.

When tissues in the body are experiencing necrosis, inflammation and mitochondrial dysfunction one of the most helpful antioxidants is the flavonoid. Once ingested, flavonoids like quercetin, which is the most abundant flavonoid in our diet, are conjugated via glucuronidation in the liver to their inactive metabolites making them easier to transport through the blood to these problem areas. Once they arrive, they must be deconjugated back into their active aglycone form so that they can be used to suppress the expression of pro-inflammatory genes such as COX-2 and scavenger receptors.

When the inactive flavonoids arrive at the inflamed tissues, phagocytic cells surround the problem area and secrete large amounts of both lactic acid and BG. The lactate is required to create the acidic environment needed for the most optimal BG function. One study shows a 13-fold increase of BG activity from pH 7.4 to pH 5.4. Then, BG secretion is needed for the bioactivation of the inactive flavonoid metabolites back to their aglycone form. From here, the flavonoids can go to work quenching the inflammation. If BG has been inhibited by fluoroquinolones or other antibiotics, flavonoids like quercetin will not be re-activated and will be unable to temper the inflammation. Here are three fascinating studies that explain this in detail (here, here, here). It appears that elevations in BG might follow inflammation, in an attempt to help resolve it

In addition to suppressing pro-inflammatory genes, the diuretic, antioxidant, anti-inflammatory, and antibacterial properties of flavonoids help inhibit the formation of calcium oxalate stones. If BG has been over-inhibited, such that these flavonoids cannot be reactivated, do we not then lose the oxalate preventative benefit that they provide? Possibly, which means oxalate levels would increase.

Ironically, flavonoids are potent inhibitors of BG. Is it possible they are used to resolve the inflammation then inactivate the BG so that its continued accumulation is not able to progress hormonal and other issues? Perhaps BG is involved in a natural feedback cycle of sorts.

Beta-Glucuronidase Effect on Glycosaminoglycans

As mentioned previously, BG is a lysosomal enzyme, which catalyzes the degradation of glycosaminoglycans (GAGs), such as chondroitin sulfate, heparin sulfate, dermatan sulfate and hyaluronan. When there is a mutation in the GUSB gene resulting in a deficiency of BG the GAGs are improperly degraded with consequent intraliposomal and tissue accumulation, creating lysosomal storage issues in a disease called mucopolysaccharidoses.

Now, there is some major interplay between oxalate and GAGs. GAGs are protective against the growth and formation of calcium oxalate crystals by having a strong binding affinity to them (here, here). There appears to be a low excretion rate of sulfated GAGs in stone formers, possibly due to improper degradation. And like GAGs, oxalate also needs to be phagocytized or engulfed into the lysosome where it can be dissolved. If they tend to bind together, it would appear that the increase in BG level by phagocytes may also be important for proper handling of oxalate.

In tendon rupture, a well-recognized side-effect of fluoroquinolone antibiotics, there is an accumulation of non-degraded GAGs (here, here). We know, through observations of people with hyperoxaluria, that oxalate crystals can accumulate around the joints and within tendon sheaths. Could the over suppression of BG by fluoroquinolones and other antibiotics contribute to their accumulation? Possibly.

Beta-Glucuronidase, Oxalate, and Estradiol

We know a consequence of elevated BG is estrogen dominance (here, here), so low BG activity could translate to lower levels of estradiol. Could repeated use of fluoroquinolones diminish estradiol concentrations such that it too influences oxalate build up? Once again, possibly.

Low estradiol (E2) might contribute to elevated oxalate in a couple of ways. Estradiol inhibits the activity of glycolic acid oxidase (GAO), thereby decreasing the amount of glyoxylate converted to oxalate within the peroxisome. Studies show that E2 is significantly lower in kidney stone patients with a significantly higher frequency of calcium oxalate stones in the lowest E2 groups.

Estradiol is the body’s natural anti-androgen via its suppression of 5 alpha reductase, which converts testosterone to the substantially more potent androgen receptor ligand, dihydrotestosterone (DHT). So, it can also help to manage oxalate level by keeping DHT levels in check. A quick look at studies will show that androgens increase oxalate level and stone formation by increasing GAO activity, and by suppressing osteopontin levels while estrogens elevate it, respectively.

However, like BG, E2 is also one of those substrates that has to be kept in balance. There can be harmful effects if E2 becomes either elevated or deficient. This study shows that E2 might attenuate oxalate transport activity via the downregulation of SLC26A6 and therefore enhance cancer cell migration, creating a potential risk for nephrolithiasis and cancer.

Fluoroquinolones, Beta-Glucuronidase, Estradiol and Tendinopathies

Estradiol is very important to maintaining connective tissue in women by improving the tendon collagen synthesis rate and increasing the number of smaller versus larger fibrils. Conversely, this study shows that the natural ageing process, whereby estradiol declines, increases a woman’s risk of tendon rupture to a similar level as seen in men. They postulate that a reduction in tensile strength, decrease in collagen synthesis, fiber diameter, density, and increase degradation in tendon tissue, all play a part. This means that both elevated and diminished estradiol influence connective tissue. Consider, for example, pregnancy in which E2 is quite elevated. It is the E2 induced changes to various collagen synthesizing genes that allow the laxity and the stretching of tendons, ligaments and skin. But, going to the other extreme could low estradiol induce excessive rigidity, also contribute to injury? When fluoroquinolones are used, they inhibit beta glucuronidase. Since BG inhibits estradiol, it is possible that this is one of the mechanisms contributing to the rigidity seen in tendinopathies and ruptures after fluoroquinolone use.

It All Comes Back to the Gut

It is in the gut where the oxalate degrading flora live. It is in the gut where the microbes that absorb and synthesize vitamins and minerals live. It is in the gut where the microbes that produce short chain fatty acids and beta glucuronidase that help balance the estrobolome and other hormones live. All of these factors intersect to manage and determine our inflammation level. When we kill these microbes with antibiotics and other ‘kill tools’ we inevitably impact oxalate metabolism. Fluoroquinolone induced inhibition of beta glucuronidase may be a key player in the cascade leading to oxalosis. While the inhibition of BG may be useful when concentrations are too high, repeated or over-inhibition may be deleterious to health.

The good news is, the body wants to regain homeostasis when pushed out of balance. The cessation of any antibiotics that are depressing BG will allow it to recover over time. Perhaps by taking these other factors and associated biomarkers into consideration we might be able to gently push into some level of homeostasis more quickly to regain health.

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Musings of a Heretic Patient: Floxed and Fed Up

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After mulling it over for quite some time, I wanted to comment on something we all encounter much too frequently in our floxed lives. That is, specifically, the negative experiences we are often forced to endure with our doctors. As patients, harmed by a widely over prescribed drug, we are often dismissed whenever we propose a connection between fluoroquinolones and the adverse side effects we experience as their patients.

