Monthly Archives: February 2014

Missing Emails

I received about a dozen emails from people who reached out to me via the Floxie Hope “Contact me” page between February 17th and 20th.  I read the emails on my phone and noted that I needed to get back to those people.  When I went to respond to the emails, all messages that I received from the 17th through the 20th were gone.  They weren’t in my inbox.  They weren’t in my deleted emails folder.  They weren’t in my spam folder.  They were just gone.

The sucktasticness of Yahoo mail is annoying.

I know that this is a really trivial thing to post about, but I wanted to put a note out on a forum where people could access it easily to let those who wrote me know why I didn’t write them back.

To those of you who are waiting for a response – Can you please email me again?  I’m sorry for not being responsive!  I truly do try to respond to every email that comes to me.  I was looking forward to responding to each of you because I remember reading interesting insights and observations.  Now I no longer have your email, or your email address, and therefore my ability to converse with you is hindered.

It was suggested by a friend that I ask the NSA for copies of the emails that have disappeared.  Hahahahhahaha!  That would take a while.

I don’t think that I’m on the radar of anyone who would want to steal my emails in a nefarious way.  It would be nifty if I was, but I doubt that I am.

Anyhow, I opened a new gmail account with the hope that it will be less annoying than Yahoo’s mail system.

When I went to forward all of my old conversations initiated through floxie hope to the new gmail address, many of them were missing.  It’s probably just a glitch in the yahoo system, right?  Or the sucky way that yahoo organizes emails that are from a similar address kept me from finding the emails that I was looking for, right?  No one is messing with my email system and stealing my emails, right?

NSA peeps – can you please retrieve my emails for me?  :p

If someone is messing with my email system, they now know that I will blog about it and out them.  If nobody is messing with my email system (most likely) y’all know not to use yahoo mail because it stinks.

And floxie friends – be hopeful.  That’s all.  Be hopeful.  Recovery does happen for many.

And once you feel better and completely recovered you can worry about trivial crap like missing emails instead of wondering about whether or not you’re going to die.  It’s kind of nice to worry about trivial crap.


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Have you seen the documentary, “I AM?”  It’s an interesting and insightful film.  I recommend it.  Here it is, for you to check out:

The film makers seek to find answers to two questions.

1.  What is wrong with our world?


2.  What are the solutions to the world’s problems?

(Spoiler alert) – The answer to both questions is the same.  It is –


I am what is wrong with the world.  I am the solution to the world’s problems.

Kinda profound, if I do say so myself.

We all have problems and solutions within us.  I assert that they are in balance as well.  Those who cause huge problems are a huge part of the solutions.  Those who cause small problems are still part of the solutions, but they’re a smaller part.  People fluctuate between perpetuating problems and perpetuating solutions.  The pendulum swings from problem to solution – in our individual lives, in our institutions and in our world.

No one is the solution without recognizing that they are the problem as well.  There are those who are the problem without being the solution, but they generally fail to recognize that they are part of the problem – they fail to see that there is a problem and imagine, out of ego and narcissism, that they are neutral.

It’s called responsibility.  I am responsible for the problems that I cause in the world and I am responsible for solutions to them.

It took a long time for me to accept responsibility for my floxing, and I sill like to think of myself as more of a contributor to the solution than to the problem of people being hurt by fluoroquinolones.  Sure, I can take responsibility for putting the pills in my mouth, for self-medicating, for having a breakdown when I got sick, for not communicating what happened to me to my doctor, for the anger that I feel toward the medical system, and plenty more.  Got it.  I am responsible for all of those things.  I am also responsible for creating this site to bring light to the problem, for offering people stories of hope and healing, along with snippets of “deep thoughts by Lisa” – these things are part of the solution.  They’re the least that I can do and I have every intention of doing more to change the situation of people becoming disabled from unnecessarily strong chemotherapy drugs being frivolously prescribed to treat infections.  My pendulum is in solution mode for the problem of fluoroquinolone toxicity.  And fluoroquinolone toxicity is a problem, a big one.

Doctors, and the medical system as a whole, don’t seem to see the problem though.  They are stuck in the narcissistic, false view that they are the solution without being part of the problem.  They fix things, cure diseases and heal people, right?  Sure – those things happen.  Doctors should be proud of every life that they save and every disease that they cure.  But those accomplishments do not diminish the pain that they inflict.  Along with the good that has come with modern medicine, harm has come as well.  The rise in “diseases of modernity” such as autoimmune diseases, obesity and its complications, ignored diseases (like fibromyalgia, chronic fatigue, gulf war syndrome, adverse drug reactions, etc.), autism, mental illness (it’s not a choice), dietary intolerances, etc. are at least partially, if not fully, caused by pharmaceuticals, doctors and the medical system.

