May 2014

Thresholds and Tipping Points in Thiamine Deficiency Syndromes

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Chandler Marrs

I recently stumbled upon on a research paper published in 1968. It was not that long ago in the overall course of modern medicine, perhaps even its heyday, when all things were still possible and before the complete fealty to pharmaceuticals arrived. To the youngsters and to those coming of age in the last 20 years, however, anything published pre 1990 is ancient history.  What could such old paper tell me about medicine that is new and useful? It turns out an awful lot.

Back in the day, research was a little simpler and more focused, not on finding out which drug could be fit to which symptoms, but on how things worked. Good experimental design, answered mechanical questions, like if we apply X to Y or if we remove X from Y what happens?

In this paper, Encephalopathy of Thiamine Deficiency: Studies of Intracerebral Mechanisms, the researchers identified a very important component about Vitamin B1/thiamine deficiency – the time course of the disease process. That is, with a diet deficient in thiamine, how long does it take before symptoms emerge, what is the corresponding level of deficiency in the brain, and at what point, after supplementation, does recovery begin; important questions clinically.

Vitamin B1 – Thiamine Deficiency

Remember, vitamin B1 or thiamine deficiency at its worst is linked to severe decrements neurological functioning, like Wernicke’s Encephalopathy that include noticeable ataxic and gait disturbances (loss of voluntary control of muscle movements, balance and walking difficulties), aphasias (language comprehension and/or production difficulties), and if it persists, Korsakoff’s Syndrome (severe memory deficits, confabulations and psychosis). Thiamine deficiency was originally observed in only chronic and severe alcoholics or with severe nutritional deficits as seen in famine. Fortification of food stuffs was thought to relieve much of the nutritional risks for deficit, especially in impoverished regions. More recent research, however, indicates that thiamine deficiency has reared its ugly head once again and this time in modern, non-impoverished, regions where the food supply is ample. How can that be?

Non-Alcoholic Wernicke’s Encephalopathies

Thiamine deficits can be mediated by a number of factors, including by less obvious nutritional deficits where food supply is abundant but nutrition is lacking (a diet of highly processed, carbohydrate and fat laden foods), with thiamine blocking factors found in medications/vaccines, environmental toxicants and some foods, after bariatric surgery and in disease processes like AIDS. Over the course of our research, thiamine deficiency has been observed in previously healthy, young, non-alcoholic patients, post medication or vaccine, along with symptoms of dysautonomia.

What has always struck me about the thiamine deficits we observe is the differential expression and time course of the symptoms. In some people, the reaction leading to thiamine deficit appears linear, progressive and rapid. In others, the symptoms appear to wax and wane and to evolve more slowly. How is that possible? Certainly, individual predispositions come into play. Some individuals may be somewhat thiamine deficient prior to the trigger that initiates the full expression of symptoms, while others have higher baseline stores. Additionally, anti-thiamine environmental exposures and other medical conditions/medications may also come into play.  In the literature, however, the progression of symptoms from bad to worse is almost always direct and rapid, perhaps mistakenly so. Indeed, Wernicke’s Encephalopathy is a medical emergency necessitating immediate IV thiamine.  How is it then, that we see more chronic, remit and relapse patterns of thiamine deficiency, even in some cases where thiamine concentrations are being managed medically?

Cerebral Thiamine Deficiency: Crossing the Black Line

It turns out, there is black line with regard to thiamine deficiency, that when crossed overt symptoms emerge, and a similar black line, that demarks recovery. It is possible then that barring a continuous blockade of thiamine, one can move above and below those lines and the corresponding symptoms may wax and wane. The paper from 1968, cited above, found those black lines, in rodents, but we can extrapolate to humans.

The research. The investigators took three groups of female rodents, a paired group of thiamine deprived and thiamine supplemented, along with a group fed ad lib (as desired) and assessed the time course and concentrations of cerebral thiamine deficiency relative to the initiation and progression of the observable neurological symptoms associated with Wernicke’s encephalopathy in rodents (ataxia, loss of righting, opisthotonos –rigid body arching). The experiment lasted about 6 weeks.