I cannot even begin to quantify the level of frustration and anger I feel whenever I’ve been confronted with this in my doctors visits. It’s demeaning and demoralizing to be treated as if I am a complete moron for broaching the subject whenever they come up empty on their diagnosis.

At first I chalked it up to ego because after all, THEY are the “experts” and I am just one of the great uneducated with the audacity to question their expertise and search for answers beyond their own. I know what it feels like to be sneeringly, denigrated for my research. To be called a GOOGLE doctor for simply not accepting their non-diagnosis as a diagnosis.

Oh, the times I felt like screaming and pulling my hair out in my doctor’s office. The times I became so frustrated I wanted to overturn the tables and rip those stupid charts from the walls are just too innumerable to count on my flox journey.

Laying the blame on ego alone was the simplistic answer but something always niggled at me every time I left the office, depressed and defeated.

Why was I always making excuses for what was so obviously a rude and demeaning attitude towards my quest for answers? Why were all my doctors so hostile to my input and so dismissive of my efforts at educating myself? What lay beneath this dismissal of my pain and the destruction of my body that even they could not deny?

Today it happened again and it sparked me into writing this post.

The Heresy of Questioning a Doctor

I have come to learn that a few of the common tactics used by doctors can be identified. Many of them are being used to work against us when confronting a doctor’s assessment of our specific issues.

The first one is utilizing our lack of a formal medical education to minimize our efforts. It’s the most obvious use of the power dynamic they conjure to silence us. Questioning a doctor is an anarchistic act. It challenges the authority of the empirical medical model, the one we’ve been programmed from childhood to believe has all the answers. The one domain that is so sacrosanct in our society that questioning it is bordering on the heretical and places you squarely outside the acceptable behavior circle.

I have come to accept that I am now a heretic and so is anyone who steps outside the medical status quo in their search for answers. Like any heretic, I need to be prepared for the onslaught of disapproval and derision I might receive for questioning the medical gods. I need to remember to arm myself psychically and mentally for every visit. The fact that I must do this saddens me. It illustrates just how meaningless and hollow the Hippocratic Oath has become to our modern medicine men.

“Nor shall any man’s entreaty prevail upon me to administer poison to anyone; neither will I counsel any man to do so.”

Plausible Deniability in Medicine

Another tactic used by physicians to dismiss patient concerns is plausible deniability. Physicians now rely on plausible deniability to explain away their non actions or worse. It is the deliberate and destructive act they use against the very people they have sworn to heal. It’s also known as covering their asses. Knowing this and accepting that this is the norm rather than the exception has been a bitter pill for me to swallow but imperative to retaining my sanity.

And Then There is Gaslighting

Another thing I’ve come to recognize as a tactic is what I call medical gaslighting. Gaslighting is a very effective but abusive form of diversion. In this case, a physician utilizes an established (though questionable) psychological diagnosis as a convenient way of absolving their non actions in your case. It also serves to stopgap any further digging into causal links and diverts attention away from the physicians own culpability. How many times have I been told that my symptoms are all in my head? Too many times to count. And since my symptoms don’t fit any known disease model, I must be suffering from a psychological malady.

This has now become a part of the DSM-5 lexicon of psychiatric diagnosis and poses further harm to people like myself and anyone whose symptoms cannot be easily pinpointed to any one specific disease. If anyone, who like myself has been previously diagnosed with a mental illness (depression, PTSD) these diagnoses further serve to de-legitimize the patient’s experience.

We need to be aware that even when we have the hard evidence of medical research to back up our claims, we will be challenged and possibly labeled. If we refuse to accept this knee jerk assessment or the drugs they will inevitably prescribe to treat our “real” issues we might find ourselves tagged with the non-compliant stamp.

I write this as a warning to everyone who finds themselves on this page. You might hit some very daunting, brick walls along this journey but know that you are not alone. One day we will be vindicated, this crime will be exposed, and Big Pharma and all colluding physicians and corrupt governmental agencies will be brought low.

For those who have been blessed with that one special physician who listens and learns, I am grateful to see that ethics still exist. It’s heartening to know that there are doctors out there who can put ego and material gain aside and remain open to their patient’s body awareness and desire for healing. Sadly, those doctors risk becoming medical heretics too, banned and derided by the more conventional experts, the same experts that employ the tactics listed above.

In the end, I know we will win and a big part of that victory comes from the massive amount of support and experience we find on our support pages. Thank you to all my fellow floxies. You are the vanguards of this battle and close to my heart.

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This post was published originally on Hormones Matter on October, 2015.

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Becoming the Person I Hoped I Was

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When life changes its mind about the size of the mountain you’re climbing, you will suddenly find that you have some decisions to make.  My husband got sick.  He was hit, badly, with long term side effects stemming from a short course of Ciprofloxacin (Cipro), a fluoroquinolone antibiotic. The side effects from Cipro can be a horrific and long term, but are often invisible. Blood tests come back normal, neurological exams reveal nothing of note, the sufferer often looks fine, and worst of all, most doctors are completely unfamiliar with these adverse reactions. This of course means that most people are completely unfamiliar.  We certainly were.  But without a doubt my husband was sick, and I had some decisions to make. The biggest decision I at first didn’t know I was making (daily, even minute by minute) continues to be this: what kind of person am I going to be?

I have unknowingly been faced with this decision before. Two years ago, James, the husband of a coworker got sick. Really sick. He had stage four esophageal cancer, and it was very unlikely that he would survive long after the “last hope” surgery.  His wife was not in a position to stay home and take care of him and she had to continue working full time. They also had two elementary age girls. Not much could be worse.

After his surgery, James had trouble getting enough calories. I like to bake so I made him some cookies, and a couple of chocolate cakes. Actually, what I really did was make cookies and cakes for my future husband and for parties, but I made sure to double the batches so I could give some to James. This was the extent of my support. James and his wife expressed their gratitude far beyond the reality of the gesture. This attention embarrassed me a little, but mostly made me feel rather pleased with myself. Yes! I am one of those people who bake when my acquaintances are ill!  What an amazing, empathetic, wonderful person I am. I did not go so far as to credit myself with James’s survival and subsequent return to health, but I allowed for how the chocolate probably helped.

I had made the decision to act on my compassion. A little. Well, not so very much actually. Almost literally the crumbs from my kitchen. Yet I now understand the level of gratitude around a few cookies. Today similar small gestures from the people around me stun me with appreciation of my own. I understand it now. My friend makes enough extra soup so that I can have lunch for three days. My coworker orders the annual holiday craft for my students without bothering me with the details. Another friend texts to see if I need anything at Trader Joes. “I’m going later, what can I get you?”  These moments stick.

