Monthly Archives: October 2014

Kratom – Painkiller for Floxies?

At the end of my last post, “Why NSAIDs Suck for Floxies (and Probably Everyone Else Too),” I mentioned some alternatives to NSAIDs that can be used as painkillers.  I forgot one that a Floxie friend specifically asked me to mention, so it’s getting its own post.

The painkiller is called Kratom.  It is reported to have helped several Floxies with pain management.  I have not personally tried it, nor have I done extensive research on it.  I highly recommend that you research it yourself before trying it.  I’m not a doctor and this isn’t a medical recommendation.  Kratom is a supplement/herbal drug and it should be considered as carefully as any other supplement/herb/drug.  Like all treatments for Floxies, what works well for one person, may not work well for another.

Now that I have put that disclaimer out there, I’ll mention some things that I read about it on the internet:

“Kratom is a tree native to Southeast Asia (Thailand, Malaysia, Myanmar [Burma], and elsewhere). Its botanical name is Mitragyna speciosa. Kratom is in the same family as the coffee tree (Rubiaceae). The leaves of kratom have been used as an herbal drug from time immemorial by peoples of Southeast Asia. It is used in folk medicine as a stimulant (at low doses), sedative (at high doses), recreational drug, pain killer, medicine for diarrhea, and treatment for opiate addiction.”

“Several Kratom supporters who commented and wrote to me said that the substance had helped them kick addictions to opiates–in some cases after many years of taking the drugs for tremendous pain. Others said it helped them get off anti-depressants and anti-anxiety medications. Some said that taking Kratom provides steady energy without increased anxiety. In general, supporters credited Kratom with remarkable benefits without side-effects.”

“The herb Kratom — Mitragyna speciosa — has become surprisingly popular for a growing number of Americans with various conditions that the pharmaceutical industry has poorly served and often ignored. Fibromyalgia, depression, diabetes, PTSD, anxiety, and chronic pain due to arthritis and injuries are some of the conditions where patients are turning to kratom out of frustration with pharmaceutical drug side-effects and lack of benefit.”

“So far, there have been only a handful of scientific studies on kratom’s effects on mammals. What is known is that there are more than 25 naturally occurring alkaloids in kratom leaves, and the two believed to be most active on opium receptors in the human brain are mitragynine and 7-hydroxymitragynine. A study by Doctor K.L.R. Jansen and Professor C.J. Prast, published in 1988 in the Journal of Ethnopharmacology, reports that kratom showed opiate-like effects (such as analgesia and cough suppression) in animals. These effects were confirmed by recent research at the Universiti Sains Malaysia and the December 2010 report published by the DEA.”

I would think (this isn’t a very educated guess – as I said, I haven’t looked into it much) that anything that affects opiod receptors could be addictive.  That is something to consider.

Kratom is legal in 49 of the 50 states.  The one state that it is illegal in is Indiana.

My basic impression is that Kratom is a painkiller that has fewer adverse effects than most of the painkillers (both legal and illegal) that are on the market.  It is reported to have helped some Floxies.  Very little research has been done on it so exactly how safe it is, is to be determined.  And, if you want to try it, you should try it now before the DEA gets too uptight about it.  Again, I’m not recommending it based off of any personal experience and you should always be careful and do your own research.  It is something that those suffering from chronic pain may benefit from though.


I had originally had the following on this post –

“Kratom can get you high.  The fact that it can get you high leads me to a couple of thoughts.  First, it’s being looked into as a controlled substance by the DEA.  There is too little research on it for them to be saying that they want to crack down on it because it’s dangerous.  But the DEA does have a history of cracking down on fairly safe drugs just because they get you high (marijuana being the main example).  As long as a drug doesn’t get you high, it can be horribly dangerous and still be encouraged by the government agencies.  The second it gets someone high though, panties get in a wad.  Blame our Puritan ancestors for that.

Second, the fact that Kratom can get you high may have some product safety and quality control implications.  If the kids are getting high off it, there is going to be a market for it.  If there is a market, there is going to be money and people may want to be shady with it (by “shady” I mean that they may lace it or otherwise tamper with it in order to gain more profits or customers).  So, please, be careful with your source and make sure that quality control measures are in place if you decide to try it.”