Neither the control group (thiamine supplemented) nor the ad lib group demonstrated neurological deficits at any time during the study. The thiamine deprived group, on the other hand, demonstrated symptoms that began with weight loss, progressive anorexia, hair loss (recall our observations about hair loss) and drowsiness at about 2.5 weeks into the experiment. Interestingly, no neurological signs of thiamine deficiency were seen at that time.

The results. At 4.5 weeks in, the researchers noted a rapid progression of symptoms and decline of health over the course of the next 5 days (the black line). These symptoms included: incoordination with walking, impairment of the righting reflex, reluctance to walk, walking backwards in circles, imbalance, rigid posturing and eventually a total loss of righting activity and severe drowsiness.

One can imagine, if a similar deprivation of thiamine were observed in humans, the corresponding symptoms might also include the initial hair loose and weight loss, perhaps noticeable, perhaps not depending upon the time frame and severity of the thiamine deficiency. It would also include incoordination and difficulty with walking, balance and voluntary movement, perhaps tremors, excessive fatigue or sleepiness and the myriad of neuro-cognitive disturbances noted in Wernicke’s syndrome.

In the cited experiment, one injection of thiamine reversed these symptoms to a nearly normal, or apparently normal neurological state within 24 hours.

Brain Thiamine Thresholds

Animals from each of the groups were sacrificed and examined at each of the stages of the experiment. Brain thiamine and other markers of thiamine metabolism were assayed to determine the cutoff levels of thiamine that demark symptoms and recovery.  This is really interesting and the beauty of this entire study.  Neurological symptoms become apparent when cerebral thiamine concentrations reach 20% of normal.  Recovery begins when those concentrations climb to 26% of normal. At least in rodents, one has to deplete 80% of the brain thiamine stores before overt neurological symptoms become apparent; 80% – that is a huge deficit.  Similarly, it doesn’t appear to take much to right that deficit, only a 6% increase in thiamine concentration set the course for improvement.

If we extrapolate to humans, where life span, genetic and environmental factors likely moderate the degree of thiamine stores and consumption, we still contemplate a rather large thiamine deficit needed before overt symptoms of Wernicke’s emerge. Similarly though, it is also evident that a rather small change in thiamine can have enormous effects on neurological functioning. In the case of the rodents, a mere 6% point change reversed the symptoms. One might suspect equivalent deficit/recovery thiamine parameters in humans.

Waxing and Waning Symptoms:  A Case for Persistent Thiamine Deficiency

If we consider the possible course of non-alcoholic thiamine deficiency, where no extraneous variables like bariatric surgery or thiamine deficient parenteral feeding are present and where dietary thiamine varies daily and is not held constant as it is during experimental conditions or during famine, we can begin to see how thiamine related neurological symptoms may wax and wane. Different exposures and triggers may decrease thiamine periodically, even to the point where overt neurological symptoms present. When those exposures are removed and barring deficiencies in metabolism and diet, symptoms may abate, at least temporarily, and until the next trigger or until the black line is crossed anew and thiamine deficiency becomes the medical emergency observed in overt Wernicke’s.

In contrast, the more persistent or chronic thiamine deficits that do not cross the 80% depletion cutoff (or the human equivalent), may also wax and wane and show all the core neurological symptoms expected in overt Wernicke’s though to a much lesser degree. Additionally, as we have speculated, persistent thiamine deficiency might disable mitochondrial functioning in such a way that the patient presents with a myriad of seemingly unrelated symptoms, that are not typically attributed to thiamine deficiency, such as cardiac dysregulation, gastroparesis, autonomic instability, demyelinating syndromes and hormone irregularities, especially thyroid, but also reproductive hormones. These too may be related to thiamine deficiencies. Although, we cannot and should not rule out other causes as well, sub-optimal thiamine may be involved with a host of complex disease states and medication adverse reactions where neurological symptoms are present. Thiamine deficiency should be tested for and ruled out before more invasive therapeutic options are contemplated.