It’s not that difficult of a concept – pharmaceuticals cause mitochondrial damage, those mitochondria create massive amounts of oxidative stress and the superoxide and/or peroxynitrate cycles within the cells cause direct and indirect (through damage to DNA and negative gene expression) harm.  Also, destruction of the microbiome and its balance are really bad ideas that cause all sorts of problems.

Of course, the whole process is complex and difficult to understand when you get into the details.  It’s too difficult for most doctors to see, not only because it’s hard and they’re too busy to look at scientific research, but also because they’re stuck in their ideas of what “should” be.  Drugs “should” metabolize out of a person’s body in a short amount of time.  Antibiotics “should” kill bacterial cells while leaving host cells intact.  Fluoroquinolones “should” not damage DNA.  Doctors “should” cure diseases.  The medical system “should” be the solution, not the problem.

Too bad what “should” be does not align with what IS.

Every doctor, every drug, even every patient that buys into the system, is part of the problem.

It is time for everyone to recognize that with the good of Western medicine, some bad has come too.  It’s time for egos to be put aside and for people (mainly the doctors) to realize that they are responsible for recognition and creation of the problem – they are the problem.

Doctors and other people in the medical system are the solution as well.  Of course they are!  Who else could be?  They have the resources to solve the problems that they cause, and no one else does.

Patients are part of both the problem and the solution as well.  The information is available for patients to realize a large amount of what good and harm drugs and procedures do.  Patients can, and should, advocate for themselves and speak out when they see something that is wrong.

But first, both doctors and patients have to see that there are problems.  They need to see that the situation that we are in, with young people falling ill to chronic, disabling diseases, is not okay.  It’s a problem.

I can only hope that doctors will be willing to put aside their foolish egos and realize that they do harm along with good.  They aren’t going to realize anything or accept any culpability without pressure.  I am sure of that.  People who have been hurt by them (and the system that they are part of) need to rise up and make them aware of the harm that they have caused; the problems that their actions have led to.

Patient activists are responsible for putting pressure on doctors, the pharmaceutical companies, pharmacists, and others in the medical field too.  We need to push harder so that those within the system are recognizing the problem and working toward becoming the solution.

I AM the solution.  (Along with cannabis – haven’t you heard?  It cures EVERYTHING.)

I AM the problem as well.  (Along with fluoroquinolones – seriously, I can connect them causally to every chronic illness out there.)

I have less power than the medical system and the pharmaceutical industry though, so, dare I say – I am less of the problem, or the solution than they are.

Solution mode is greatly needed.  From everyone.  Especially from those with power and influence.

Maybe my perceived lack of power is a cop-out though.  Maybe the answer is simple.  What is the problem?  I AM.  What is the solution?  I AM.

You are too.

“No man sets aside his old ways to seek the new until he personally feels the need for it.  This is why the great teachers urge men to see the awful condition they are actually in, rather than living by pretty words and nonexistent ideals.  Talking about love and peace when neither love nor peace are in their hearts is a cunning and destructive evasion of the facts.”  – Vernon Howard


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Article Breakdown – “Mechanisms of Pathogenesis in Drug Hepatotoxicity Putting the Stress on Mitochondria”


Do you have a headache?  Do you want one?  If so, read this article –

Mechanisms of Pathogenesis in Drug Hepatotoxicity Putting the Stress on Mitochondria” written by

Dean P. Jones, John J. Lemasters, Derick Han, Urs A. Boelsterli, Neil Kaplowitz

If you want a headache that lasts a while, read these articles that give background information as to why what is in “Mechanisms of Pathogenesis in Drug Hepatotoxicity Putting the Stress on Mitochondria” is important.

Drug Metabolism and Disposition, “Acyl Glucuronidation of Fluoroquinolone Antibiotics by the UDP-Gulucuronosyltransferase 1A Subfamily in Human Liver Microsomes


Current Drug Metabolism, “Acyl Glucuronides: Mechanistic Role in Drug Toxicity?