If it did get you high, I don’t, personally, think that’s a bad thing, but, it does NOT GET YOU HIGH.

Please see Linda’s comment below.

Also, in conversing about painkillers on facebook, both Noni juice and corydalis were mentioned as painkillers that have worked for Floxies.


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Why NSAIDs Suck for Floxies (and Probably Everyone Else Too)

After fluoroquinolone toxicity, many people have trouble handling NSAIDs.  By “have trouble handling” I mean that NSAIDs lead to an explosion of fluoroquinolone toxicity related symptoms for many (but not all) people.  I know that the last time I took a NSAID corresponded with the flox-bomb going off in my body – my hands and feet swelled and were painful, I had hives all over my body, my energy was gone, my tendons were weakened, my memory and concentration were shot, I had a massive amount of anxiety and many other symptoms.  I intend to avoid NSAIDs for the rest of my life because of this, and other people’s similar experiences.

That’s nice anecdotal evidence, Lisa, but it’s anecdotal and therefore not very convincing. 

From the warning label for Cipro/ciprofloxacin

“NSAIDs – Non-steroidal anti-inflammatory drugs (but not acetyl salicylic acid) in combination of very high doses of quinolones have been shown to provoke convulsions in pre-clinical studies.”

Also, from Pharmacology Weekly, “convulsive seizures have been reported in patients taking fluoroquinolones, especially if they are also taking nonsteroidal antiinflammatory drugs (NSAIDs).”

Well, that sucks, but I’m not taking NSAIDs concurrently with fluoroquinolones and I haven’t had seizures.  The question remains – Why shouldn’t I have NSAIDs after fluoroquinolone toxicity?

Nasty Carboxylic Acid Molecule

The answers, I think, come from the fact that both fluoroquinolones and NSAIDs have a carboxylic acid molecule in them.

When not metabolized properly, carboxylic acid molecule containing substances can form poisonous acyl-glucuronides and acyl-CoA thioesters.  Poisonous metabolities.  And, unfortunately, “When such metabolites react with critical proteins, cellular functionality may be disturbed or an immune response may be induced, eliciting adverse effects that in serious cases can be fatal” (from the article, Metabolic activation of carboxylic acids – all quotes in this post are from that article, unless otherwise specified).

Carboxylic acid molecules are found in various xenobiotics (a chemical or substance that is foreign to an organism or biological system), including fluoroquinolones and NSAIDs, as well as in biological systems “such as fatty acids, keto-acids, bile acids, messenger molecules and breakdown products from hormones and other endogenous molecules.”  The existence of carboxylic acids in our natural environment and processes has led us to be able to metabolize carboxylic acid molecules well.  Usually.  Until we aren’t able to metabolize them well any longer.  The conversion of carboxylic acid molecules into poisonous metabolites that react with proteins has to do with the following:

“It was also recognized early on that the isomers of acyl glucuronides (formed as a result of intramolecular acyl migration) can be equally or even more potent electrophilic species than the parent acyl glucuronide, and that these iso-glucuronides covalently bind to proteins via another mechanism [4]. Furthermore, acyl glucuronides are not only able to directly acylate cellular proteins, but they can also transacylate the cysteine thiol of glutathione (GSH), leading to drug-Sacyl- GSH, which in turn is a highly reactive species [5]. However, we still know very little about the overall toxicological significance of acyl glucuronides or their derivatives. A discussion about the causal role of acyl glucuronides in drug toxicity must not only consider the differential reactivity of the drug acyl glucuronides (e.g., type of substitution at the alpha carbon, half life [6-8]) but also the nature of the nucleophilic targets”  from Editorial [Hot Topic:Acyl Glucuronides: Mechanistic Role in Drug Toxicity? (Guest Editor: Urs A. Boelsterli)] by Urs A. Boelsterli (213-214).

