I believe that I did have some predisposing factors that contributed to my getting floxed and the severity of my reaction and subsequent decline. This does NOT mean that I think I was responsible in any way for the fact that I was floxed. If I am correct that I had some predisposing factors, I certainly didn’t know any of this when I took the drugs. Neither, apparently, did my doctors, the FDA, or Pharma (at least, not that they’re admitting to). So just because in hindsight I believe I had a predisposition, does not mean this absolves Pharma and the FDA from their responsibilities in all of this, which I think are substantial.
In prior writings of my descriptions of my acute floxing, I have always said that there was nothing in my family history or my own history to make me suspect that I may have had any kind of predisposition to being floxed. This is true, in the sense that there was no medical or physical indication that stood out for me at the time. And certainly I didn’t fit the category of the “elderly person over 60 in renal failure and on steroids”. But here I will amend my earlier statements somewhat because hindsight is everything. At the time I took the antibiotic, as well as for the first couple of years after, had you asked me if there was anything to indicate that I had a predisposition to this reaction, I would have said “No way”. But it’s five years later, thousands of research papers later, 500-600 pages of my own notes condensed into this website later, and over 1800 days, and 2,592,000 minutes later of thinking about “Why the hell me?” Naturally, I can’t help but have come up with a few hypotheses.
I think virtually everyone who gets hit with a “chronic invisible illness” spends time looking back at their life prior to this illness and tries to make sense of “why it happened to me”, or “what I did to cause this”, and I am no exception. Things that never would have taken on any significance suddenly become questionable. I can look back and remember times where I felt a little shaky, and experienced what I thought might have been a benign essential tremor. I can remember times where I felt more anxious and “revved up” than I should have. I can remember the depressive episodes I’ve experienced, and the one situational panic attack I experienced. I think of the pizza and cookies I’ve eaten, the anti-depressants I tried a few times for a few days, the malathion I was exposed to back in the 80’s in California as they sprayed entire neighborhoods trying to prevent the fruit fly or whatever from invading, the tap water I drank, the lifetime of flame retardants I’ve been exposed to, the leaded gasoline and second hand smoke while growing up, the fluoride in the water and in my toothpaste, my less than ideal childhood . . . the list is endless. It’s easy to get caught up in “why me” or “what did I do to cause this”. When your life completely stops as a result of something like FQT, it’s also easy to forget that there are billions of people out there who can take these antibiotics without a known problem, who are living with all the same toxins we were exposed to, eating all the same “toxic foods” or perhaps far worse than we did, and had more “stress” or “psychiatric problems” than we did, and they continue to live their lives just fine. I know plenty of people my age and older, who also grew up on white bread in the 60’s, and did more legal and illegal drugs than I ever have, and they are healthy and active today, riding their bikes 50 miles at a stretch, stopping at all the little road cafes along the way to eat three or more hearty meals of the SAD (Standard American Diet) downed with a couple of beers.
I believe that eating a healthy diet, along with adequate exercise, probably are a couple of the best things a person can do for themselves over a lifetime to help maintain their health. But it’s certainly no guarantee. A “healthy diet” (whatever that is) is no guarantee you’ll remain healthy for 100 years, any more than an “unhealthy diet” is a guarantee that you won’t. Even Ötzi the 5300 year old Ice Man had degenerating joints, hardened arteries, gall stones, advanced gum disease and tooth decay, worms, Lyme’s disease, high levels of arsenic in his system, and some kind of chronic illness (Lyme’s/Arsenic poisoning?) for several months before his death at the ripe old age of 45 (due to trauma) – and you can pretty much guarantee that he got plenty of exercise and his diet was fully Paleo and organic too (it turns out the arsenic could have been from natural sources as well and as a result, some people have a genetic ability to metabolize it differently and get rid of it easier).
So this of course, is when people start looking to genetics to give us clues. Here too, though, there are no guarantees, and of course every single person on the planet has some genes that are less than ideal, expressed or not, but we’ve learned to survive and thrive despite this.
Overall, most people will agree that both genetics and environment (both nutritional as well as emotional) contribute to our health, and I agree with this. Looking back with the gained wisdom of hindsight, I can make my own best guesses as to what genetic, environmental, and situational influences contributed to my floxing.