Cipro toxicity isn’t like cancer. It isn’t something that people already understand to be a struggle. Like many chronic conditions, it can become invisible to those not suffering. It is easy to ignore something (or someone) who disappears from daily life, without any official medical diagnosis. So easy in fact that this is many people’s natural inclination. To ignore or minimize. This was my inclination.

On the best days the gratitude I now feel for small acts of kindness can seem a fair trade for the unawareness that formerly accompanied our good health.  The rarity of these acts makes them more powerful. Many people who know our story ask my husband how he is, but more often people don’t. Ever. I suspect these people do care (or at least I am deciding to believe they do). So what is the disconnect?

From my own experience, reaching out to help anyone in need takes an ability to look beyond, briefly, the ever present squawk from the needs of your own life. That was me.  Since my husband has been sick I have heard from many people about their own struggles. How did I not notice my sister has been fighting through horrible digestive issues? How did I miss my friend having constant headaches for four months (after taking Cipro, by the way!)? How did I miss my coworker’s father passing away?

When I did used to look beyond my life, I would often be immobilized by anxiety. There is a real courage involved in moving past the fear and discomfort of saying something wrong. In the past I lacked that courage. I justified with thoughts that generally began, “I don’t want to remind her of….”  Really? Did I think there was a moment that she had forgotten that her father had died, her husband had cancer, her head was pounding, whatever? No. It may hide for a moment but she always knows it’s there. What she does not know is that I remembered it’s there. And that I cared. It is the rare person who can push past these obstacles and offer something anyway.  It is the rare moment when they do.

I am also grateful because I believe acts of compassion, small as they may be, give me a glimpse into the very best selves of those around me. My father and sister could not be more supportive. My aunt has been lovely. Our closest friends have rallied throughout. Although I already knew this information about my family, many of the friends I have chosen in my life are turning out to have a depth to them that has not been apparent to me before. Perhaps this was always true and I just never had occasion to see it. Or perhaps this is something that my friends are deciding about themselves, in the same way that I am deciding about myself. Maybe with every decision we make there is an associated change in ourselves. I don’t know. I do know that the way this has deepened my feelings for these people is as if, from the mountain, I thought I was looking at the edge of a lake in the distance. But now after climbing a little higher, it turns out it is the beach of an ocean. What a dazzling view.

Since my husband’s illness began 6 months ago, every person in my life has been presenting me with an unintended gift the moment I started paying attention. The gift of example. Everyone has and is modeling the kind of person I want (and don’t want) to be.  Who do I want to be when the people around me are in need?  Do I want to be the person who texts from the grocery store?  The person who takes over chores without being asked? Or the person who is so unsure of what to say that she says nothing at all? (How many times have I been that person? Too many to count.)  It’s an obvious decision once you’re aware of it. It’s a choice that I did not even know I was making before this experience. Non-action is a decision. Generally it’s the worst decision.

I have come to believe more and more that it is our actions that define us, not our thoughts, our intentions, or even our feelings. Still, I wish I could go back in time two years and smack the feelings right out of myself. The silent self-satisfaction over a chocolate cake… how very shameful. There is no way to go back and offer to babysit, or cook a meal, or shop, or just ask (frequently) how things are going, and what can I do for you today to help? Or better, just do something that needs to be done, without asking. I can’t go backward and do that. Most disgraceful for me is that cancer is a very “visible” disease and I did my best to not see it. There is only one way to atone. Open my eyes for the rest of my life, and act on what I see, and even what cannot be seen. It is not a coincidence that every time I see James, he asks if there is anything he can do for us. My husband is sick and I am here now. Life is full of decisions. Today I am deciding to be grateful for the chance to have a do over. From now on I get to decide to be the kind of person I always hoped I was.

 

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This post was originally published in December of 2013. 

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Glabrata – A Deadly Post Fluoroquinolone Risk You’ve Never Heard About

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I would like to share information on a little known, rare infection that all too often is overlooked or misdiagnosed, by the medical profession. It is an infection that shows no mercy to its victims and is deadly  in 67 to 90% of the cases, depending upon the severity of the infection. It is called Candida Glabrata (C.Glabrata), and I, like thousands of other victims, have had to learn the harsh realities of what this infection is capable of. I have also learned that it is an infection that our medical profession knows little about and our scientific community knows even less about how to beat it. In 2007, it was listed as the fourth leading cause of bloodstream infection in United States hospitals. The fact that the medical professionals know so little about how one contracts C. Glabrata, who gets it and when to look for it, persuaded me to speak out about this, so others do not suffer as I am.

What is C. Glabrata?

First C. Glabrata is a fungus from the Candidias family, which is the same family of candidias albican  (the yeast infection that most people are familiar with), however, there are several other forms in the Candidias family. These other forms are actually known as non-albicans and they are much more serious types of fungi. There are approximately five different species in this category with Glabrata being the most serious form.

What makes Glabrata so serious is the fact that it is only one of a few fungi that do not have hyphae, which are like the tenticles. Without hyphae, it is very difficult to culture, biopsy or see under a microscope. Due to the fact that it cannot be easily diagnosed, it is usually is not discovered in a person until they are very sick and by then it is a race against time to save the individual. The other problem with fungi without hyphae is that they are able to morph and adapt for survival. This means they have the ability to live in both alkaline and acidic environments. This is the part that makes them so deadly, because we only know how to kill fungus by changing the PH balance of the environment to basically make the living conditions unconducive to their life cycle. So, when you have a fungus like C. Glabrata that cannot be easily detected, diagnosed and then treated, you have what is known by the CDC as a deadly fungal infection.

The History of Glabrata

The fortunate thing about Glabrata is that it is a very rare form of fungus that is almost never seen in the general population. It was discovered during the 80’s when the AIDs population came to awareness. Prior to that, it had never been found in humans. Once the HIV population became infected, the fungi were impregnated in hospitals all over the country. Through the 90’s, the only people identified with this infection were the critically ill and immune compromised population, end stage HIV or end stage cancer patients in ICU units. With compromised immune systems these patients had no resistance to the fungus, and unfortunately, the mortality rate was 100%.

By the early 2000’s a new population of people were beginning to show up with C. Glabrata, only now it had moved beyond the immune comprised HIV and end-stage cancer patients. A study in 2010, found that 73% of C. Glabrata cases occurred in patients previously given fluoroquinolones. This new, previously healthy group of people falling ill to Glabrata had all been treated with a broad spectrum fluoroquinolone antibiotic often in conjunction with a steroid. Steroid treatment alone is a risk factor for the C. Glabrata infection. According to my current physicians, when fluoroquinolones are combined with steroids, the risk for contracting C. Glabrata increases significantly.