Despite their headache inducing capabilities, the articles are actually quite interesting and important.  To highlight how and why they are important, here is my breakdown of “Mechanisms of Pathogenesis in Drug Hepatotoxicity Putting the Stress on Mitochondria.”  As I have done with other journal articles, I have taken quotes from the article and commented under them.

“Mitochondrial impairment is usually a final event common to pathways leading to necrotic and apoptotic cell death.”

Since mitochondrial impairment leads to cell death, perhaps it would be nice for the FDA to examine how pharmaceuticals affect mitochondria before approving them.  Sadly, they don’t think so, as “mitochondrial toxicity testing is still not required by the US FDA for drug approval.” (

“it is important to consider whether drug-induced participation of mitochondria in hepatocellular death is a direct result of drugs acting on these organelles (e.g., drug accumulation, inhibition of electron transport and fatty acid oxidation, or depletion of anti-oxidant defense) or an indirect result ensuing from mitochondrial participation in programs of cell death.”

They found that both were the case.  This stuff is very complex and not linear.  One reaction causes another reaction, on and on for a while.  It’s not an either/or situation.

“Oxidative stress is often defined as an imbalance of pro-oxidants and antioxidants; however, the finding that thiols [i.e., glutathione (GSH) and cysteine (Cys)] in plasma are not in redox equilibrium with their disulfide products [i.e., respectively, GSSG and CySS] (1, 2) and that their plasma concentrations are substantially displaced from cellular values (3) has significantly altered concepts of oxidative stress (4, 5). For example, the in vivo “balance” of pro-oxidants and antioxidants cannot be defined by any single entity, such as an equilibrium constant, and our growing knowledge of signaling mechanisms indicates that oxidative stress may be better defined as a disruption of redox signaling, rather than as an imbalance of pro-oxidants and antioxidants. The failure of large-scale, double-blind interventional trials with free-radical scavenging antioxidants may likewise reflect an oversimplified therapeutic approach.”

If you have too many oxidants/oxidative stress in your system, you should just add antioxidants to restore the balance of oxidants and antioxidants, right?  Well, it’s not that simple.  Once the signaling mechanisms within mitochondria start the process of oxidative stress and apoptosis (programmed cell death), you can’t stop the process or repair the damage by adding more antioxidants to the mix.  If it was as simple as a disruption in the balance between oxidants and antioxidants, we would all be cured by glutathione drips and vitamin C supplements.  Unfortunately, there are complex feedback loops that make the process much more difficult to fix than that.  I’m not saying that glutathione drips and vitamin C supplements aren’t worth a try, it’s just that adding antioxidants to make up for the excess of oxidative stress (in the form of Reactive Oxygen Species and Reactive Nitrogen Species) is an oversimplified approach.

“Cells that overexpress the mitochondrion-specific thioredoxin Trx2, however, have been found to be resistant to tBH-induced loss of mitochondrial membrane potential and apoptosis”

Mitochondrion-specific thioredoxin Trx2 ( is protective.  I’m not sure exactly what the implications of this are, but I suspect that those of us who got “floxed” have low levels of mitochondrion-specific thioredoxin Trx2.  (We probably are deficient in cellular magnesium and have a genetic predisposition toward susceptibility to mitochondrial injury and oxidative stress too.)


“Mitochondrial Trx2 responds to changes in the extracellular redox potential of Cys/CySS ( (EhCys/CySS) over a range that is relevant to cardiovascular disease in humans.” and “Previous in vitro findings support a cause–effect relationship for plasma CySS in cell signaling pathways associated with cardiovascular disease.”

Cardiovascular disease is related to mitochondrial function and oxidative stress / antioxidants.

Every chronic disease that plagues humans has its roots in mitochondrial dysfunction.  That may be Lisa’s theory, or it may be the truth.  TBD.  But there are enough journal articles noting how mitochondria relate to all sorts of chronic diseases that you’d think that our regulatory agencies would require that the effects of pharmaceuticals on mitochondria be tested before they are released to the market.  But no, they don’t.  They’re incompetent fools.  And because of their foolishness the pharmaceutical companies really have gotten away with creating customers, not cures.

“Mass spectrometry-based redox proteomics show that several classes of plasma membrane and cytoskeletal proteins involved in inflammation respond to this redox switch (Trx2), including vascular cell adhesion molecule, integrins, actin, and several Ras family GTPases.”