First off, I believe I had a genetic tendency to develop some form of hyperthyroidism, most likely autoimmune in nature. Major phenotypic clues here are the fact that I’m a tall, thin ectomorph, who basically was able to eat whatever I wanted whenever I wanted. I shot up to 5’ 8” in sixth grade, and remained 100 pounds throughout high school until I put on the “freshman 10” in college. I think I’ve written elsewhere that it was nothing to scarf down half a dozen eggs, 6 pieces of toast slathered in butter and jam, 6 pieces of bacon, 6 pancakes on the side, and almost a gallon of whole fat milk for breakfast. Later on, I might have a Quarter pounder with cheese, large fries, and another ½ gallon of milk. I guess the good news is that I never drank sodas, and rarely had candy or processed snacks and didn’t like ice cream. I was super active, always outside, had plenty of energy, and all 100 pounds of me was that lean type of “marathon runner muscle”. An even bigger clue is the unusually low cholesterol I had for most of my life: under 100 in my twenties (actually had a 76 once), up to 120 or so in my thirties, up to 140 – 150 or so in my 40’s, and 160’s when I was floxed; currently about 170-180). From a clinical perspective, low cholesterol is a hallmark biomarker of hyperthyroidism (just as high cholesterol is a hallmark for hypothyroidism). When I asked the physician if I should be concerned that my cholesterol was 76, he said he didn’t know what it meant, but didn’t think it would be a problem as at that time, high cholesterol, and what caused it and the drugs to prevent it, were all the rage and the only concerns. And I obviously didn’t have that problem, despite my heavy diet of eggs. Anyway, the two take away points from here are: tall, thin ectomorphs with low or low-normal cholesterol phenotypes may be a big clue for potential hyperthyroid tendency genotypes. When I think of phenotypes who might have this tendency, I think of Princess Kate, who actually suffered from Hyperemesis Gravidarum – which can be associated with a transient “hyperthyroid state” in about 20% of women who experience it. Or Taylor Swift is another person who comes to mind who looks the physical phenotype.
Another clue is that I always had very regular, but brief light periods – which also can occur during hyperthyroid states (heavy prolonged periods with clotting can occur with hypothyroid states). I also had a tendency to sweat a lot when exercising or when nervous. I don’t think that I was ever frankly or symptomatically hyperthyroid, or if I was, I didn’t know it. But what I strongly suspect now is that I have a genetic tendency, the underlying genes, for hyperthyroidism, and for the antibodies for both Grave’s (hyperT) and Hashi’s (swinging back and forth between hyper and hypo).
Further clues are that I have a tendency to be a quick talker and thinker, and can be quick to anger. I also was described as “moody” as a child, and although I learned to control those moods, I think the underlying moodiness persisted, which I would now interpret as possibly due to Hashi’s/Grave’s antibodies. Or, just as likely, I think lead toxicity might have easily been a factor, as people in my age group for the most part were exposed to levels that would be considered toxic today (and I can still see all those large flaky paint chips layered like snow over the little porch I used to play on when I was 4 years old, and living in the inner city, with astounding levels of lead in the air and soil). Interestingly enough, I was actually suspected of having autism in my early years. Thankfully, my parents and physicians ignored these tendencies and recommendations, and for the most part, I grew out of it. I say “thankfully” because now a days, it seems throwing more drugs at the problem is always the first action to take, and knowing what I know now about myself and pharmaceuticals, I shudder to think of the consequences, both in the short and long term. I also have had a tendency towards depression, which occurs with both Grave’s and Hashi’s, and I now attribute this tendency to this as well. Although I tried anti-depressants a few times, I didn’t like the side effects, and they didn’t really seem to work, so I preferred diet, exercise, meditation, and counseling to drugs. I’ve since discovered that hormones, including thyroid hormones, make all the difference in the world in that department. Adding just a tiny dose of estrogen/testosterone in my forties made a rather amazing difference in both my emotional mood and physical state at that time (I was in perimenopause), and was my first clue as to the power of natural hormones and their effect on me physically as well as psychologically. This tiny dose of hormones never changed my natural menstrual cycle, which hummed along as regular and brief and light as ever. I really felt so much better though, that I haven’t been able to imagine my life without these hormones since, even though I’m now postmenopausal. These past five years have elucidated quite clearly the extreme effect that tiny differences in thyroid hormones, and iodine, can have on my emotional and psychiatric state.