Research shows that the fluoroquinolones wipe out all gut flora (good and bad). When combined with immunosuppressive steroids, the patient’s ability to fight bad bacteria and fungus is compromised. When all the gut flora are killed, the first flora to grow back are those that are the strongest and most resilient. Much like weeds in your garden, fungus and bad bacteria grow at a faster rate and are stronger mutants than the good bacteria. If the patient was also prescribed steroids, their own immune system can no longer come in to fight off the bad gut flora. This leaves the gut vulnerable to serious infections especially fungal ones like Glabrata. Fluoroquinolones are one of the most potent gut flora destroyers on the market. There is no other class of antibiotics that so totally annihilate gut flora to the level that the fluoroquinolones do. Combining fluoroquinolones with steroids is a recipe for disaster.

In sum, there are only four ways to develop a C. Glabrata infection, end stage HIV, end stage cancer, patients with neutropenia – a genetic or chemo-induced condition that limits white blood cells needed to protect the body from fungal invasion – or by using a broad spectrum antibiotic, like the fluoroquinolones combined with a steroid.

Diagnosing Glabrata – Why So Many Victims of Glabrata Die

Glabrata is very difficult to diagnose, leaving the infection to take hold before it is recognized. The Glabrata fungus does not have hyphae and does not present like all other forms of candidias. This fungus does not produce a white cheesy like curd discharge from the gut / stool, vagina or penis. Instead, it produces a milky white to grayish thin discharge, often seen with bacterial infections. It also produces minor to severe swelling of the tissues and erythema (redness). The infection causes horrific burning (often described as grinding glass into the tissues and then pouring acid on them) with very little itching.

In the early stages, before a doctor thinks to look for C. Glabrata, the infection is frequently misdiagnosed as a bacterial infection. The patient is put on antibiotics; often the same antibiotics that created the susceptibility to the infection to begin with. When these fail again and again, the doctors are often at a loss as to what is going on, especially if the person was a young, healthy individual prior to being given antibiotics with steroids. Since most physicians have been trained to only look for Glabrata with HIV or seriously ill cancer patients, they never think to look for it. It usually takes until the person becomes critically ill with the infection before they realize that it is a fungal infection, at which point the doctor will order specific tests looking for a non albican fungus. In more than half of all cases of Glabrata it is not realized until autopsy. These are not like other fungal tests because they have to be grown in special agar (petry dishes) and then stained with special stains and then looked at under high powered microscopes. The final drawback is that this fungus needs 6 to 8 weeks to grow out, which costs precious time that most patients do not have.

Treating Glabrata

Once Glabrata is diagnosed the next hurdle is how to treat. Currently, there are only a few drugs that have any potential to kill it: Diflucan (fluconazole), Caspofungen and Amphotericin B. Each is problematic. Diflucan has to be used at ten times the normal level for months on end, to kill C. Glabrata. Most people are unable to tolerate this course of treatment and in 99% of cases it fails and in many cases, the fluconazole induces resistance to it and other azole fungicides. Caspofungen or microfungen, are additional options. They can cause serious liver and kidney problems, leading to failure of one or both organs. These drugs work in about 70% of all cases, but again must be used for months on end and many patients are unable to tolerate the treatment.

The last drug known to kill C. Glabrata is Amphotericin B. This drug is only used when the person is on their death bed because it is so toxic that it causes acidosis within minutes of being administered. Over 90% of patients go into multi-organ failure and die within three hours of infusion (discussions with my doctors). This drug too must be used for months on end to kill it.  Amphotericin B has a 90% success rate if the patient can survive the drug itself.

In very serious and resistant cases, Flucytosine is combined with the Amphotericin B. Flucytosine is thought to open the cell walls and lets the Amphotericin B in to kill. Flucytosine is an old chemo drug that is quite potent drug. When combined Amphotericin B, the results can be deadly. These are the only drugs known to treat this fungus.

Glabrata Becomes Resistant

As if Glabrata isn’t difficult enough to diagnose and treat, the fungus is very adaptive. If the patient survives the drugs, the fungus can, and often does, become resistant to the drug that it is being treated with, leaving the person with no options to kill it. This means that you get ONE shot with a medicine because it will become resistant the second time around. Glabrata has to be killed totally. If not and it returns, there is no treatment.

But as a fungus, Glabrata does not die on contact with the medicine. Let me explain this in an easier way. Look at it like this a bacteria is like a spider or bug, when you spray it with Raid it stops dead in its tracks and dies right there where you sprayed it. With fungus it is like a weed in your yard, when you spray it with weed killer the first day it begins to droop the next day it turns brown and by the third day it falls to the ground. If you then then pull the weed up and if you did not get the roots too within a week you will have a new weed back again. Fungi work in the same way, which is why it must be treated for months on end. Fungal infections are notoriously hard to treat and some of the most deadly infections to have. This is why Glabrata is fatal in 90% of all cases.

I Have a Glabrata Infection

I have a Glabrata infection and am fighting for my life. How did I contract this deadly fungal infection? I was prescribed Cipro plus a steroid for a misdiagnosed and assumed GI infection. I had a stomach bug, likely the flu, but since I have a diagnosis of IBS and the doctor was unable to see me for four days, she suspected I had a small intestine bacterial overgrowth (SIBO). I was prescribed an antibiotic, Cipro, plus steroids. That is, I was prescribed these meds on the assumption that I had a bacterial infection. I did not.

Three days after starting Cipro, I fell ill to Cipro toxicity. My gut flora were wiped out, I just didn’t know it yet and neither did my doctors. A week later, I found out that I never had an infection and didn’t need Cipro to begin with, but it was already too late for me. In the coming months, the GI bleeds began and other GI issues that would be misdiagnosed as Crohn’s Disease and bacterial infections ensued. It was not until last month that my doctors determined that all my problems were due to a deep seeded or disseminated infection with Glabrata.

We tried the Diflucan, which failed miserably. My WBC count and neutraphil count rose and I was now in serious trouble. We put a central line in and started the microfungen. After the first seven days, my counts dropped drastically, but by day nine, I began to step backwards. The fungus was morphing to survive and was becoming resistant to the drug. We are now looking at Amphotericin B. We will give it two more weeks and then make that call but it is not looking good right now. My symptoms have begun to ramp up again. I know the odds are against me with less than a 10% cure rate, I am fighting an uphill battle but I need to win this one for my life!

Why I Am Telling My Story

Patients must understand the dangers of this class of drugs especially when combined with steroids, because many doctors do not! Fluoroquinolones are the most commonly prescribed antibiotic in the US and combining them with steroids seems to happen frequently.