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Epigenetics and Common Medications: Now What?

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Medications induce epigenetic changes

A recent article in The Guardian noted that, “Epigenetics is one of the hottest fields in the life sciences. It’s a phenomenon with wide-ranging, powerful effects on many aspects of biology, and enormous potential in human medicine.”  It is certainly true that epigenetics is a “hot” topic and that epigenetics research is paradigm shifting.  But because the field of epigenetics is so new, we currently have more questions about epigenetics than we have answers.

Questions about Epigenetics

What is epigenetics?  What positively affects epigenetics?  What negatively affects epigenetics?  Do some things have a greater influence on epigenetics than other things?  How do things that negatively affect epigenetics affect health?  How do things that positively affect epigenetics affect health?  How does epigenetics affect the health of our offspring?  At what point in time or development can epigenetic changes in a parent affect the health of a future child?  How likely is it that something that affects the epigenetic profile of a parent will be passed on to a child?  How will epigenetic traits passed from parents to children show up in the children?  What happens on a biochemical level to induce epigenetic changes?  How does the recent research on epigenetics change disease models?  What can I, personally, do to influence my epigenetics?  What should I do if I suspect that a toxic substance has negatively affected my epigenetics? Can negative or positive epigenetics lie dormant then show up in future offspring?

There are hundreds of questions around epigenetics that scientists are diligently working to answer.  Most of the answers to the questions listed above have partial answers that can be found in journal articles and text books. None of the answers are complete or comprehensive yet. There is much that is unknown and there is much to be learned in this relatively new field of research. Just touching on what is known about each of the questions listed would make this post long and convoluted, so I won’t go into details about each one.  However, it should be noted that the answers to these questions are meaningful for determining how people live their lives.

In this post, I will give a brief overview of what epigenetics is, I will point out that many popular pharmaceuticals have been shown to have a deleterious effect on epigenetics, and I will explore the question – What should you do if you have been exposed to a pharmaceutical that has been shown to cause persistent epigenetic changes?

What Does Epigenetics Mean?

The underlying DNA sequence that each individual has is static, but those genes can be turned on or off depending on conditions in the environment. The process of those genes turning on and off is epigenetics. The term “gene expression” is often used when describing epigenetics.

In “Epigenetic side-effects of common pharmaceuticals: A potential new field in medicine and pharmacology,” epigenetics is described as:

The term “Epigenetics” refers to DNA and chromatin modifications that persist from one cell division to the next, despite a lack of change in the underlying DNA sequence. The “epigenome” refers to the overall epigenetic state of a cell, and serves as an interface between the environment and the genome. The epigenome is dynamic and responsive to environmental signals not only during development, but also throughout life; and it is becoming increasingly apparent that chemicals can cause changes in gene expression that persist long after exposure has ceased.

This BBC Horizon documentary, The Ghost in your Genes, more thoroughly describes the mechanisms and the study of epigenetics:

In The Ghost in your Genes, both famine and stress are noted as things that not only change gene expression in the person who is experiencing famine and/or stress, but also change the gene expression / epigenetics of the children and grandchildren of those who experience stress or famine at critical times in their development.  In both a NOVA documentary on epigenetics and a study published in Nature Communications in 2014, it was noted that not only famine, but what a mother eats before and during her pregnancy can affect gene expression in her offspring.  Additionally, the authors of the article “Epigenetic side-effects of Common Pharmaceuticals” hypothesize that, “commonly-used pharmaceutical drugs can cause such persistent epigenetic changes.”

I took one of the drugs highlighted in “Epigenetic Side-effects of Common Pharmaceuticals” (Ciprofloxacin – a fluoroquinolone antibiotic) and had an adverse reaction to it.  According to the article, my adverse reaction may have been due to an epigenetic mechanism causing the adverse effects.  This leads me to the question of:

Now What?