This really cryptic, difficult to understand sentence may actually say a lot about FQ toxicity.  The Trx2 redox switch ( is protective against loss of mitochondrial membrane potential and apoptosis (see above).  So, perhaps underexpression of the Trx2 redox switch  leads to inflammation of  vascular cell adhesion molecules, integrins, actin, and several Ras family GTPases.  What are these things, you ask?  Wiki will tell us!

Vascular Cell Adhesion Molecules – “The VCAM-1 protein mediates the adhesion of lymphocytes, monocytes, eosinophils, and basophils to vascular endothelium. It also functions in leukocyte-endothelial cell signal transduction, and it may play a role in the development of atherosclerosis and rheumatoid arthritis.” (I’ll let you look up all of the words you don’t know in this – ugh.)

Integrins and – “Integrins are cell-surface receptors that mediate cell-cell adhesion and are of great importance in binding and interactions of cells with components of the extracellular matrix (ECM) such as fibronectin (and cell-matrix). Importantly, integrins facilitate “communication” between the cytoskeleton and extracellular matrix, allowing each to influence the orientation and structure of the other.”  When your integrins are messed up, your cytoskeleton can get messed up.  Or something like that.

Here is an about how fluoroquinolones that mentions how they relate to integrins – – “Lack of extracellular Mg2+ impairs the function of integrins.  These transmembrane proteins connect the cells to extracellular matrix”  This stuff has something to do with how fluoroquinolones mess up tendons.  Yeah.

Actin  It’s important for cellular function.  (That’s all I’ve got for you – read the wiki :p )

Ras Family GTPases –  It’s important for cellular function.  (That’s all I’ve got for you – read the wiki :p )

You could get completely lost looking up all of the different systems described within this sentence.  Now that I have dug through it, maybe the authors of the study stated things as succinctly as possible.  This stuff is hard.

If someone significantly smarter than me wants to figure out how each of these cellular functions relate to magnesium, and, of course, floxing, that would be great.

Chelatable Iron, Oxidative Stress, and Cell Death

This whole section is about how iron relates to drug induced liver injury (DILI).  I’m not going to go over it piece by piece.  One thing that makes me curious about this section is that iron helped me to feel better than any other supplement.  I wonder why that is.  If the answer is in the article, I don’t understand chemistry well enough to get it from the article.

“In the mitochondrial permeability transition (MPT), high-conductance permeability transition (PT) pores open that make the mitochondrial inner membrane nonselectively permeable to all solutes of molecular mass up to approximately 1500 Da (59, 60). Calcium ion, oxidative stress, and numerous reactive chemicals induce onset of the MPT, whereas cyclosporin A (CsA) and pH less than 7 inhibit pore opening. After MPT onset, mitochondrial depolarize and undergo large-amplitude swelling driven by colloid osmotic forces, which are the hallmarks of the MPT. Swelling leads to rupture of the mitochondrial outer membrane and release of proapoptotic cytochrome c and other factors from the intermembrane space.”

Calcium + oxidative stress = apoptosis.  I’ve seen this elsewhere –

Interplay of Signal Transduction and Mitochondria in the Acetaminophen model

This section goes over how acetaminophen causes mitochondrial damage and drug induced liver injury.  It’s not a one-step process – it’s really complex and multiple things have to go wrong, at a cellular level, at once.  But it can happen.

As I mentioned above, I hypothesize that pharmaceutical induced mitochondrial injury is the cause of most chronic diseases.  Per Dr. Richard Boles, an expert in mitochondrial dysfunction and diseases:

these are partial defects. Mitochondrial dysfunction doesn’t really cause anything, what it does is predisposes towards seemingly everything. It’s one of many risk factors in multifactorial disease. It can predispose towards epilepsy, chronic fatigue, and even autism, but it doesn’t do it alone. It does it in combination with other factors, which is why in a family with a single mutation going through the family, everyone in the family is affected in a different way. Because it predisposes for disease throughout the entire system.”  (

Is acetaminophen causing mitochondrial damage???  Is it damaging or depleting mtDNA?  Is that damage hereditary????  Because if ACETAMINOPHEN is leading to a variety of chronic diseases, ugh, well, we might just be fucked (sorry, I couldn’t think of another word for the situation).

Fluoroquinolones deplete mitochondrial DNA content – “Interestingly, as an inhibitor of bacterial topoisomerase II and an inducer of DNA double-strand breaks, ciprofloxacin was also shown to deplete the mitochondrial DNA (mtDNA) content, thus leading to mitochondrial dysfunction and retarded cellular growth (15–17).”  Awesome, huh?