Also know that 78% of the time Glabrata starts in the gut. Other times it starts in PIC and central lines. In either case, one initiated, it infiltrates the prostrate for men and the vagina for women. It has been known to seed itself any organ throughout the body. If you are suffering with an infection in any of these areas that does not respond to antibiotics and you are also suffering with GI issues, you need to ask your doctor about checking you for a fungal infection, especially if you have used a fluoroquinolone antibiotic with a steroid prior to the onset.

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More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

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Featured image: GMS stained skin punch biopsy demonstrating fungal spores of C. glabrata, eScholarship, University of California.

This story was published originally in December 2013.

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Who Reads the Drug Warning Labels?

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drug side effect labels

I have a confession – I didn’t even glance at the warning insert that came with my Cipro prescription. I didn’t even think about reading it. I didn’t think for a second that I needed to be worried about the side-effects of an antibiotic. I assumed that all antibiotics were safe, thoroughly tested, had few side-effects and that any side-effects that they had wouldn’t hurt ME. After all, I was a fit, strong 32 year old with zero health issues other than the urinary tract infection that I was trying to treat. I thought that I had nothing to worry about and that medicine generally and antibiotics specifically fell into the category of things that do good, not harm. So when I developed severe Central, Peripheral and Autonomic Nervous System malfunctions and inflamed tendons after taking Cipro, I was shocked and shaken that an ANTIBIOTIC that is prescribed every day to treat simple urinary tract and other infections, could cause me, a healthy and fit woman, to be suddenly systemically sickened.

I suppose that, since I didn’t read the warning label, I have to take a certain amount of personal responsibility for what happened to me. Officially, I was warned. I should have known that Cipro, one of the most popularly prescribed broad-spectrum antibiotics on the market, could cause tendonopathy, renal failure, rash, anemia, hepatic failure, hallucinations, seizures, permanent peripheral neuropathy, etc. I should have read the warning label so, at the very least, I would have known that when I experienced inflammation and weakening of every tendon in my body (lightly referred to as tendonopathy – as if that even comes close), hives all over my body, loss of memory and reading comprehension, inability to concentrate, peripheral neuropathy, anemia, etc., that I was experiencing an adverse reaction to the drug that I had taken. Should’ve, would’ve, could’ve. I lived and learned and will certainly read warning labels in the future. However, I don’t think that I am unusual in not bothering to read the warning label that accompanied my prescription for antibiotics. Do other people read drug warning labels?

Doctors certainly don’t seem to read drug warning labels. Every single doctor who I asked whether or not Cipro could have caused my symptoms said that it couldn’t have, despite the fact that the majority of my symptoms are listed on the warning label.

And even if I had read the warning label, would I have been sufficiently warned? I assumed, as I think most people do, that drug side-effects are transient, that they are stopped as soon as administration of the drug is stopped, or at least as soon as the drug is fully metabolized. I had no idea that a drug could cause a syndrome that would take me years to recover from. Nowhere on the warning label does it say that side-effects can be long-lasting and, when I took Cipro in 2011, nowhere on the label was the word “permanent.” It was only added to the warning label in 2013 in reference to permanent peripheral neuropathy.

Who would think that a drug, an antibiotic no less, could cause a chronic syndrome that includes pain and nerve destruction? Again, doctors certainly don’t because not a single one acknowledged that my cascade of physical and mental issues that cumulatively was a toxicity syndrome, was caused by Cipro. This was despite not only the warning label but also thousands of patient reports, lawsuits, media reports and studies that show that I was not crazy or suffering from sudden onset of an autoimmune disease; I was poisoned by a prescription antibiotic.

Even if I had read the warning label, I likely would have assumed that side-effects were rare. The people who acknowledged that Cipro caused the damage that it caused in me dismissed the possibility that what happened to me could happen to them by saying that adverse effects of fluoroquinolone antibiotics (Cipro, Levaquin and Avelox) are rare. How, I wonder, would anyone have a clue whether or not Fluoroquinolone Toxicity Syndrome is rare? Given that the onset of symptoms is often delayed by days, weeks or even months after administration of the drugs has stopped; that doctors and patients alike are looking for allergic reactions when they are looking for adverse drug reactions, not systemic breakdown in the form of a syndrome; that the doctors who prescribe fluoroquinolones (general practitioners and emergency care doctors) are typically not the same doctors who treat the symptoms (rheumatologists, neurologists, psychologists, etc.); that there appears to be a tolerance threshold for fluoroquinolones (meaning that you can take it up to your threshold point without incident but once you cross your threshold point you suffer from a severe onslaught of symptoms), a concept that those who are doing drug studies don’t even seem to consider; and that almost everyone in the medical field is in complete denial about the dangers of these drugs, how in the world would anyone, including the FDA, have a clue what the frequency of adverse reactions to these drugs is???

Risk is not properly communicated via drug warning labels. Risk is a function of severity and frequency. Individual adverse symptoms are listed on drug warning labels, but nowhere does it state how severe each symptom can be, or whether multiple symptoms can occur simultaneously, or if the drug can trigger a long-lasting syndrome that itself is a chronic disease. How can people possibly assess the risk of experiencing severe, life-altering, long-term side-effects if it’s nowhere on the warning label that those things can happen? And if frequency of adverse reactions is systematically under-acknowledged for the reasons listed above, how can people possibly assess the likelihood that an adverse reaction will happen to them?

Perhaps doctors and patients alike are doing the sensible thing in not bothering to read drug warning labels. If the information that they give is arbitrary and they don’t help people to assess the actual risk associated with a drug properly, they should be ignored.

The only party that the warning labels are truly serving is the drug companies, because if they can say that they warned you through the paperwork that accompanies dangerous drugs, you can’t sue them.

So who is appropriately communicating the real risk of adverse drug reactions to patients? Who is communicating the risk to doctors? How is anyone supposed to know the real severity and frequency of adverse drug reactions? We’re not getting that information – from anyone. The FDA is failing to provide that information. Neither doctors nor patients are demanding that information. Everyone is assuming that adverse drug reactions are rare, while the number of deaths from prescription drugs climbs and the number of chronic diseases that people suffer from, many of which are caused by adverse drug reactions, skyrockets.

Perhaps it is time that we start demanding that drug warning labels mean something. They should accurately and completely reflect the real dangers associated with each and every drug. Frequency of adverse events should be noted on the warning labels. This is not too much to ask for. Patients, doctors and everyone else involved should insist on it. We deserve to know.

For a list of warnings that should be on the label for fluoroquinolone antibiotics, please visit www.ciproispoison.com.

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More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter. 

Photo by Bruno Guerrero on Unsplash.

This article was published previously in October 2013.  

 

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Shades of Grey – The Good and Bad of Fluoroquinolones

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Lisa Bloomquist flouroquinolone antibiotics

A friend of mine recently commented on one of my posts about fluoroquinolone toxicity, “I totally appreciate these articles and my heart goes out to those suffering, but are there people who have benefited from these antibiotics? I’m not trying to stir the pot, I’m curious as I would think many readers would be.”