Some of the drugs described in “Epigenetic side-effects of common pharmaceuticals: A potential new field in medicine and pharmacology” as having adverse effects through an epigenetic mechanism are: synthetic estrogens, combined oral contraceptive pills, fluoroquinolone antibiotics, beta-blockers, statins, cox-2 inhibitors, neuroleptics, SSRIs, Ritalin, Adderall, chemotherapeutics and general anesthetics. With 70% of Americans taking prescription drugs, and many of the drugs noted being popular, the question of what people are supposed to do after exposure to these drugs – in order to minimize and repair the epigenetic damage done – is not a trivial one.

I had an adverse reaction to Cipro/Ciprofloxacin, a fluoroquinolone (also called quinolone) antibiotic that has been shown to “inhibit eukaryotic DNA polymerase alpha and beta, and terminal deoxynucleotidyl transferase, affect cell cycle progression and function of lymphocytes in vitro, and cause other genotoxic effects.”  That sounds like pretty severe cellular genetic damage and it leads me to wonder – what am I supposed to do now that I have taken, and had an adverse reaction to, a drug that has been shown to cause, “extensive changes in gene expression….suggesting a potential epigenetic mechanism for the arthropathy caused by these agents?”

Should I change my diet so that I only eat things that are good for my liver and heart because, “It has also been documented that the incidence of hepatic and dysrhythmic cardiovascular events following use of fluoroquinolones is increased compared to controls, suggesting the possibility of persistent gene expression changes in the liver and heart?”  Will foods that are good for my heart, or a liver cleanse, trigger positive gene expression that can reverse the negative gene expression induced by the Cipro?  Are nutrient dense foods and liver cleanses powerful enough to combat the ill effects of a pharmaceutical that is specifically designed to disrupt the DNA replication process?  (Fluoroquinolones are supposed to disrupt the DNA replication process for bacteria while leaving eukaryotic cells intact. Unfortunately, fluoroquinolones also have deleterious effects on  mitochondrial DNA replication and chromosomes of eukaryotic/human cells.)  How do I know whether or not gene expression for liver and heart disease have been turned on in me?  If heart or liver disease genes have been turned on, can I turn them back off?

Epigenetics across Generations

Should I not have kids?  A chemotherapeutic agent, Topotecan, with the same mechanism of action as fluoroquinolone antibiotics – the disruption of DNA replication through interrupting topoisomerases – was found to “profoundly affect the expression of long ASD (autism spectrum disorder) candidate genes” according to the study, “Topoisomerases Facilitate Transcription of Long Genes Linked to Autism” published in Nature in September, 2013.  Autistic kids are just as much of a blessing as non-autistic kids, but the question remains; did Cipro negatively affect my epigenetic profile in a way that will cause negative gene expression in my children, should I choose to have them?  I wasn’t pregnant when I took Cipro though. Does that matter? Does the timing of exposure to the pharmaceutical that negatively influences gene expression make a difference?

A friend’s son was given a drug to keep him from wetting the bed.  Shortly thereafter he developed Tourette’s-like symptoms.  Several drugs used to prevent bed-wetting fall into the category of “Neuroleptics, SSRIs, Ritalin, Adderall.”  Per Epigenetic Side-effects of Common Pharmaceuticals, “The long-term use of these drugs causes an iatrogenic disease termed ‘‘Tardive Dyskinesia” (TD), which refers to a variety of involuntary, repetitive movements such as grimacing, tongue protrusion, lip smacking, puckering and pursing of the lips, and rapid eye blinking.”  Those symptoms are awfully similar to my friend’s son’s symptoms and it made us wonder, should he talk to his son about the possibility that he carries epigenetic errors that can be transcribed to his future children?  Should his son take that into consideration when he is of an age to have children?  Could my friend’s future grandchildren be adversely affected by a drug that was given to his son to stop bed wetting?  If so, how might they be affected?