Got that?  Don’t worry, most people don’t.  Even the author of that quote, Urs A. Boelsterli, goes on to say that, “Like for other signaling paradigms, it seems that the complex balance between bioactivating and protective pathways may ultimately determine the outcome in vivo, rather than one single factor (reactivity of an acyl glucuronide) alone. Thus, the exact role of acyl glucuronides in drug safety assessment is simply not known and cannot be generalized.”  Basically, it’s not known why carboxylic acid containing drugs sometimes turn into poisonous metabolites that form covalent adducts with critical protiens.  They don’t always.  But sometimes they do.  And when they do, a whole load of bad health outcomes occur.

Removal of carboxylic acid containing drugs from the market

Many carboxylic acid containing drugs, including NSAIDs, have been removed from the market because of safety issues.  “Many of the carboxylic acid containing drugs that have been associated with toxicity – idiosyncratic or otherwise – belong to the therapeutic class of NSAIDs.” And “Of 29 drugs withdrawn from the market in the UK, Spain or USA between 1974 and 1993, nine were carboxylic acid-containing drugs, making this compound class the most frequently involved in drug discontinuations in this period.”

Several fluoroquinolones have been removed from the market.  Omniflox/temafloxacin, Raxar/grepafloxacin, Trovan/trovafloxacin, Zagam/sparfloxacin, and Tequin/gatifloxacin have all been taken off the market in the U.S.


Interactions between carboxylic acid containing drugs and mitochondria

Diclofenac is a NSAID that is still on the market despite its association with immune-mediated toxicity and hepatic failure.  “studies have shown that diclofenac inhibits mitochondrial function, minimising ATP production and mitochondrial permeability transition [85,86] . Uncoupling of oxidative phosphorylation may be a class characteristic of NSAIDs and other carboxylic acid drugs; they act as proton ionophores.”

There is quite a bit of evidence that fluoroquinolones interfere with mitochondrial function “Bactericidal Antibiotics Induce Mitochondrial Dysfunction and Oxidative Damage in Mammalian Cells” and “Delayed cytotoxicity and cleavage of mitochondrial DNA in ciprofloxacin-treated mammalian cells” are two of my favorite articles.  Also, the FDA admits that mitochondrial damage is the likely mechanism through which fluoroquinolones cause peripheral neuropathy.

Acyl-CoA thioester formation is one of the metabolic pathways through which carboxylic acid molecule containing substances can form “chemically reactive metabolites that are capable of participating in nucleophilic-type reactions leading to the formation of covalently bound protein adducts.”  Acyl-CoA formation is “an integral part of mitochondrial energy metabolism.”

Delayed reactions and tolerance thresholds

A couple explanations for the delayed adverse reactions that people experience from fluoroquinolones come from the metabolites formed by the carboxylic acid molecules in FQs and NSAIDs, and also from their reaction with mitochondria.  Urs Boelsterli notes that, “On the other hand, although glucuronidation of carboxylic acid-containing drugs may cause delayed toxicity due to reactive acyl glucuronide intermediates, this process may at the same time protect from the acute toxicity of the aglycone or its oxidative metabolite(s).”  (Uhhhh…. Thanks for the delayed reaction that made this whole ordeal deniable for doctors?  Well, it’s better than acute death, so there’s that.)

In “Mechanisms of Pathogenesis in Drug Hepatotoxicity Putting the Stress on Mitochondria” it is noted (by Urs Boelsterli and others) that:

“…damage to mitochondria often reflects successive chemical insults, such that no immediate cause for functional changes or pathological alterations can be established. There is indeed experimental evidence that prolonged injury to mitochondria, such as that which typifies oxidative injury to mitochondrial DNA or to components of the electron transport chain (ETC), has to cross a certain threshold (or a number of thresholds) before cell damage or cell death becomes manifest.”

To put this section in more simple terms, delayed reactions and tolerance thresholds are real and there are several hypotheses for why people experience delayed adverse reactions to fluoroquinolones, NSAIDs, and other carboxylic acid containing, mitochondria damaging drugs.

Staying in the Lipids

Another possible explanation for delayed reactions and relapses is that fluoroquinolones and NSAIDs stay in the body.  I’ve always been skeptical about that possibility, but maybe they stay in the lipids.  “For example, several studies have shown the ability of xenobiotic carboxylic acids to be incorporated into complex lipids (e.g., formation of ‘hybrid’ tri-acyl glycerols by ibuprofen or fenbufen [90-92] ), thus prolonging the time the drug stays in the body, or potentially causing adverse effects through inhibition of lipid-metabolizing enzymes etc. [93] . The toxicological effect of such hybrid lipids is not known at present.”

