Tag Archives: adverse drug reactions

The Gaslighting of Patients

Gaslighting: A form of manipulation that seeks to sow seeds of doubt in a targeted individual or members of a group, hoping to make targets question their own memory, perception, and sanity. Using persistent denial, misdirection, contradiction, and lying, it attempts to destabilize the target and delegitimize the target’s belief.

Gaslighting occurs far too often to patients who experience adverse reactions to pharmaceuticals. Often, it is done by the people patients turn to when they are sick–our trusted advisors, our healers: our doctors.

I don’t think that most doctors mean to gaslight their patients, or that many of them are narcissists or abusers who intentionally manipulate people. I think that most doctors want to heal and help their patients. They use the information and tools that they have to move their patients toward health and well-being.

Yet, gaslighting is occurring.

When “floxed” patients approach their doctors with symptoms of fluoroquinolone toxicity (or FQAD-fluoroquinolone associated disability) they often face denial, derision, and hostility from the doctors who they are requesting help from. The doctors say that the symptoms that the patient is experiencing can’t be from the Cipro (ciprofloxacin), Levaquin (levofloxacin), Avelox (moxifloxacin), or Floxin (ofloxacin), even though most of the symptoms of fluoroquinolone toxicity / FQAD are listed in the 40+ page warning labels. They say that the drugs should be out of the patient’s body, even though the black box warning label notes that fluoroquinolones “have been associated with disabling and potentially irreversible serious adverse reactions.” They say that they’ve never seen a patient who has had an adverse reaction to a fluoroquinolone–and that may be true, but are they looking? They say that delayed reactions can’t happen–but they’re documented. They deny that adverse reactions can happen, probably because they are in denial about the very real possibility that the drugs that they prescribe can cause serious, severe, and irreversible pain to their patients.

Then, they suggest that the patient see a psychiatrist and get on antidepressants.

Some people who experience adverse reactions to fluoroquinolones benefit from seeing a psychiatrist and taking antidepressants (though others are hurt further by both–be careful), and those things aren’t inherently bad, but the implication in suggesting psychiatrists or antidepressants is that patients who are experiencing adverse reactions to fluoroquinolones are crazy. We’re not crazy. Though some fluoroquinolone toxicity / FQAD symptoms are psychiatric, none of the symptoms, not even the psychiatric ones, are choices, decisions, or even the result of being crazy. All the symptoms of fluoroquiolone toxicity / FQAD stem from fluoroquinolone use and the damage done by these drugs.

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When a person, especially a doctor, suggests that all the symptoms of fluoroquinolone toxicity / FQAD are in a patient’s head, they are gaslighting the patient and making him or her feel crazy.

It’s dismissive, it’s obnoxious, sometimes it’s abusive, and it’s always wrong.

It happens all the time though, and I wish that it would stop.

Adverse reactions to fluoroquinolones (and other pharmaceuticals) are real, and they happen more often than they should. Denying that adverse reactions occur, then blaming the victim and telling him/her that he/she is insane, is not only useless, it is destructive. It hurts the patient/doctor relationship, and, more importantly, it hurts the patient. As I said above, I don’t think that many doctors intentionally seek to manipulate or hurt their patients. It’s happening though, and it needs to stop.

In the stories of patient pain and suffering from fluoroquinolones described on Fluoroquinolone Stories and The Fluoroquinolone Wall of Pain, doctor denial and gaslighting are described.

Sherry describes the gaslighting and denial that she experienced after taking Floxin and Flagyl:

“I went from doctor to doctor trying to convince them that these drugs did this to my body. They looked at me as if I had ten heads. They couldn’t believe that these medications could stay in one’s body for that long. I was crazy. I would bring them papers to show them proof and one doctor said to me that the medical community would use these papers for toilet paper!”