One thing to note is that I’ve always had low to normal blood pressure, about 110/70. So despite this potential underlying propensity for hyperthyroidism, I never experienced high blood pressure pre-flox. The only time my blood pressure increased was during severe flares post flox, getting up to 140-150 systolic. I injured my back in my early twenties, and did suffer from bouts of back pain ever since. Stretching, walking, and exercise seemed to help the most — it always felt like a ligament and muscle problem ultimately, which seems significant now. My back pain flares often felt severe, and I think a few doctors thought I was exaggerating about my pain, but I now suspect that I did, in fact, have more pain because of these predispositions to the muscle and ligament problems. During the later years, I came to suspect an underlying connective tissue disorder more and more, and there is a close association between connective tissue disorders and thyroid disorders, as I discuss in “Thyroid Damage Due to Collagen/Connective Tissue Damage”. One clue that I now think is important are the vertical ridges on my nails indicative of a keratin problem; these ridges actually started in my thirties. I would notice maybe one ridge on one nail, and then over the years, it slowly increased. Post flox, this progression increased significantly, and my nails are now severely dry and brittle, with numerous multiple ridges on all nails. So far, I haven’t lost my nails, as some flox victims have, but I have to be careful as they crack and chip so easily now. I also often had “cold feet”, especially in my later years. This can be a symptom of hypothyroidism and hyperthyroidism.
No one that I know of in my family history has ever had a thyroid problem or been diagnosed with one, or with any other autoimmune disease. But diagnoses for the thyroid antibodies didn’t exist back then, so no one would have been aware of a subclinical, or silent condition, until or unless it went clinical or progressed to an overt thyroid condition. I now suspect this same tendency for hyperthyroidism in my father though: a thin, wiry man, who kind of looked like Mick Jagger physically, ate whatever he wanted whenever he wanted, and had a lot of “nervous energy” as well as some rage issues. He was always tapping his feet and hands or fingers, and I seem to have inherited this from him (which came in handy when I played the drums). My mother was also of fairly slight build, only gaining weight when eating fairly massive amounts of fatty and carbohydrate loaded foods topped off with a lot of ice cream daily. Both my parents grew up with severe food and nutrition shortages in World War 2 torn Europe, which only escalated post war as they lived in DP camps scrounging for whatever food they could bargain for on the black market. My mother commented to me once how it seemed so many people had “huge lumps on their neck” (goiters) during this time, presumably due to lack of iodine and selenium as well as other general nutrition scarcities. For both of them, Wonder Bread truly was a “wonder”, and all the processed foods lining the US food stores, and McDonald’s when it came along, was considered “health food” by them in a real serious way. If it is true that epigenetic modifications from the scarcities and excesses in nutrition of the prior generation can affect the current generation, then I probably got a few of those too. My father smoked like a chimney his entire life, and except for one back episode, was basically never sick a day in his life or ever went to a doctor that I can remember until finally succumbing to pancreatic cancer in his seventies. He was probably one of the physically healthiest people I’ve known up until the end, so he got a good twenty more years of excellent health than I apparently will. My mother, currently in her mid eighties, is definitely slowing down with numerous “old age” symptoms, but still swims and exercises for several hours daily, and continues to eat out at family restaurants (like Denny’s) every day, which is way more than I can do in my current state.