I think that fluoroquinolone induced mitochondrial damage, both direct and hereditary, is responsible for the increase in every chronic disease that has increased in prevalence along with fluoroquinolone use.

“One of the most striking and puzzling clinical hallmarks of idiosyncratic (host-dependent) DILI is the delayed onset of the disease. In fact, the time between initiation of daily drug treatment and the presentation of biochemical markers and clinical symptoms of liver injury can vary from a few weeks to several months, sometimes even exceeding a year (89). The reason for the long lag, often followed by an abrupt progression to DILI, is currently not known. However, it is clear, for the vast majority of drugs, that the delayed time to onset is not related to a gradual accumulation (of drug or drug metabolite) that would eventually lead to critical and toxicologically relevant concentrations in the liver. Instead, the lag time could be explained by an accumulating effect of a drug. This notion, together with experimental findings, is in line with the concept that mitochondria are involved in the etiology of DILI, because 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 (Figure 4A).”

Underlining added by Lisa.  This paragraph explains both delayed reactions and the fact that most people have a tolerance threshold for fluoroquinolones.  If your doctor, or anyone else, tells you that your reaction that came months after you stopped administration of a fluoroquinolone “couldn’t have happened because of the FQ, because it was metabolized already,” or something like that, tell him or her to read this paragraph as many times as it takes to understand it.  Damage to mitochondria, whether related to DILI or not, is not linear and it is not (necessarily) immediate.  Unfortunately, this is not understood by anyone other than the authors of this study, and probably a few other scientists, so suing based on a delayed reaction to a drug that you have tolerated well in the past is difficult to impossible.

“This non-linear response can be explained upon consideration that the molecules that subserve mitochondrial function (e.g., mitochondrial DNA, mRNA, and ETC proteins) are present in excess of amounts required for normal cell function. This reserve (or buffering) capacity acts as a protective mechanism; however, at a certain stage of damage, the supply of biomolecules needed to support wild-type mitochondrial function becomes compromised.”

For each of us Floxies, the reserve capacity of our mtDNA has been depleted.  I have no clue if it can be built up again or not.

“a number of human mitochondrial genetic diseases that are clinically discreet are being diagnosed at unexpected rates”

It is REALLY IMPORTANT that it be determined whether or not pharmaceutical induced damage to mitochondria is hereditary.  Seriously scientists – important stuff – answers will be greatly appreciated.

“First, all the investigated drugs (including trovafloxacin, a fluoroquinolone) invariably decreased the activity of key mitochondrial proteins that are sensitive to oxidant stress (e.g., aconitase-2, complex I) and often decreased the expression of mitochondrial (but not nuclear) genes (120). Second, we found that these markers of mitochondrial injury became apparent only after four weeks, although a number of cytoprotective pathways were activated within two weeks. It thus appears that an initial adaptive response was followed by a toxic response (121), possibly also involving a threshold.”

What happens when expression of mitochondrial genes are decreased?  What are the implications of this finding?

The fact that there is an initial adaptative response followed by a toxic response (to pharmaceutical induced mitochondrial injury) may explain why there are so many different results to studies of fluoroquinolones (and other mito damaging drugs).  Long-term studies need to be done.  Studies that take into consideration that delayed reactions occur, need to be done.  Studies that take into consideration tolerance thresholds need to be done.  Please.

“First, superoxide that escapes dismutation to hydrogen peroxide cannot cross the inner mitochondrial membrane and can oxidize [Fe-S]-containing enzymes (e.g., aconitase and complex I/III subunits). Alternatively, superoxide can rapidly react with mitochondrial nitric oxide (NO) to form peroxynitrite (ONOO−). For example, the fluoroquinolone antibiotic trovafloxacin (TVX), a typical DILI-associated drug, raises steady-state levels of NO in hepatocellular mitochondria (unpublished data). The mechanisms are not known, but TVX also increases cytosolic (non-ferritin-bound) Ca2+, likely activating the Ca2+-dependent mitochondrial NO synthase (123) to produce ONOO−. Peroxynitrite is dangerous for a number of reasons: i) under acidic conditions, it can be degraded to form the extremely reactive hydroxyl radical; ii) it may directly cause the nitration of aconitase, Sod2, and the [Fe-S]-containing subunits of ETC complexes; and iii) it can induce mitochondrial permeabilization (Figure 4B) (124). This superimposed oxidative/nitrative stress could ultimately push the cell across the threshold to observable injury.”