Lessons Learned and Forgotten from Thalidomide and DES

How does pharmaceutical induced epigenetic damage affect a person’s children or grandchildren?  Some drugs, such as thalidomide and DES, have demonstrably shown that intergenerational adverse epigenetic effects of pharmaceuticals are possible, and can be severe.  “Diethylstilbestrol (DES), which was used to prevent miscarriages and other pregnancy complications between 1938 and 1971, is known to cause cancer in the male and female reproductive tracts later in life. Many other adverse associations have been identified in DES-exposed women and their offspring, and animal studies have shown effects in the next generation (grandchildren), a clear demonstration of transgenerational epigenetic effects.”  You can read about some of the effects of DES on children and grandchildren of exposed women HERE, HERE, and through doing a search for “DES” on Hormones Matter.  The transgenerational adverse effects of DES and thalidomide are frightening, and you’d think that lessons would have been learned from those experiences, but did we actually learn any lessons?  The effects of DES and thalidomide on the children of the women given those drugs were rooted in epigenetics, yet some of our most popular pharmaceuticals today also have deleterious effects on epigenetics. Is it possible that we learned nothing and that the harm brought on by drugs given to millions of people today (drugs like fluoroquinolone antibiotics, SSRIs, statins, and others are prescribed to millions of people annually) are going to show up as amplified harm in our children and grandchildren?

It is not yet known what the intergenerational effects of fluoroquinolone antibiotics, most chemotherapeutics, statins, beta-blockers, SSRIs, etc. are. But it is a question that is worth asking and it is certainly a question that is worth exploring and answering in a scientific way.  With millions of people taking pharmaceuticals daily, and many of those people having children, we should all demand answers to the questions of how pharmaceuticals are affecting not just our individual gene expression, but also how the genes of our children and grandchildren are going to be expressed.

Until those studies come out, what are we, collectively, supposed to do with the information that pharmaceuticals are adversely affecting gene expression?

What I’m Going to Do

I know what I’m going to do. I’m learning as much as possible to empower myself; I’m not having kids; I’ll try to live a healthy lifestyle. I feel okay about these things. I grieve a bit for the loss of my trust in the medical system, and for the decision not to have biological children, but on an individual level, these decisions aren’t tragic. However, if many people follow my lead, there would be quite a bit of trouble in the world. It’s not realistic for everyone who has taken a SSRI, beta-blocker, fluoroquinolone, statin, etc. to forego having kids. It’s not going to happen. Honestly, I don’t even know that it should happen. There are too many questions that are still unanswered about how pharmaceuticals affect epigenetics and what those epigenetic effects look like, for anyone to make an informed decision.

But we still should ask the difficult questions.  And we should still demand answers to the difficult questions.  We deserve to know – what should we do if our gene expression has been negatively affected by a pharmaceutical?  There won’t be easy answers, but the hard questions, and the hard answers, are valuable.

Note:  Unless otherwise specified, quotes are taken from “Epigenetic side-effects of common pharmaceuticals: A potential new field in medicine and pharmacology”

Information about Fluoroquinolone Toxicity

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

We Need Your Help

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

Yes, I would like to support Hormones Matter. 

Image by kjpargeter on Freepik.

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From Lupron Victim to Victims’ Advocate

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Lynne Millican Lupron Victims Hub

After being prescribed Lupron for endometriosis and several IVF attempts during the years 1989 – 1992, I began to experience multiple symptoms and adverse health – virtually all of which were deemed by my physicians as “unrelated to Lupron”. But because there had been such an abrupt change in my health since taking Lupron, I strongly suspected Lupron was responsible, and so started scouring the medical, pharmaceutical, scientific, and government literature for any validating bits of information. Lupron (a.k.a. leuprolide, leuprorelin) is used on women, men, and children for A-Z indications.