Fluoroquinolones thoroughly mess up lipids.  The article “Comparison of the Effects of Subinhibitory Concentrations of Ciprofloxacin and Colistin on the Morphology of Cardiolipin Domains in Escherichia Coli Membranes” goes over how ciprofloxacin adversely affects cardiolipin, “an important component of the inner mitochondrial membrane, where it constitutes about 20% of the total lipid composition” (wiki).  “Characterization of the Interactions between Fluoroquinolone Antibiotics and Lipids: a Multitechnique Approach” is also an informative article.

Something to note is that the tests for autoimmune diseases aren’t testing the activity of the immune system, as one might assume, they are testing for cellular damage antibodies.  Antibodies to phospholipids are a category of tests for lupus, and the one of the tests in that category is that for a cardiolipin antibody.

Autoimmune Diseases and reactions

Some of the things said in “Metabolic activation of carboxylic acids” made me think that carboxylic acid containing drugs may be (causally) related to autoimmune diseases.

“high intra-cellular or plasma concentrations of acyl glucuronides may lead to the nonspecific formation of haptenated proteins that are able to invoke an immune response in susceptible individuals.”

“When such metabolites react with critical proteins, cellular functionality may be disturbed or an immune response may be induced, eliciting adverse effects that in serious cases can be fatal”

I’m honestly not sure whether or not the “immune response” noted is the same as an autoimmune disease.

It makes me wonder though – What is the relationship between carboxylic acid molecules and autoimmune diseases?  The fact that both NSAIDs and hormones contain carboxylic acid molecules makes me wonder whether carboxylic acid metabolites are the reason that women have more problems with autoimmune diseases than men.  (Women have a lovely monthly cycle of hormonal fluctuations that typically cause pain that is often treated with NSAIDs.)

The flox bomb went off in me 2 weeks after I finished my course of cipro, while I was taking NSAIDs (ibuprofen) because I was starting my period.  Triple whammy.  And it most definitely felt like my body was being attacked from the inside.

GABA issues

I honestly have no idea how GABA receptor issues relate to mitochondrial issues or carboxylic acid metabolism.  I do know that messing with GABA-A receptors is another reason to avoid both fluoroquinolones and NSAIDs, and especially to avoid them together.  From Pharmacology Weekly:

What role do NSAIDs have in the predisposition for developing seizures while also taking a fluoroquinolone antibiotic?

Interestingly, the presence of an NSAID or NSAID metabolite can significantly augment this effect and result in an even greater inhibition of GABA-A receptor activity.  It is, however, important to note that majority of this effect is related to an NSAID that is only available outside of the United States called fenbufen (Afiancen®, Bifene®, Cincopal®, Cinopal®, Lederfen®, Reugast®).9-11,14  It appears that the metabolite of fenbufen, 4-biphenylacetic acid (BPAA), augments the ability of the fluoroquinolone to inhibit GABA binding to the GABA-A receptor.9-11,14  It is important to note that BPPA itself does not inhibit GABA binding to the GABA-A receptor, but rather when BPAA and the fluoroquinolone come in close proximity they interact in such a way that it results in the ability of the fluoroquinolone antibiotic to inhibit GABA binding to a greater degree than by itself.  It is possible that the interaction between a fluoroquinolone antibiotic and BPAA causes some other biologic effect that influences the activity of the GABA-A receptor.  In fact, there is some evidence that some fluoroquinolones (mainly enoxacin and norfloxacin) can increase the activity of nuclear activator protein 1 (AP-1) DNA- and cyclic AMP responsive elements (CRE)-binding activities in both the hippocampus and cerebral cortex.14  It has been suggested that increased activity of AP-1 mediated gene expression is important for activity-dependent plasticity in these regions of the brain and thus contribute to the increased risk for seizures.14  Even though fenbufen has been the main NSAID implicated in this adverse drug reaction, other NSAIDs such as indomethacin, ketoprofen, naproxen, ibuprofen have also been shown to augment fluoroquinolone induced GABA-A receptor inhibition in animal studies.9