I really appreciate the inquiry, and I’m sure he’s right in thinking that many people have the same question. Here is my response:

Yes – absolutely – lives have been saved by fluoroquinolone antibiotics (Cipro/ciprofloxacin, Levaquin/levofloxacin, Avelox/moxifloxacin and Floxin/ofloxacin). They are powerful, broad-spectrum antibiotics and, as such, they have saved the lives of people who are suffering from severe, life-threatening infections.

Unfortunately, fluoroquinolones come with severe side-effects that include cellular damage. They have been shown to deplete mitochondrial DNA and induce large amounts of oxidative stress (also known as reactive oxygen species or ROS). Both mitochondrial damage and oxidative stress have been linked to many chronic, multi-symptom diseases, including chronic fatigue syndrome / M.E., Alzheimer’s, diabetes, Parkinson’s, fibromyalgia, autism, Gulf War Syndrome, and many others. Fluoroquinolone toxicity syndrome is a multi-symptom, chronic illness that is often misdiagnosed as fibromyalgia, CFS/ME, an autoimmune disease, etc. Fluoroquinolones have been shown to cause destruction of tendons, cartilage and muscles, as well as permanent peripheral neuropathy and severe central nervous system reactions.

Fluoroquinolones are being used Inappropriately

Because of the severity of the side-effects of fluoroquinolones, it is inappropriate for them to be used when other, more benign, antibiotics will effectively fight an infection. They are only appropriate for use in situations where more benign antibiotics have failed, and a person’s life is threatened by an infection.

Unfortunately, many people are given Cipro/ciprofloxacin, Levaquin/levofloxacin, Avelox/moxifloxacin or Floxin/ofloxacin for sinus infections, urinary tract infections, respiratory infections, and prostate infections. Fluoroquinolones are even prescribed when no infection is present for suspected infections (they are often prescribed prophylactically for travelers’ diarrhea).

Think of Fluoroquinolones as Chemo Drugs – They Are

Fluoroquinolone antibiotics should be thought of as anti-cancer chemo drugs. In fact, they have been investigated for their cancer-fighting / tumor killing properties. Chemo drugs can save lives – there is no doubt about that. But, because of the harm that the drugs themselves do, it is not appropriate to give them to people unless they have cancer or are in a life-or-death situation. Similarly, it’s not appropriate to give people fluoroquinolones for simple infections that could be treated with more benign antibiotics.

The Hippocratic Oath and Informed Consent – Forgotten Bedrocks of Medicine

Despite the fact that fluoroquinolones have severe side-effects, very few people are advocating for their removal from the market. When they are needed to save a life, they should be available. What most people (myself included) are advocating for is sensible, appropriate use of fluoroquinolones. Neither Cipro/ciprofloxacin, Levaquin/levofloxacin, Avelox/moxifloxacin nor Floxin/ofloxacin should be prescribed to people who can be helped by a more benign antibiotic. (Adherence to the Hippocratic Oath should prevent this from happening, but it’s not). Fluoroquinolones should not be given to people without a warning about the severe cellular damage that can be done by these drugs. (Informed consent is important.) In order for fluoroquinolones to be thought of and administered appropriately, both physicians and patients need to be aware of how dangerous fluoroquinolones are, and how severe their adverse effects can be.

Through people telling their stories of how fluoroquinolones hurt them, awareness of the dangers of fluoroquinolones will come. Hopefully, sensible and appropriate use of these powerful, dangerous drugs will follow.

Fluoroquinolones can do good, but they can do harm too. Categorizing things in terms of good or bad is the natural inclination of most people, but it’s never that simple for drugs. All drugs can do good, but they can do harm too – hence the list of side-effects that comes with each prescription. We can’t yet ask for drugs to only do good, and never do harm – that’s not the way the world works. But we can ask for dangerous drugs to be used appropriately. It is ONLY appropriate for fluoroquinolones to be used in life-or-death situations when other antibiotics aren’t effective. To use them flippantly, and when they aren’t entirely necessary, is inappropriate and a violation of the Hippocratic Oath.

Information about Fluoroquinolone Toxicity

Information about the author, and adverse reactions to fluoroquinolone antibiotics (Cipro/ciprofloxacin, Levaquin/levofloxacin, Avelox/moxifloxacin and Floxin/ofloxacin) can be found on Lisa Bloomquist’s site, www.floxiehope.com.

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Participate in Research

Hormones MatterTM is conducting research on the side effects and adverse events associated with the fluoroquinolone antibiotics, Cipro, Levaquin, Avelox and others: The Fluoroquinolone Antibiotics Side Effects Study. The study is anonymous, takes 20-30 minutes to complete and is open to anyone who has used a fluoroquinolone antibiotic. Please complete the study and help us understand the scope of fluoroquinolone reactions.

Hormones MatterTM conducts other crowdsourced surveys on medication reactions. To take one of our other surveys, click here.

To sign up for our newsletter and receive weekly updates on the latest research news, click here.

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Hormones MatterTM is completely unfunded at this juncture and we rely entirely on crowdsourcing and volunteers to conduct the research and produce quality health education materials for the public. If you’d like help us improve healthcare with better data, get involved. Become an advocate, spread the word about our site, our research and our mission. Suggest a study. Share a study. Join our team. Write for us. Partner with us. Help us grow. For more information contact us at: info@hormonesmatter.com.

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A Fragmented Balance: Life Post Cipro

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Fluoroquinolone reactions

It has been seventeen months since I took three doses of Cipro and seventeen months of endless education of a degree in which I will never receive nor have ever been interested in to begin with. Pushed into an unfamiliar world due to a prescription of an antibiotic for an infection I did not even have.

I have never been one to like medications and because I have always been generally healthy, I have rarely ever needed them. A suspected urinary tract infection is what started this whole mess.  As it turned out, it was bladder irritation due to ice tea, not an infection. If I had listened to my gut I would not have swallowed the poison. Instead, I listened to my doctor. Why? Because I had been going to her for quite a long time, she knew me best; she is supposed to have my best interest at heart. In fact, she knew me so well that when she gave me the prescription she told me NOT to look at the side effects because I would choose not to take it. She knew I hated taking medication. It was JUST an antibiotic. That’s what she said and that is what I told myself.

Well Cipro is NOT just an antibiotic for some people. For some people it is poison; it is a game of Russian roulette with all chambers full.  I will spare you the details of the thirty plus symptoms it has caused and continues to cause, but know that my life has not been the same since and it never will be.  Even if my body recovers, it will never be the same. It can never give me the time back that I have not been able to spend with my children because I was laying in bed icing my hamstrings, or the hikes I have had to avoid because of the muscle loss; the time I have spent researching alternative ways to heal because the medical community has NO clue. Life will be different, from here on out.