Cheryl notes the following experience after taking Ciprofloxacin XL:

“I went back to the pharmacist and told him the reaction I had. He said it can happen and it certainly sounded like I had an adverse reaction but he did not report it. I went back to the doctor how prescribed the drug to me and he did not believe me that I had reacted in that manner. Again, no reporting back to any authorities that I had an adverse reaction. I tried to show him the evidence of how many people have been damaged by this group of drugs and how dangerous they are and I was blown off. He told me he prescribes this drug all the time and has never had anyone react. I beg to differ because I bet people do have negative reactions but because they happen after the drug has been used, the connection between the aching muscles, nausea, anxiety, stiffness etc are not connected to the drug they took a month or more ago.”

There are many others.

Floxies are not alone in getting gaslighted by doctors. In the post “The Unintentional Gaslighting of Women and a Goodbye” Kerry Gretchen describes how her stroke that resulted from hormonal birth control wasn’t taken seriously by the doctors who treated her. Support groups for people who have had adverse reactions to a variety of pharmaceuticals and medical devices are full of patients who are frustrated and hurt when their doctor denies both their pain, and the cause of it.

The pain caused by pharmaceutical injuries is real, and patient pain should never be dismissed or denied. When denial of pain occurs, and patients are told that their symptoms are all in their head, it hurts the patient psychologically, and destroys the trust and bond between the patient and his or her doctor.

Doctors can stop this cycle through listening to their patients, not dismissing or disregarding adverse drug reactions as “rare” or “all in your head,” and being conscious of gaslighting as a phenomenon. Good, thoughtful, kind doctors don’t want to hurt or manipulate their patients, but, in order to maintain their worldview about the safety and efficacy of the drugs they prescribe, they often deny and deflect. Hopefully, with awareness of both gaslighting as a phenomenon, and how adverse drug reaction symptoms appear, the cycle will be halted.

 

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Lessons from Entrepreneurs

One of my favorite podcasts is Entrepreneur on Fire with John Lee Dumas. It’s a fun and interesting podcast that fits just about perfectly into my commute. In it, John Lee Dumas interviews business owners about their entrepreneurship journey.

Because I relate everything in my life back to fluoroquinolone (FQ) toxicity, some things brought up on Entrepreneur on Fire often made me think about flox-related issues.

One thing that is brought up regularly on Entrepreneur on Fire is the power of networking. It seems that every time I talk with someone about FQ toxicity they say, “that happened to me,” or, “that happened to my husband, wife, sister, brother, mom, dad, uncle, aunt, child, neighbor, etc.” However, it also seems that no one outside of the “floxie” community really knows about FQ toxicity. It’s a strange combination of common and unheard of. It’s as if everyone thinks that they’re a rare case, or they internalize the lack of recognition of FQ toxicity in the medical community, or they assume that there must be other factors at play because antibiotics “don’t do that,” or they get better and don’t think about it any more.

I’m honestly not sure where the dissonance lies, and I am certainly biased in thinking that I see FQ toxicity everywhere, but I wonder if there just aren’t enough people talking about it. I wonder if, like in business, what is necessary for getting the word out about FQ toxicity is a whole lot of chatting about FQ toxicity and a whole lot of networking. If all of us who know about FQ toxicity shared something on our social media sites about FQ toxicity on a regular basis (daily, weekly, monthly – whatever you feel comfortable with), maybe more people would connect the dots and start talking about FQ toxicity. If people see articles or blog posts about FQ toxicity, maybe they’ll realize that they’re not alone in their suffering, or maybe people will start to believe that their loved one who is sick after taking a FQ isn’t just “being difficult,” or maybe people will think twice before taking a FQ themselves, or giving a FQ to a loved one. Maybe, if people hear about FQ toxicity enough, they’ll see that it’s a problem, and that something needs to be done about it.