Over the course of decades I visited nearly every university and medical library in Boston and had read countless studies and articles, accumulating a significant body of adverse information about Lupron’s effects and risks. Ultimately my health deteriorated further, and home-based internet searches replaced trips into libraries. All this information sat on shelves, doing no one any good, until finally in 2008 a friend created the basic website and the Lupron Victims Hub was born.

The Inception and Goals of Lupron Victims Hub

Lupron Victims Hub was founded in 2008 to serve as a central resource for information not otherwise readily found concerning the drug ‘Lupron’.  Lupron (a.k.a. leuprolide or leuprorelin) belongs to a class of drugs known as “GnRH analogs/agonists” or the “relins” – i.e., Lupron = leuprorelin;  Synarel = nafarelin;  Trelstar = triptorelin;  Zoladex = goserelin; buserelin; histrelin).  Because of personal exposure to the relin, and the large market share that this drug has enjoyed, the website’s focus has been upon Lupron. To a lesser extent, the website also includes risks of other relins, as well as general risks to the relins/GnRH analogs as a whole.

The website exists as a resource for information on the risks and adverse effects of Lupron for consumers, medical professionals, attorneys, academia, and the media.  All my research, information, support, and assistance has been provided pro bono. Contact from victims and families frequently centers on their search for doctors and lawyers to help them – but at present time there is no such ‘Post-Lupron doctor/lawyer referral list’.  Hopefully the future will contain ‘Post-Lupron clinics’, with ample physicians and various specialties devoted to the diagnosis and care of Lupron victims – but currently, although there is a real nationwide need for such clinics, the thought is but a wishful pipe dream.

Twenty five years ago I felt like a lone voice, no one knew anything about Lupron, and no doctors or lawyers entertained a thought of this drug’s lingering adverse events. Now there are thousands of Lupron victims clamoring for help, lawsuits are in the courts and in the pipeline, and several physicians have gone on record about Lupron’s dangers, Lupron’s hidden data, and the serious permanent adverse effects upon women’s bodies.  It would seem that a critical mass is being reached, more media coverage is occurring, and more and more doctors are in earnest trying to understand ‘what the hell happened’ to the health of their formerly vibrant patients.

It took me personally a dozen years of searching post-Lupron to find understanding, caring, and appropriate medical care – a totally unacceptable situation. When doctors and the FDA (see ‘Open Letter to FDA’ ) are uninformed of the drug’s data and risks, they are ill-equipped to understand or accurately assess Lupron’s effects.  The atrocious “doctor visit stories” women recount post-Lupron (including my own) are hair-raising and nothing short of nightmare scenarios. Compassionate, diligent, and proper attention and care of these patients is urgently needed, yet negligently absent.

What We’ve Learned about Lupron

Information pooled on ‘Lupron Victims Hub’ should clearly identify that ‘Houston (and elsewhere)  … “we have a problem”’.  As for goals, I hope that my website will facilitate long-overdue acknowledgement of this public health crisis, and that those entrusted with our health and safety will initiate an investigation into Lupron’s long term adverse effects, remove the drug from the market, and establish appropriate medico-legal advocacy for these Lupron victims.  And any order will do.

Participate in Research

Hormones Matter is conducting research on the side effects and adverse events associated with Lupron. If you have taken Lupron, please take this important survey. The Lupron Side Effects Survey.

To take one of our other Real Women. Real Data. surveys, click here.

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Postpartum Fluoroquinolone Toxicity

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Sarah Flynn

In March of 2011, two months after the birth of my daughter, I experienced a bout of acute illnesses. My birth experience had been difficult, delivering five weeks early via emergency C-section after my water broke at 35 weeks gestation. My recovery was complicated by the need for an appendectomy just six weeks later. As if two abdominal surgeries weren’t enough, all of the trauma apparently dislodged two kidney stones in my right kidney. I woke up one morning with blinding pain in my stomach that migrated to my back and my side. I had passed a kidney stone once before, so I immediately knew what was causing the pain. Many who have experienced a kidney stone compare it to the pain of childbirth; I would argue that the pain is actually much worse. Unable to manage the pain on my own, I was taken to the emergency room for treatment. In the ER I was given IV pain medication and sent home with a short-term prescription for hydrocodone. I was also sent home with a prescription for a seven day course of the antibiotic Cipro. This medication was given to me as a preventative measure in case the stone ripped through my ureter.