My sister was also very slender, suffered from depression, and when she committed suicide at the age of 30, her therapist told me that she believed it was due to starting Prozac – which now seems significant to me. Both of us had a tendency to “space out” at times, for lack of a better phrase (the positive aspect of having this ability is that I was a good meditator). My father also had a tendency to “space out”. After everything I’ve gone through with these thyroid hormones, I now believe this was due to this “genetic tendency for thyroid problems” as well. The brain fog, and “catatonia-like” CNS symptoms I’m now experiencing are far beyond this “spacing out”, which was very mild in comparison, but I can’t ignore the similarities to that feeling of depersonalization that occurs with both and often occurs with both hyper and hypo thyroidism. Additionally, according to my 23andMe results, I have an elevated risk for A-Fib at 20.0% (average risk 15.9%) and Bipolar Disorder at 0.20% (average risk 0.14%). I definitely have cardiac arrhythmias, including A-fib, and severe “mood swings” post Cipro, but there’s no doubt both are heavily influenced by my TH/Iodine/Antibody status. Of course, both A-Fib and Bipolar Disorder have a strong association with thyroid hormone abnormalities in general as well. Lastly, and perhaps somewhat interestingly, my parents were first cousins, so that certainly increased my chances slightly of getting something from both sides, so to speak.
Large linkage studies in families indicate a polygenic inheritance with no single locus playing a dominant role in autoimmune thyroid diseases. So I suspect I’ve gotten a few of those genes. Recent genetic modeling based on twin studies has concluded that as much as almost 80% of the predisposition to Graves’ disease is attributable to genetics. I strongly suspect in my case that I have this genetic predisposition, along with a predisposition for Hashi’s, but that for most of my life I was subclinical. As I’ve mentioned elsewhere in this document, perhaps what I really have are genes for some kind of “alternate metabolism of iodine” more prevalent in me, or these genes were “switched on” post floxing. I didn’t start having TSH screens done until I was in my forties; at that time, it was always around 1-2, and I myself wasn’t aware of how prevalent the antibodies are overall (and certainly I didn’t realize then that TSH is an unreliable screen anyway whenever the antibodies are present). I wish I had known then what I know now. I wish I had tested for the antibodies regardless of TSH, because it would have been nice to know if I had them before being floxed.
As stated elsewhere in this document, I think the Cipro either caused these antibodies, or triggered a subclinical state within me to go clinical. I think this process started with my first Cipro in Jan 2009, and exploded in my March 2010 extreme acute reaction. In hindsight, due to symptoms I now recognize, I also believe I was, in fact, experiencing a mild hyperthyroid/Hashi’s flare with resultant Interstitial Cystitis (and not just a simple UTI), when I took the March 2010 Cipro. Hyperthyroidism is essentially a hypermetabolic state, so I probably already had an increased metabolism with increased proliferation of cells, enzymes, and receptors going on when I took the March 2010 Cipro (and remember that FQ’s target TOPO’s involved in rapid turnover more). According to my 23andMe testing, I am a “fast metabolizer” of some substances. I also probably had all the antithyroid antibodies, which caused the flare and “mild hyperthyroid state”. The Cipro then induced a massive, immediate presumed TH/Iodine hyperthyroid flare, increasing the rate of my metabolism even more while on the Cipro.
When I was on TH I found out that only 55-62.5 ug TH will shut off my axis completely (TSH = 0 ), which is literally half the thyroid replacement dosage that most people need. Indeed, with this second round of thyroid hormone, I can’t seem to get above 50 ug total without bringing on severe cardiac and neurological symptoms along with other symptoms of hyperthyroidism. Consequently, a mere 10 ug change in dose results in about a 20% change in serum levels for me. This seems significant (and somewhat unusual) to me, and helps explain the extreme sensitivity I have to thyroid hormones in general and my very narrow therapeutic range. With this knowledge, perhaps my low cholesterol, and extreme sensitivity to all the steroid hormones now, is also supportive of an overall “lower normal range” of hormones for me. Being a tall thin ectomorph is also indicative of a lower amount of natural estrogen. As such, I probably was being “overdosed” with Cipro (even though I was on the low dose of 250 mg twice a day) because of my slender build and light weight (what we call the “greyhound effect” in vet med). I’ve heard it said that us thin, athletic folks are bigger “whiners” and complainers in our suffering when we get floxed, but I think it’s just that we may be getting double and triple dosed due to our lean mass and it’s actually affecting us more. Of course, on top of this, women tend to be overdosed in general (See 60 Minutes story http://www.cbsnews.com/news/sex-matters-drugs-can-affect-sexes-differently/ ). The Cytochrome P450 enzyme activities can vary greatly among individuals (see the FQ-CYP1A2/3A4 connection here), and perhaps those involved in steroid hormones and xenobiotic metabolism in me are either much greater or much less than the statistically normal population, thereby affecting my overall susceptibility to some drugs in general as well as my current sensitivity to steroid hormones. Interestingly enough, greyhounds normally have thyroid hormone levels lower than other breeds, often leading to erroneous diagnoses of hypothyroidism. In my case, I seem to do best with frees at about 30%-40% of normal range, and if they are pushed up over 60% of normal ranges, I tend to experience hyperthyroid symptoms. So the lab ranges provided as “normal” for most (95%) of the population don’t apply to me (I’m probably in that outlying 5%). Greyhounds also tend to be “super sensitive” and “thin skinned” to everything (they scream with the tiniest of needles, and yell when coming out of anesthesia – not unlike me, I’ve heard). Some greyhounds will even do an activity known as “trancing” – standing as if in a trance – or perhaps just spacing out or meditating. I don’t know if this has anything to do with their thyroid genetics, but it’s interesting none the less.