I failed to mention the worst side effect of Cipro toxicity – how all of this can consume you, swallow you whole and spit you out in pieces. Fragments. Trying to fix yourself while being sick is not an easy task. It is an unfair task actually. It can make you angry; it can make your friends and your family angry. They don’t want to hear it and you are too tired to listen to yourself anymore.

I became silent.

During my silence an evolution occurred. It has started me on a new journey; a delicate balance of before, after, and mostly today. The object of my new journey is to gather the fragments each day as if they are new and polish them, repaint them and do my best to put them back together again. The object is to make a new art piece, a new me, post Cipro injury and to hope that people will admire the new me, but more importantly, that I will admire the new me, the stronger me, the less naive me. I think will call my art piece “Fragmented Balance”.

Participate in Research

Hormones Matter is conducting research on the side effects and adverse events associated with the fluoroquinolone antibiotics, Cipro, Levaquin, Avelox and others: The Fluoroquinolone Antibiotics Side Effects Study. The study is anonymous, takes 20-30 minutes to complete and is open to anyone who has used a fluoroquinolone antibiotic. Please complete the study and help us understand the scope of fluoroquinolone reactions.

Hormones MatterTM conducts other crowdsourced surveys on medication reactions. To take one of our other surveys, click here.

To sign up for our newsletter and receive weekly updates on the latest research news, click here.

What Else Can I Do To Help?

Hormones MatterTM is completely unfunded at this juncture and we rely entirely on crowdsourcing and volunteers to conduct the research and produce quality health education materials for the public. If you’d like help us improve healthcare with better data, get involved. Become an advocate, spread the word about our site, our research and our mission. Suggest a study. Share a study. Join our team. Write for us. Partner with us. Help us grow. For more information contact us at: info@hormonesmatter.com.

To support Hormones Matter and our research projects – Crowdfund Us.

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Truth Seeker or Conspiracy Theorist? You Decide.

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Lisa Bloomquist

I’ve always believed that the simplest answers to most problems are the ones that are closest to the truth. I don’t particularly like conspiracy theories. I generally find them to be offensive. So as not to offend the people who believe in conspiracies, I’ll refrain from giving an example, but I tend to think that what you see is what you get and that there aren’t any evil masterminds controlling the world. I don’t think that there is anyone smart enough to have evil plots that control the world. Rather, I believe that there are complex feedback loops that keep certain parties in power and others powerless. Of course, those in power work to protect their power, sometimes through greed, lies and cover-ups, but it’s not necessarily a conspiracy per se. It’s just people being people and trying to maintain the status quo because people generally don’t like change (and a million other complex psychological and sociological reasons why people like to keep those in power who are in power and those without power without power).

Then I got sick. I got sick because a prescription pharmaceutical, an antibiotic no less (Cipro), hurt me.  I was poisoned by a prescription drug that is considered to have an “enviable record of safe and efficacious use.” (1)  I started screaming about how it’s not okay to take away people’s ability to walk, sleep, work, etc. to treat their sinus or urinary tract infections.  I started screaming about how fluoroquinolone antibiotics (Cipro, Levaquin, Avelox, Floxin and a few other less commonly used drugs) are dangerous and over-prescribed. I started researching how fluoroquinolones work and was appalled to find that they dismantle and disrupt replication of DNA.  I began making connections between the side-effects the fluoroquinolones, and the various diseases that fluoroquinolone toxicity mimics.

Diseases of Fluoroquinolone Toxicity

Fluoroquinolones cause peripheral neuropathy (2), peripheral neuropathy could easily be mistaken for Fibromyalgia. Fluoroquinolones cause destruction of tendons (3) and cartilage (4), both of which are found in the joints, and thus fluroquinolone toxicity could be misdiagnosed as Rheumatoid Arthritis. Fluoroquinolones have many psychological side-effects including anxiety, depression and even psychosis (5), and thus they may be connected lead to psychiatric disorders. I found a study that connected topoisomerase interrupting drugs (6) (fluoroquinolones are topoisomerase interrupters (7), along with several chemotherapy drugs) with Autism. A conspiracy theorist was born.

Fluoroquinolone antibiotics can take an acute infection and convert it into a chronic illness (Fluoroquinolone Toxicity Syndrome). The new, chronic illness likely will be misdiagnosed and not recognized as a drug side effect, and the treatment of the misdiagnosed disease often leads to prescriptions for additional drugs. And, even though that line of thinking leads to more profits for Big Pharma, I don’t think that it’s a conspiracy. I don’t think that it’s intentional, even on the part of the companies that initiate and perpetuate it, Bayer and Johnson & Johnson (J&J). Though making people chronically ill through an antibiotic that is viewed as benign by almost everyone is convenient and profitable for them, I don’t think that it’s their intention. Perhaps I’m naive.

Somewhere between naively believing that Bayer and J&J have no idea what they’re doing, and pessimistically believing they are poisoning us all to turn us into lifelong customers, lies the truth.

The Truth about Fluoroquinolones

The truth, especially when dealing with something as complicated and multifaceted as biochemistry, cellular biology and genetics, is very difficult to comprehend. But the fact that it is too difficult for most of us to understand does not mean that there is no truth. The correct answers are probably not the easiest answers. They don’t fit into a box of good or evil. They aren’t linear. The truth about fluoroquinolones involves inconvenient things like delayed reactions, tolerance thresholds, system-wide cellular destruction that results in a wide array of disease states, enzyme depletion, etc. The truth about fluoroquinolones defies common sense because our common sense tells us that antibiotics are benign, that drug side-effects are rare, that when side-effects happen they’re treatable and transient, etc.  That “common sense” approach, unfortunately, is not the truth.

The truth is that fluoroquinolones disrupt and dismantle DNA.  This has been shown repeatedly.  Per a 1998 study entitled “The Mechanism of Inhibition of Topoisomerase IV by Quinolone Antibacterials,” Fluoroquinolones are “among the first antibacterial agents that efficiently inhibited DNA replication.”  (8).  The mechanism for action for Ciprofloxacin, as listed on the FDA warning label is, “The bactericidal action of ciprofloxacin results from inhibition of the enzymes topoisomerase II (DNA gyrase) and topoisomerase IV (both Type II topoisomerases), which are required for bacterial DNA replication, transcription, repair, and recombination.” (7) Disrupting the DNA replication process is how these drugs work (or at least part of how they work).  Denying that fluoroquinolone antibiotics damage DNA because it’s not a pleasant thing to acknowledge, is futile and it does not get us closer to the truth.