Floxies – that’s what happened to you (and me).  It’s really hard to understand, I know.  I have a headache right now and I’m guessing that you do too if you’ve gotten this far in the post.  It’s important information though.

On a light note, I think that it’s funny that fluoroquinolones convert “NO” into “ONOO” in our cells.  Yup, that’s about what it feels like – “no” turning into “oh no” turning into “oh fuck” which turns into “fuck you Bayer / Johnson & Johnson.”  🙂

The end of the article and my comments.

Dean P. Jones, John J. Lemasters, Derick Han, Urs A. Boelsterli and Neil Kaplowitz are brilliant.  I thank them very much for this article.  It answers a lot of questions.  It still leaves many unanswered, of course – as any good article does.  I hope that they, and more scientists, are doing more work on the relationship between pharmaceutical induced mitochondrial injury and disease states.
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Fluoroquinolone Caused Mitochondrial Damage and Oxidative Stress – What are the Consequences for Floxies?

Pill Pic 021014

I’m working on a couple of posts/articles/essays right now about how all sorts of chronic diseases, from diabetes to alzheimer’s to autism, are caused by mitochondrial damage and oxidative stress.  I’m pointing out that pharmaceuticals cause mitochondrial damage and oxidative stress.  Of course, I’m focusing on my least-favorite pharmaceuticals, fluoroquinolones, and am trying to make a case that fluoroquinolones cause many chronic diseases.

That line of thinking is scary as hell for those of us who have had a bad reaction to a fluoroquinolone.

What does the connection between fluoroquinolone induced mitochondrial damage / oxidative stress and chronic diseases mean for us?  What is our prognosis?  Are we going to come down with diabetes or Alzheimer’s?  Are our kids going to be autistic?  Scary stuff – aaaarghhhh!!!  New plan – run and hide on a tropical island far from the internet.

Just so you all know, I’m not sure what it all means.  I am doing my best to put together the pieces of the puzzle.  I’m doing my best to draw conclusions from reputable sources.  I’m doing my best to understand what happened in my body when the Cipro bomb went off in me.  In trying to understand what happened, I’m stumbling upon articles that point to the possibility that the problem is bigger than we think.  It is possible that fluoroquinolones are causally related to fibromyalgia, chronic fatigue syndrome / M.E., all autoimmune diseases, depression, anxiety, bipolar disorder, diabetes, Alzheimer’s, autism, some kinds of cancer, and more.  Are all cases of those chronic diseases caused by fluoroquinolones?  Of course not – most of the diseases are older than fluoroquinolones.  But it’s possible that they have increased hand in hand with fluoroquinolone use because of the damage that fluoroquinolones do to mitochondria, and the oxidative stress that they induce.

It’s also possible that other drugs are the primary culprits.  And I suppose that it’s even possible that junk food that is full of free radical producting chemicals is the culprit behind all the oxidative stress that people who have chronic diseases experience.  Or maybe the problem is GMO corn or childhood vaccines or pesticides or something else.  There are pretty reputable sources that note that pharmaceuticals cause mitochondrial damage and oxidative stress though, so I’m betting that the culprits are Bayer, Johnson & Johnson, Merck, Pfizer, Abbvie and all the other pharmaceutical giants that are very good at making customers and very bad at actually promoting health.

Anyhow, the theory that fluoroquinolones cause mitochondrial damage / oxidative stress and that mito damage / oxidative stress are behind all sorts of chronic diseases is the theory that I’m going with.  Whether I’m right or wrong is yet to be seen.  Even though my theory may scare the crap out of you, your support is still greatly appreciated.  🙂

If I’m wrong, the case against fluoroquinolones is still pretty damning.  With fluoroquinolones, one can convert an acute problem, an infection, into a chronic syndrome that includes destruction of connective tissue (tendons, ligaments, cartilage, fascia, etc.) throughout the body, damage to the nervous systems (central, peripheral and autonomic), and more.  Fluoroquinolone toxicity can develop slowly or quickly.  It can last for months or years.  Tragically, some people don’t recover.  But most people do – with time.

How fluoroquinolones cause the damage that they do is hugely complex and difficult to understand.  Part of the damage mechanism is mitochondrial damage and oxidative stress, hence the trip down chronic disease lane.  Other aspects of how fluoroquinolones work – DNA adducts, RNA transcription errors, disruption of tubulin assembly, etc. are equally daunting and potentially harmful.  Ugh.  Bad news.