Initial Symptoms of an Impending Cipro Reaction

About 48 hours after beginning the Cipro, I noticed an unusual feeling of nervousness. I was also having trouble regulating my internal body temperature. I would either be sweating profusely or so bone-chill cold that the only relief I could get was standing in a hot shower. I attributed these symptoms to being overwhelmed by the beating my body had taken in the last two months all while trying to care for my two month old preemie daughter. The anxiety was met with severe insomnia, and after a few days of almost complete sleeplessness (on top of the getting up with a newborn every few hours), I saw a general practitioner at a local walk-in clinic to get some advice and hopefully some relief. The doctor agreed that I was likely overwhelmed by all that had happened on top of adjusting to caring for a newborn. However, she also mentioned that I should stop taking the Cipro, and that “Cipro can do funny things” to some people. I took her advice and stopped the Cipro. Within a few days I started to feel more normal, and I shrugged off the experience. Little did I know my nightmare was just beginning.

Neurocognitive Deficits and Cipro

Two weeks later I returned to work. I was staring at the computer screen working on a research project when I noticed that my vision had become blurry. I went to the bathroom and put saline drops in my eyes when I discovered that my pupils were enormous. My eyes looked completely black instead of the normal light greenish-blue hue. I decided to leave work and go home early, and I had to squint and blink furiously just to keep my car on the road. When I returned home, my husband noticed my eyes and told me to lie down. I was exhausted, yet sleep would not come.

Cipro and the Central Nervous System

In the next few months I deteriorated rapidly, suffering from extreme anxiety, muscle twitches, myoclonus jerks, sweating, chills, weakness, tendonitis in my wrists, confusion, PVC heart arrhythmia, among roughly 30 other terrifying and painful symptoms. The worst of them, by far, was the completely intractable insomnia. I would go days at a time without being able to sleep even for one minute, finally crashing for two or three broken hours, and then the cycle would repeat itself. I sought out several doctors who ran tests after test and found nothing. I was finally steered toward psychiatry, where I was diagnosed with “anxiety” and given a slew of prescription psychiatric medications. Luckily, I declined to take most of them.

Continued Deterioration and Delayed Reactions to Fluoroquinolones

Weeks went on and my symptoms did not abate. I decided to leave my job and stay at home to take care of my precious baby daughter, the only thing giving me hope or the will to keep moving forward at that point. I was simply too sick to work, and my work environment was extremely stressful during that time. I was still very confused as to what had befallen me. After months of suffering, I remembered the doctor who had advised me to stop the Cipro. One simple Google search of “Cipro side effects” opened literally thousands of pages of information, with stories exactly like mine, of delayed reactions and unexplainable, debilitating symptoms. Because the severe symptoms were delayed for weeks after I stopped the Cipro, I never attributed my symptoms to this medication. I was unfortunately unaware that close proximity of the effect was not a necessary condition for causation when it came to pharmaceutical side effects.  However, as I began to research this class of antibiotics, called fluoroquinolones, I became aware that the most severe reactions are often delayed.

Fluoroquinolone Toxicity

I saw the top expert in the medical field on fluoroquinolone adverse reactions, and he diagnosed me with fluoroquinolone toxicity syndrome after a careful assessment. Almost a year after my first symptoms appeared, I finally had a name for my suffering. It took me almost two and a half years to recover ninety percent. My recovery focused on nutrition, stress management, and the power of positive thinking. Instead of taking medications, I found a sleep psychologist and underwent CBT for insomnia, and it helped dramatically. I still have symptoms, including the PVC arrhythmia, transient insomnia and peripheral neuropathy, but I consider myself very lucky. Many individuals with fluoroquinolone toxicity are disabled for life. You can read more about fluoroquinolone (FQ) toxicity here.