Very little is known about the consequences of disrupting DNA replication through pharmaceuticals. The truth that fluoroquinolones disrupt and dismantle DNA is only part of the puzzle; it is only part of the truth. As complicated and poorly understood as the effects of these drugs on DNA are, there are still multiple levels of questions regarding the effects of fluoroquinolones on the human body. Some of the questions, answers and truths likely lie in understanding the effects of these drugs on mitochondria. A thorough understanding of article “Mechanisms of Pathogenesis in Drug Hepatotoxicity Putting the Stress on Mitochondria” (9) and how it relates to fluoroquinolones will likely give you some answers about how these drugs do damage. There is evidence that fluoroquinolones cause cerebellar ataxia (10). The carboxylic acid molecule that is part of fluoroquinolone drugs likely leads to the formation of hazardous acyl glucuronoids (11). The interaction between broken mitochondrial DNA, acyl glucuronoids and cerebellar ataxia, combined with other ill understood and complex factors, is probably where the truth lies. It is hugely complex. It is impossible for the average person to comprehend and it is difficult for even the smartest person to understand. So, instead of seeking understanding and truth, the majority has chosen to ignore the fact that no one knows how these chemicals work in the human body and what their consequences are. We will take them because we know one small element of what they do – they kill bacteria – and believe that all other effects of these drugs are coincidental, accidental or rare.

Willful Ignorance about Fluoroquinolone Dangers

Willful ignorance has taken over, and faith-based assumptions about the good or evil that the medical system is have come to dominate the conversation. The established medical system is the entrenched party with the power, so those who support it are the majority; they are those with “common sense.” Those who rebel against the assumptions that the medical system is doing good are accused of being conspiracy theorists or worse. No one is really qualified to say that they have a position based on truth though, because there are too many unknown variables to know the truth (at this time). No one, not even the smartest researchers and scientists, fully know how fluoroquinolones, and probably many other drugs, affect every system in the human body. The human body is too complex and too little is known (at this time) about it, and how each of its systems interact, for anyone to truly know how everything works together. So little is known about the human body that ligaments, something that you can see with the naked eye, are still being discovered (12). If we don’t even know every ligament in the body, you can certainly bet that we don’t know every enzyme or neural pathway. Yet enzymes, neural pathways, mitochondrial DNA and other really important parts of human physiology are being disturbed by pharmaceuticals. And people are getting sick because of it.

Though the truth about how adverse drug reactions occur is difficult to ascertain, it should be sought. Questions should be asked. Experiments should be done. The effects of drugs on all bodily systems should be explored.  Perhaps answers to difficult questions about how drugs effect mitochondria, neurons, enzymes, etc. should be asked before drugs are released into the public.

Back in 1992, when fluoroquinolones were first gaining popularity, Scientists raised concerns about their use in an article published by the Proceedings of the National Academy of Sciences of the United States:

“the interaction (of fluoroquinolones) with DNA is still of great concern because of the possible long-term genotoxicity of quinolone compounds, which are increasingly adopted as first-choice antibiotics for the treatment of many infections, and because it addresses the real mechanism of action of this class of molecules.” (13)

The question hasn’t been asked though.  People have been stuck on the faith-based assumption that fluoroquinolones have “enviable record of safe and efficacious use” because the only side-effects that they’re willing to see are allergic reactions. They have been intent on willful ignorance. Willful ignorance protects them. It keeps them from seeing that in frivolously over-prescribing dangerous and poorly understood drugs, we may have damaged our precious DNA, and that the consequences of doing so may be many of the “mysterious” systemic diseases that plague us.

There is a fine line between screaming about willful ignorance on the part of the majority and being a conspiracy theorist.  I’d like to think that I am reasonable; that my assertions are backed up by scientific findings, and that I’m right.  Of course, all conspiracy theorists also think that they’re right, so my conviction does very little to convince naysayers.  I hope that my screams are heard though. I hope that some people in power do something to stop the foolish over-use of these DNA damaging drugs.  I hope that it’s not too late to be prudent and cautious.

The real world is complicated. Sometimes human bodies work in ways that aren’t simple.  Sometimes problems are complex and difficult to understand. Sometimes pharmaceuticals work, or don’t work, in ways that are poorly understood. The power to do a massive amount of both good and harm is possible with modern medicine. Perhaps it is time that we start admitting that the harm that some drugs do is disproportionate to the good that they do. Perhaps it is time that we start recognizing that adverse drug reactions are not always immediate or easy to remedy. Perhaps it is time that we start insisting that the mechanisms of action for drugs be fully understood, at least by Scientists, before they are mass marketed to the public.

I don’t think that these suggestions and assertions make me a conspiracy theorist.  But if they do, so be it. The notion that the pharmaceutical/medical system is killing and sickening innocent people is a “conspiracy theory” that I know to be true.  So I will continue to fight to expose it, whatever the consequences may be.

Information about Fluoroquinolone Toxicity

Information about the author, and adverse reactions to fluoroquinolone antibiotics (Cipro/ciprofloxacin, Levaquin/levofloxacin, Avelox/moxifloxacin and Floxin/ofloxacin) can be found on Lisa Bloomquist’s site, www.floxiehope.com.

Participate in Research

Hormones MatterTM is conducting research on the side effects and adverse events associated with the fluoroquinolone antibiotics, Cipro, Levaquin, Avelox and others: The Fluoroquinolone Antibiotics Side Effects Study. The study is anonymous, takes 20-30 minutes to complete and is open to anyone who has used a fluoroquinolone antibiotic. Please complete the study and help us understand the scope of fluoroquinolone reactions.

Hormones MatterTM conducts other crowdsourced surveys on medication reactions. To take one of our other surveys, click here.

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References

  1. Expert Review of Anti-Infective Therapy. Levofloxacin: update and perspective on one of the original respiratory quinolones.
  2. FDA Drug Safety Communication: FDA requires label changes to warn of risk for possibly permanent nerve damage from antibacterial fluoroquinolone drugs taken by mouth or by injection.
  4. Quinolone Arthropathy in Animals Versus Children.
  5. Levofloxacin-induced acute anxiety and insomnia.
  6. Topoisomerases facilitate transcription of long genes linked to autism.
  7. FDA: Flouroquinolone warning label.
  8. The Mechanism of Inhibition of Topoisomerase IV by Quinolone Antibacterials*
  9. Mechanisms of Pathogenesis in Drug Hepatotoxicity Putting the Stress on Mitochondria.
  11. Current Drug Metabolism (v.12, #3).
  12. Surgeons discover new ligament in human knee.

Related posts:

beyond the ER with FQWhen Investigating Fluoroquinolone Reactions, Move Beyond the ER Bactrim reactionFrom Healthy to Barely Functioning After Taking Bactrim and Keflex

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