From an overall “autoimmune” perspective, when I look back on my life, I was a pretty healthy person, not prone to infections in general. I grew up playing in dirt, with animals such as dogs, cats, horses, and whatever little wild critters I could rescue. I assume I’ve had strep throat, as many children have, but if so, I never knew it, and I’ve never been tested for it. I assume the same about the flu, and I’ve never had a flu shot. I never had earaches as a child or adult, or bronchitis that I know of. I’ve never had a sinus infection that I know of. I’ve only had a few UTI’s in my life, the requisite ones when I started having sex, and then not another one until menopause. I got my annual colds, which I’ve always cleared well within 3-4 days. I also didn’t take any drugs whenever I got a cold; I simply rode them out for a few miserable days. I had no known allergies, and could eat whatever I wanted. As a result, I was only rarely exposed, maybe 5-6 times, to antibiotics of any kind in the first 50 years of my life. For me, the significance of this is that I think I basically had a pretty strong immune system. This worked well and in my favor when it came to dealing with natural threats such as bacteria and viruses. But from an immune perspective, I wonder if this is working against me when it comes to FQ’s. I get the feeling my body was hell bent on protecting me from the Cipro, and for some unknown reason, still is when it comes to metabolites even remotely resembling FQ’s. This article “Autoimmune diseases may be side effect of a strong immune system” suggest the same. So perhaps this may be a factor as well.
Tall, thin ectomorphs such as myself are also a phenotype at risk for harboring genetic predispositions for Ehlers-Danlos (EDS) and Marfan’s connective tissue disorders. Neither my 23andMe genetic data, nor a more comprehensive specialized genetic test looking specifically for Marfan’s SNP’s, revealed any risk. My 23andMe genetic data for EDS was unremarkable for the SNPs they provided; however, I have not had the more comprehensive testing looking at specific genes contributing to EDS. I also have never been hypermobile or double-jointed; if anything, I tend to have had tight muscles and ligaments and was never super limber. Interestingly, the one and only time my tendons felt like “wet noodles” and felt severely susceptible to rupturing was when I was on T3 only for a few weeks (no T4). Despite my lack of genetic markers for EDS or Marfan’s, this doesn’t mean it doesn’t exist. I think flox victims may have one or more genetic variants within EDS/Marfan’s genes which predispose us to being floxed, but they’re just not identified and known yet. Only full genetic testing for these genes, including the non-coding regions, can rule this possibility in or out conclusively.