While the data most strongly implicate certain fluoroquinolone antibiotics and NSAIDs, CNS side effects and seizures have been reported with many of the fluoroquinolones, including the ones currently on the market.1-5  This is the reason that the product package inserts for the fluoroquinolone antibiotics not only list the above as potential side effects, but also describe the drug interaction with NSAIDs.1-5  As such, until further evidence suggests otherwise, it would be prudent, especially from a medical legal perspective, for healthcare providers to avoid the use of fluoroquinolones with or without NSAIDs in patients who are at greater risk for seizures (e.g., history of epilepsy, severe cerebral arteriosclerosis) or those with a lower seizure threshold (e.g., patients on medications known to do this, renal dysfunction).

Heart Disease

Even if one has never taken a fluoroquinolone, NSAIDs should be used with caution.  The number of NSAIDs removed from the market because they were too dangerous is high.  Vioxx, ibufenac, benoxaprofen have all been removed from the market because of severe toxicity issues.  Vioxx is thought to have directly caused hundreds of thousands of heart attacks.

The Reuters article, “High doses of common painkillers increase heart attack risks” notes that, “Long-term high-dose use of painkillers such as ibuprofen or diclofenac is ‘equally hazardous’ in terms of heart attack risk as use of the drug Vioxx, which was withdrawn due to its potential dangers, researchers said on Thursday.”

Concluding thoughts

Before I got floxed, I would pop ibuprofen like it was candy.  I would take it to ease menstrual cramps, whenever I felt even a little bit achy, and even to help me sleep.  I never had any sort of adverse reaction to it.  I thought of it as “vitamin I.”

It was only after my second exposure to cipro that I could no longer handle ibuprofen.  As I mentioned, the explosion that occurred in my body after taking cipro corresponded with taking ibuprofen for menstrual cramps.  I have not taken an NSAID since and I intend to avoid them, along with every other carboxylic acid containing drug, indefinitely.

Maybe my frequent use of ibuprofen set me up for getting floxed later.

Maybe the horrible reaction that I had to the triple whammy of carboxylic acid molecule containing substances – cipro, ibuprofen and hormones – saved me from future long-term consequences of regular NSAID use.  I don’t know.  I do know that they’re nasty drugs.  Shoot, NSAIDs can cause Stevens-Johnson Syndrome – aka, the worst thing ever, so I’m glad I stay away from them now.

Got it, no NSAIDs.  Problem – I’M STILL IN PAIN!  Any suggestions?

A paragraph at the end of an already-too-long post isn’t the place to fully address this, but I will acknowledge that the lack of safe painkillers is a serious problem.  Here are some options that I have heard good things about (I’m not a doctor, this isn’t medical advice, yadayada) –

  • Tumeric
  • Tart Cherry Juice
  • Vitamin D3
  • Cannabis / Marijuana
  • Opiates (a crappy option in many ways)
  • Acetaminophen / Tylenol (it’s hard on your liver, but it’s not a NSAID)

Here’s an article from Dr. Mercola that lists some additional alternative to pharmaceutical painkillers –


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Out of Balance: The Unbridled Power of the Pharmaceutical Industry

How did we get to this point where fluoroquinolones, drugs that have been shown, over and over again, to have hugely deleterious effects on cells, are prescribed to millions of people each year?

No one stopped it.

No one kept the pharmaceutical industry from doing what they do – turning an acute problem into a chronic problem via throwing a wrench into carefully calibrated biochemical pathways.  Lifetime customers are born from chronic health problems.  I don’t think that it’s a conspiracy, but I do think that the pharmaceutical companies aren’t incentivised to stop hurting people with pharmaceuticals.

As Chandler Marrs noted, “Unbridled power – that’s what pharma has and we allowed it. It’s funny, we go up in arms when there is the perception of too much power in government, but not in corporate America and not in medicine. Those are sacred cows that must be slaughtered. Otherwise, we might as well go back to the snake oil salesman and circus callers because w/o checks and balances in the medical industry, there is no product safety, none.”

Please read this post about the lack of checks and balances on the pharmaceutical industry –


Shares are greatly appreciated too.  Thanks!