But people do recover from fluoroquinolone toxicity.  I did.  I’m fully recovered.  So are the other people who have shared their stories on  I wonder if the chronic disease prognosis for those who recover is any different from the prognosis for those who don’t, or for those who take fluoroquinolones but don’t have an adverse reaction.  I don’t think that a study to answer that question has been done.  It would be interesting to find out the answer.

Right now, we don’t know the answers though, so we have to make assumptions about our health and our future.  If you’re going to make baseless assumptions about your personal health prognosis though, they may as well be hopeful ones.  Try to believe that you will heal and that once you heal you will be as capable, resilient and durable as you were before a fluoroquinolone knocked you down.  Or, better yet, believe that floxing gave you some sort of health super-powers.  Here is a crazy thought – what if our floxing reaction was actually protective against damaged cells and the conversion of those cells into chronic diseases?  What if our horrible reaction was because of mass apoptosis (programmed cell death), and in dying, those cells kept from reproducing and leading to a chronic disease at some later time?  Now that is a far-fetched hypothesis, but I kind of like it.  I just hope that my recovery doesn’t mean that my bad cells are sticking around now.  :p

Back to fluoroquinolones being related to the chronic diseases – what if I’m right?  What if fluoroquinolone caused mitochondrial damage and oxidative stress is behind all of the chronic diseases of modernity?  Well, it’s a sad state of affairs.  But people should know about it.  They should hear about it.  They have the right to know.

But you are going to be fine.  Try to believe it.


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Fluoroquinolone Antibiotics and Fungal Infections – A Real Problem

Hormones Matter Logo

When antibiotics kill the good bacteria in the gut, fungal infections can take over.  I wonder how many of our floxing symptoms have to do with fungal overgrowth?  Here are some thoughts.

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Keep Going

Not Giving Up

A friend wrote this to me –

Dear Lisa,

I don’t believe I am going to get better, and I don’t know what to do anymore. This feels like a nightmare from which I cannot wake up. I know people say to stay positive, but I don’t know how, especially when, every day, I read comments in the group with people who are several years out, and have not improved. I know people say everyone is different, but after more than a year, I have a feeling I am one of the unfortunate few that never recover. What should I do?

Here is my response –

Dearest friend,

I think that you should just keep going. That’s all that is really required of you, or anyone else – just not giving up. In not giving up you are being hopeful. Eventually, it will become easier to not give up. Eventually, it will be effortless. At least that’s what I hope for you.

I recently got an email from someone who recovered after 8 years. 8 years is frightening, for sure. But she recovered. It did happen.

I encourage you to find something that makes you feel just a little bit better. Maybe that’s sunshine, or funny movies, or acupuncture, or magnesium, or whatever – and do that thing every day until the little incremental improvements add up.

And just don’t give up.

Try to believe that it will get better. It’s okay to not always believe that you will improve. But as long as you’re not giving up, things will change. Maybe they will change for the better. I hope that for you!

That’s what I think you should do. I hope that what I said doesn’t seem to trivialize your situation in any way. I know that it’s scary and I know that fear that it won’t end is normal. I think that just continuing on is difficult sometimes. That’s what I suggest you do though.



Post Script To All:

I wish you all healing, love, happiness, recovery and everything else that your heart desires.  I’m sorry that this whole ordeal happened to you.  I’m sorry for the pain.  I’m sorry for the suffering.  I’m sorry for the fear and the hopelessness.  I hope that it all passes.  I hope that you find your way back to health and happiness.

I know that sometimes it feels like it won’t pass, like you’re stuck in a hole and will never be able to crawl out of it.  It will pass though.  I can’t promise that you will recover completely, or that you’ll get your former abilities, or yourself, back.  But I can promise you that this difficult moment will pass.  It will change.  Eventually you will stop falling down the hole, and you will start to improve; to emerge.

When you emerge, you’ll have all sorts of gifts that you didn’t ever want.  Empathy and compassion for those with chronic, mysterious diseases, patience for yourself, faith in your resilience, etc.  Those things are possible.  They’re down that hole – look around and you’ll find them.

I am inclined to write trite sayings about this, and I’m not sure if they help or hurt.  Hang in there.  It will pass.  Breathe.  And just keep going.  That is my advice.

And know, in every part of your being, in every breath you take, that you are loved.

It helps.  I swear, it does.



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