As far as some “situational aspects” that may or may not be significant when I took the March 2010 Cipro, there are several things I’ve thought of. One, is that I stopped taking a Calcium supplement while on the Cipro, as the drug insert recommended not taking Calcium (such as in dairy products) at the same time. I wanted to “make sure” I wasn’t “binding” up or compromising the medication(affecting the absorption) in any way, so I figured a few days of stopping the Calcium supplement wasn’t going to hurt (yeah, I know . . . really stupid in hindsight, but what can I say, other than the truth of my own stupidity. Scroll down to “V-ATPase” here for more info on this). I didn’t exercise or go jogging while on the Cipro, but I did continue with my daily walking of a couple of miles, which also meant I was out in the sun for that time. I also was drinking orange juice for breakfast and eating other fruits – but NOT grapefruit or other citrus fruits. I also was on the oral low dose estrogren/testosterone supplement, with progesterone supplementation every two weeks of the month (ie, steroids); I was not taking the progesterone at the time I took the Cipro though. Lastly, and what I think was very important, is that I think my overall iodine stores and status was low. It is true that for much of my life I ingested a fairly high iodine diet. However, as I was getting older, I was trying to cut down on the dairy (not drink so much milk), and although I still ate 3 egg omelets with cheese, it was not every day anymore. I had been a lacto-ovo vegetarian for about 20 years, so I hadn’t had any red meat or chicken during that time; I also didn’t eat fish or seafood products, and I don’t like salty foods and didn’t salt my foods. Consequently, I can see how my iodine intake had probably been slowly decreasing overall as I got older. I strongly suspect it was this factor, in concert with probably anti-thyroid antibodies, that greatly contributed to my FQ-induced TH/Iodine pathology in general. It started with the Jan 2009 Cipro, and exploded with the March 2010 Cipro.
Lastly, I tried to look back at other times in my life when I experienced adverse reactions to drugs or substances, to see what, if anything, they may have had in common with my Cipro-induced reaction. In general, I haven’t taken many drugs in my life, as for the most part, I’ve never had anything more serious than my annual colds, which I would simply ride out without taking anything. I never even took an aspirin or NSAID growing up. However, this doesn’t mean I haven’t tried some things. I think even before being floxed, I sensed that perhaps I needed lower dosages of drugs than most people, and always did my best to take as little as possible or the lowest dosages as possible. Despite this, I have experienced some adverse reactions.
- I tried Prozac once, prescribed after the death of my sister. I only lasted a few days on it, because of the “funny way” it made me feel. What really stands out for me is the feeling of “eye pain” and disorientation that occurred – now, a very familiar symptom. At the time, it was such a weird disorienting feeling, I knew I didn’t want to continue taking it. To me, this is not only interesting, but significant: the molecular targets of Prozac include all 5 muscarinic (M1-M5) receptors, along with a number of other targets. And I suspect that damage to these muscarinic receptors are what has affected my eyes now since being floxed. The molecular structure of Prozac also is highly fluoridated. Of course the big thing with Prozac is the increased serotonin, and I certainly have experienced symptoms similar to “serotonin syndrome” during this ordeal, so I’ve come to suspect that serotonin is really involved in my eye problems and other flox symptoms as well.
- I then tried St. John’s Wort a couple of times. Again, I only lasted a few days on it both times, mostly because the reactions I felt were a weaker version of the same or very similar effects I had with Prozac, including the eye issues. I also developed a brown vaginal discharge both times which started within one day of starting it, and stopped within one day of stopping it. I don’t know what that was about, but certainly I didn’t like it.
- I then tried amitryptiline once, and again, only lasted about a week on this due to severe mouth dryness (and I suspect, eye dryness as well that I may not have noticed at the time). I couldn’t even eat, my mouth was so dry, and the feeling of this severe dryness no matter how much water I drank was simply intolerable and rather scary. Among the numerous mechanisms of actions of amitryptiline, muscarinic receptor antagonism is one of them, along with mild NMDA receptor modulation.
- I tried over the counter pseudoephedrine once in a cold formula, and felt like I had a pretty scary reaction. This included insomnia, nervousness, excitability, dizziness and anxiety – I was up all night feeling like I could go “psychotic”, with the “wanting to jump out a window” feeling for several hours. This is certainly similar to what I’ve felt plenty of times since being floxed. Pseudoephedrine targets adrenergic receptors, and stimulates the sympathetic nervous system and “fight or flight” response (which is exactly what it feels like to me). Needless to say, I never took anything with pseudoephedrine in it again.