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Fluoroquinolones as Chemo Drugs – Some Thoughts

Lisa and Dad

Lisa and her dad (Bill) in 2011

Several posts about fluoroquinolones being cell-destroying chemotherapeutic drugs have been posted lately. A couple of them are written by me (Lisa Bloomquist), CIPRO, LEVAQUIN AND AVELOX ARE CHEMO DRUGS published on Hormones Matter, and FDA ALLOWS CHEMO DRUGS TO BE PRESCRIBED AS ANTIBIOTICS published on Collective Evolution. Another post about fluoroquinolones being chemo drugs is David Melvin’s, FLUOROQUINOLONE DELAYED ADVERSE REACTIONS: SIMPLE THREE STEP LOGIC published on My Quin Story. And another is Paul Fassa’s, WHAT IF YOUR ANTIBIOTIC WAS REALLY A FAILED CHEMO DRUG published on Real Farmacy. They’re all good posts with good source articles that are well worth reading and sharing (please do)!

For my pedantic friends – yes, of course, I know that all antibiotics are chemotherapeutic drugs by definition. I’m using the term “chemo drug” to mean a drug that damages human cells and is used for the purposes of fighting cancer. You know what I mean when I say “chemo drug,” – no snottiness allowed. :p

When one realizes that fluoroquinolones are cell-destroying chemo drugs, a lot of things about them make sense.

First, people have a tolerance threshold for fluoroquinolones because they have a tolerance threshold for cellular damage. The same is true for many recognized chemo drugs. An individual can handle the damage done by the chemo drug – until they can’t. The threshold is one that can be crossed over a lifetime and damage is cumulative. (More about tolerance thresholds for fluoroquinolones can be found HERE.)

Second, the severity of the adverse reactions to fluoroquinolones make sense when it is recognized that they are cell-destroying chemo drugs. How does it make sense that every system in a Floxie’s body goes hay-wire after crossing his or her tolerance threshold for fluoroquinolones? Well, he or she was given a cell-destroying chemo drug that specifically attacks the mitochondria – the engines of the cells. When cellular engines are attacked, multiple systems can have multiple problems. Symptoms that are recognized as occurring with chemo drugs are common among Floxies – brain fog, neuropathy, fatigue, etc.

Third, delayed adverse reactions make sense when one recognizes that fluoroquinolones are chemo drugs. David Melvin explains how delayed reactions make sense when noting that fluoroquinolones are cell damaging chemotherapeutic drugs in his post, FLUOROQUINOLONE DELAYED ADVERSE REACTIONS: SIMPLE THREE STEP LOGIC published on My Quin Story. The three simple steps to understanding delayed adverse reactions to fluoroquinolones are recognizing that:

  1. Fluoroquinolones are powerful drugs
  2. Fluoroquinolones are chemotherapy
  3. Chemotherapy can cause “late effects”

Delayed reactions are often the most difficult things for people to get their heads wrapped around. I have a little story to make sense of it –

My dad was diagnosed with non-hodgkins lymphoma in 2004. He went through one round of chemo and kicked its butt. He’s going strong and doing well today. (I didn’t get my “dwell for years on a period of sickness” tendencies from him.) Even though he’s constantly climbing mountains and repelling into canyons (he’s doing really well), he has said several times that his cardiovascular system isn’t as strong as it used to be before he went through his round of chemo. Some cardiovascular system damage is certainly worth it – the chemo saved his life and got rid of his cancer – so he’s not complaining when he notes that it did some damage to his heart and lungs. He just doesn’t have the endurance or cardiovascular capacity that he probably would if he hadn’t had cancer/chemotherapy. No one thinks twice when my dad says that chemo drugs damaged his cardiovascular system. It makes sense because it is known that chemotherapeutic drugs do systemic damage that can be long-lasting, and that the adverse effects from that damage can happen long after administration of the drug has stopped.