I think that there is a lot of value in in-person networking and discussion of FQ toxicity as well as social media networking. Conversations can be initiated, and a lot of people can learn about the dangers of Cipro, Levaquin, Avelox and the other fluoroquinolones if, when we are asked, “What do you do?” those who know about FQ toxicity answer, “I’m a ____, and I also advocate for fluoroquinolone toxicity awareness,” or something like that. I understand that it’s not entirely healthy to base your identity in your sickness, but, in my case it’s an accurate description of my life. I spend more time and energy working on FQ toxicity advocacy than I do on my “real” job. If we all opened up the door to talk about FQ toxicity when networking, maybe we could not only make people more aware of FQ toxicity, maybe we could chat with the “right” person to advance our cause. You never know who someone is connected to. Maybe the next person that you chat with at a networking event is connected to a powerful doctor, or someone influential in the media, or whatever.

The book, “The Tipping Point” by Malcolm Gladwell, was brought up on Entrepreneur on Fire the other day. According to the back of the book, “The tipping point is that magic moment when an idea, trend or social behavior crosses a threshold, tips, and spreads like wildfire.” One day, FQ toxicity is going to reach a tipping point where it “spreads like wildfire,” and people know that fluoroquinolones are dangerous drugs that cause multi-symptom illness. One day, everyone will know how foolish it is to disrupt the DNA and RNA replication process of bacteria and mitochondria with chemo drugs masquerading as antibiotics. One day, it will be seen as a crime against humanity that these drugs were given out to children with ear infections. We’ll get to that tipping point where everyone realizes the dangers of fluoroquinolones, as us “floxies” do. Talking about FQ toxicity incessantly, and networking and sharing information, insights and stories is how we will reach the FQ toxicity awareness “tipping point.” And once the tipping point is reached, change will occur.

As Margaret Mead said, “Never doubt that a small group of thoughtful, committed citizens can change the world; indeed, it’s the only thing that ever has.” We change the world, and we reach the tipping point, one person at a time. We contact people, we take opportunities that are in front of us, and we create change – through networking, sharing and talking. It will behoove us to take tips from successful entrepreneurs – network, talk, spread ideas and knowledge, sell our world-view, etc. until the tipping point is reached.

 

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The Floxie Hope Podcast Episode 3 – Rachel Brummert

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Rachel Brummert, Executive Director of the Quinolone Vigilance Foundation, is interviewed on Episode 3 of The Floxie Hope Podcast.  Rachel goes over her history with fluoroquinolone toxicity; and gives information on the history, mission and activities of the Quinolone Vigilance Foundation (QVF).

The QVF is engaged in research, advocacy, outreach and other activities related to helping victims of fluoroquinolone toxicity.  The Mission of the QVF is to understand and reduce Quinolone/Fluoroquinolone Toxicity as a cause of human suffering in the world.

Per the QVF’s web site, www.saferpills.org, they fulfill this mission by networking medical professionals and researchers; fostering, initiating, and directing fundamental research to discover underlying toxicity mechanisms; funding research that will produce the most promising results; translating new discoveries into effective medical practices, therapies and public health approaches; and develop and applying discovered knowledge to educate the medical community and help alleviate individual suffering.

You can learn more about the QVF through listening to Episode 3 of The Floxie Hope Podcast.  It is available through the following links:

iTunes – https://itunes.apple.com/us/podcast/floxie-hope-podcast/id945226010

Floxie Hope Podcast Web Site – http://www.floxiehopepodcast.com/floxie-hope-podcast-episode-003-rachel-brummert/

Thank you for listening!

Please share The Floxie Hope Podcast with your loved ones and help us to get the word out about the dangers of fluoroquinolones.  Thank you!

All reviews of The Floxie Hope Podcast on iTunes are appreciated!

Enjoy!

 

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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.

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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 – http://articles.mercola.com/sites/articles/archive/2014/10/02/narcotic-overdose-deaths.aspx

 

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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 –

SIDE EFFECTS AND UNINTENDED CONSEQUENCES OF POPULAR PHARMACEUTICALS

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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