- I have always been sensitive to caffeine, and basically never drank anything with it as a result. I avoided commercial teas for the same reason. I am a “fast metabolizer of caffeine” according to my 23andMe results (which I think in theory should have allowed me to tolerate more of it than I do). Methylxanthines (caffeine, theophylline, and theobromines) are adenosine receptor antagonists, as well as phosphodiester inhibitors. Theophylline and Cipro are both metabolized by P450 1A2. I think that the FQ-CYP1A2/3A4- theophylline/caffeine connection is an important one in terms of ferreting out mechanisms for these ADR’s. For an interesting and detailed discussion on this, see the hypotheses I present here, under CYP1A2/3A4 topics.
- I think I tended to be sensitive to chocolate at times, especially if I hadn’t eaten anything else. I would feel kind of “revved up” a bit sometimes, similar to caffeine. I rarely ate chocolate by itself as a result. Again, see the discussion on CYP1A2/3A4 for relevance.
- I never liked getting drunk, and therefore rarely drank alcohol. It never made me feel good, just kind of dizzy, out of it, and tired, so it was easy to stay away from. I don’t know why this is – possibly a tyramine/MOA connection? I could eat cheese fine, although it’s true I never ate it alone or in large amounts, just in an omelot or in other foods. I also think it could be related to an “aldehyde toxicity”, scroll to “Aldehyde Dehydrogenases” topic in the same link as above.
- When I was first floxed in the acute phase, there was a recommendation going around the FQ forums that undenatured whey protein was good to take to try and increase glutathione production. Of course being only a week or two into my reaction, I was desperate to try anything that would thwart off this reaction, and this was one more. Whey protein is isolated from milk, and this means plenty of iodine, tyrosine, tryptophan, casein, glutamic and aspartic acid (depending on what you read; it’s not supposed to be in the undenatured stuff), branched chain amino acids, possibly lactoperoxidases and myeloperoxidases, possibly tyramine , and who knows what else is in there that could now be considered totally “toxic” to me. And toxic it was. Within minutes of trying it, I felt like I could start having seizures, and as if I would start vocalizing uncontrollably; I felt this incredible “psychotic” feeling develop, and my entire body started with the “finger in the electric socket” feeling, buzzing, going numb, and eventually stiffening up to the point I literally almost could not move. I managed to get to the bathroom a few feet away and vomit most of it up, but I ended up in the ER anyway — but not before screaming and begging my partner to “Just let me die, don’t call 911, just let me go”. Believe it or not, I actually tried this again, using a second brand of whey (both came from Whole Foods and were organic), just to make sure it was the whey. I think I still couldn’t believe it, given the fact that I had been drinking TONS of milk for my first 50 years, and now, suddenly, I’m reacting to whey? The second time I was prepared for the reaction, and managed to vomit it all up as soon as it started and avoid the ER trip. There is absolutely no doubt in my mind that there was something in whey that I was reacting to, but as I’ve listed above, there are several possibilities that I know of, and probably some unknown ones as well. It was a totally terrifying reaction, to a product that days earlier I would not have had a problem with at all. Because I can’t isolate one cause for this reaction, I can’t hypothesize a mechanism for it either, but certainly there are multiple culprits on the “differential list”.
There are a number of known risk factors that have been published, and are in the drug inserts, as to who should “use caution” (whatever that means) when using the FQ’s. In the paper “Musculoskeletal Complications of Fluoroquinolones”, http://www.myquinstory.info/wp-content/uploads/2012/03/Hall-Finnoff-Smith-2011.pdf on Page 136, Table 3, the following risk factors are given for FQ adverse effects: Increasing age, Systemic corticosteroid use, Participation in a sport, Magnesium deficiency, Trauma (tendon or joint), History of organ transplantation, End-stage kidney disease, Hemodialysis, Osteoarthritis, Rheumatoid arthritis, Psoriatic arthritis, Systemic lupus erythematosus, Ankylosing spondylitis, Reiter syndrome, Polymyalgia rheumatic, Ulcerative colitis, Crohn disease, Diabetes mellitus, Hyperparathyroidism, Hypothyroidism. (Note the at risk population includes people and related family members with autoimmune or endocrine disorders (diabetes, thyroid, etc.), steroid usage (ie, Prednisone, inhalers), and “participation in a sport”(almost everyone else at some point in time in life).