But I’m betting that 9 out of 10 doctors would say that David Melvin’s near heart attack (described HERE) had nothing to do with the fluoroquinolone that he took seven years earlier. I don’t doubt for a second that David’s cardiovascular problems have to do with fluoroquinolone toxicity though. Fluoroquinolones are chemo drugs. They damage cells. It makes just as much sense for David to blame his near heart attack on the Levaquin that he took seven years ago as it makes for my dad to note that his endurance was decreased by his round of chemo nine years ago. Both have been exposed to chemo drugs. It makes sense when it’s realized and comprehended that fluoroquinolones are chemo drugs.

Now you may be thinking, “Great, Lisa, thanks for telling me that I’m going to have a heart attack. Thanks a lot. I thought this was supposed to be Floxie HOPE.” Enter expletive directed toward me.

I’m going to scream about fluoroquinolones being chemo drugs until people “get it” and doctors stop prescribing them for stupid stuff. But I don’t want the thought of fluoroquinolones as chemo drugs to steal your hope. People recover from chemo. They do. Many people go on to live full, happy, long lives after going through multiple rounds of chemotherapy. They recover their health and vitality. Their brain fog recedes and their energy returns. They go on with their lives.

Even though my dad notes that his cardiovascular system isn’t as strong as it was before he went through chemo, he’s living a really good and full life. He’s turning 69 this month and I can’t keep up with him. He’s literally climbing up mountains and repelling down canyons every weekend. He has a lot of love and joy in his life. He’s strong and capable. He has recovered from both the cancer and the chemo.

It was wrong that I was given a chemotherapeutic drug when I didn’t have cancer. The same is true for all of my Floxie friends. There is nothing that is okay about the damage that these stupid drugs inflict on people. But recovery is possible. Take a look through the stories on this site. People have recovered from fluoroquinolone toxicity and have gone on to lead good, happy, healthy, full lives. I wish the same for all of you!

Post script – Here are some tips for recovery from chemo from the National Cancer Institute – FACING FORWARD: LIFE AFTER CANCER TREATMENT. I think MY TIPS are better, but I’m a bit biased.



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Unintended Consequences of Pharmaceuticals (Especially Fluoroquinolones)

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Before I started studying adverse drug reactions / biochem / cellular biology, I thought that there were people who had a pretty good grasp of how everything within the human body works. I was wrong about that – I was ignorant. It took a lot of research for me to realize that the body is so incredibly (beautifully) complex, and that systems are so unpredictably intertwined, that no one really grasps how it all works. We aren’t even close. But pharmaceuticals throw a wrench in many biochemical pathways whether we are aware of them or not. Ignorance is not bliss. The complexity of life is mind-bogglingly amazing. How ’bout we stop messing with it in ways that hurt us?

A post about how complex and interconnected all of our biological systems are, and about how messing up any or all systems with pharmaceuticals is probably not the best idea, can be found here –


Many of the thoughts behind the post are based on THIS CHART.

There is nothing simple about biochemistry, but there is something that is beautiful and incredible about it.  All of those systems work together, and amazingly, they work together perfectly most of the time.  I find it to be mind-blowing and I’m a bit awe struck by what incredibly complex creatures we are.

Pharmaceuticals have the power to disrupt our biochemical systems.  I wish that we were using a bit more prudence with powerful concoctions that can hurt us in multiple ways.


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Repeated Use Doesn’t Make Fluoroquinolones Safe

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I posted “REPEATED USE DOESN’T MAKE FLUOROQUINOLONES SAFE” on on 10/1/2014.  Please check it out and share it – thanks!!!

When doctors say things like, “I’ve prescribed fluoroquinolone antibiotics to hundreds of patients and I’ve never seen problems like yours. It’s a good drug with an excellent safety record.” it really irks me.  It irks me for the nine reasons listed, but the one that irks me most is that it’s so illogical.  Doing things wrong repeatedly does not make them right.  Thousands of prescriptions for Vioxx, Thalidomide and DES were written before they were taken off the market or restricted. I’m sure that the doctors who wrote those prescriptions thought that the drugs that they were prescribing were perfectly safe. They weren’t. Fluoroquinolones are not safe either. Lack of recognition of the severe adverse effects does not make them safe – it just means that doctors are as biased and blinded as anyone else. Look at the studies. Look at what Cipro, Levaquin and Avelox do to cells. Cellular destruction results in multi-symptom, chronic illness – in case that fyi is needed.


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