And how many people know they are low on Mg before taking an FQ? How many of their physicians know this or have considered this? Sadly, how many people know they are diabetic or pre-diabetic when taking an FQ? — there is a huge epidemic of undiagnosed diabetes, pre-diabetes, and metabolic syndrome occurring in this country. How many people know they have anti-thyroid antibodies before taking an FQ? How many people know they might have a parathyroid adenoma before taking an FQ? I can tell you that taking an FQ is a hell of a way to “find out” these possibilities.
So, my list of additional potential risk factors for getting floxed would include the following (Some of these are repeats of the above). This is by no means an exhaustive list. I’m sure others could add to this list, and I’m sure I’ve forgotten a few things of my own that I’ve thought of in the past:
- Tall, thin, lean mass, athletic ectomorph.
- Anyone with anti-thyroid antibodies of ANY type.
- Anyone with lower than normal cholesterol.
- Anyone already on thyroid hormone replacement therapy for any reason.
- Anyone with a history of thyroid disease in the family or themselves.
- Anyone with any type of clinical autoimmune disease or a history of it in the family.
- Anyone with any type of known endocrinopathy: Addison’s Disease, Cushing’s, Hyper/Hypoparathyroidism, Diabetes or Metabolic Syndrome, Polycystic Ovarian Syndrome, etc., or family history of such.
- Anyone in “hormonal flux” – teens, pregnancy, perimenopausal, and menopausal.
- Anyone with known tendon disorders, pain, or prior ruptures.
- Anyone with known Ehlers-Danlos or Marfan’s genetic predisposition.
- Anyone with prior mental health issues of any type.
- Anyone with autism or autism spectrum disorders
- Anyone with sensitivities overall to drugs.
- Anyone on psychotropic drugs or antidepressants, or has experienced adverse reactions to them in the past.
- Anyone with existing neuropathies or neurological problems, or known genetic tendencies or family history of such, such as Charcot-Marie-Tooth.
- Anyone with known or diagnosed mitochondrial disorders, or family history of such.
- Anyone on statin drugs, steroids, NSAIDS, benzodiazepines, or any other drugs which might potentiate reactions.
Again, by writing up what I feel may have been my own personal predispositions, as well as other hypothesized predispositions, this does NOT in any way absolve the pharmaceutical companies and the FDA from their responsibility for the safety of these drugs. Indeed, when I look at the list I wrote along with the existing known potential predisposing factors, the question becomes not “Who should not take these drugs”, but rather, “Who should”?
It also doesn’t matter if I had a predisposing factor or not: It is Pharma’s and FDA’s responsibility to do their best to ensure the safety of the drugs they manufacture and market, and to provide truthful and fully informed consent to the medical professions, and ultimately, to the consumers (see here). If there are predisposing factors, discovered pre or post marketing, it is Pharma’s and the FDA’s responsibility to study these factors, learn from them, and either improve the drug safety, recall the drug, or at a very minimum, advertise loud and clear warnings about these factors to both the medical professions and the public (see here). In my opinion, not only has none of this occurred, but Pharma and the FDA have instead have done their best to minimize, deny, and turn a blind eye to the very real danger of these drugs. It’s been over 45 years since the first quinolone antibiotic nalidixic acid began in use clinically, and the reports of these severe and permanent reactions have continued unabated ever since. As I’ve said elsewhere, Pharma and the FDA have the capability, resources, knowledge, power, and funding to the tune of billions of dollars to learn from these adverse reactions right now. It shouldn’t be me – an FQ victim without any of the capabilities, resources, knowledge, power, or funding that Big Pharma has – trying to figure out what the hell happened to me, what my predisposing factors, if any, were, and trying to warn to the public about them. It shouldn’t be me spending whatever little quality of life time and capabilities I have left, trying to do their job. It’s almost ludicrous to think I’ve had to do this, if it wasn’t so horrifically sad and disgusting.
But the sad reality is, it is only the victims, who learn this information too late after the fact, that do their best to warn the rest of the population.