The pharmaceutical companies will lead you to believe that these side effects are rare, and therefore insignificant compared to the population of people that the drugs help. However, the truth is that most medication side effects are never reported, if they are even attributed to the drug at all. In actuality, doctors are generally uninformed about the complex array of side effects that these drugs can cause and are often unwilling to attribute patients’ symptoms back to the medications that they themselves prescribe. It is unlikely that we have an accurate picture of the side effect profiles of many prescription drugs, not just fluoroquinolones. In fact, many have speculated that a variety of idiopathic illnesses such as fibromyalgia are not organic illnesses but are all manifestations of fluoroquinolone toxicity or other adverse medication reactions. Each individual tends to have a unique threshold for toxicity, so it is entirely possible to have taken these antibiotics before without trouble only to experience a severe adverse reaction the next time they are taken. Since my diagnosis, it has become my mission to educate my friends, family and the world on FQ toxicity. Knowledge is power, and sometimes it can even be life-saving.

Participate in Research

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

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

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Chemicals in Sunscreens, Soaps, Plastics and Livestock Disrupt Sperm

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Endocrine disruptors impair sperm motility

Guys, considering having children?  New research shows you might want to avoid endocrine disruptors lest you alter the swimming, navigational and fertilization capacity of your sperm. Yes, endocrine disruptors, those synthetic chemicals that enhance or reduce endogenous hormones and are found in sunscreens, soaps, plastics, herbicides, pesticides, human and animal antibacterials, can render your sperm incapable of fertilization by some pretty striking mechanisms.

Why Hormones Are Important

Hormones control every aspect of human life from the most basic sexual function and reproduction, through metabolism and even brain function, so disrupting the natural balance of hormones can, and often does, have serious consequences on human health. In recent years, researchers have begun to untangle those effects. Almost to a tee, the studies run by independent scientist, show a myriad of negative effects linked to hormone disrupting chemicals. The study published just this month: Direct action of endocrine disrupting chemicals on human sperm is no different, except that the researchers not only identified the direct mechanism by which these chemicals affect sperm, but also, how a combination of exposures magnifies the deleterious response.

Endocrine Disruptors and Sperm Competence

The process of fertilization is a remarkably complex act. After ejaculation, sperm must swim upstream, against a pressurized force, against a chemical gradient to reach and then penetrate the oocyte or egg. Before reaching the egg, the sperm has to shed part of its native endocrine structure (acrosomal exocytosis) in order to successfully withstand penetration. The navigation, motility, and penetration are mediated by complex and perfectly timed set of chemical reactions between endogenous hormones secreted from the female and the activity of a calcium (Ca2+) channel called CatSper in the sperm. Sperm from animals lacking the CatSper gene are infertile because they cannot respond appropriately to the hormones released by the female. Many endocrine disruptors inappropriately activate the CatSper Ca2+ channel by mimicking those female hormones (progesterone and prostaglandins), thus impairing the sperm’s ability to reach its destination and perform the task at hand.

The present study found that physiological concentrations of many endocrine disrupting chemicals, concentrations the average person is expected to be exposed to and designated as safe, were deleterious to sperm competence. The chemicals in sunscreens that provide the UV-filters, the precursors for surfactants in soaps and commercial resins, growth hormones in livestock, insecticides, antibacterial and antifungal preservatives in foods and personal products such as soap, toothpastes, incorrectly activated the CatSper Ca2+ channel rendering the sperm incompetent. Most interesting, the researchers found that combination exposures increased the endocrine disrupting capacity of these chemicals. Since these chemicals are pervasive in modern life, it is reasonable to suggest that almost all exposures to endocrine disruptors happen in combination rather than in isolation. The potential to magnify the negative affects on health is likely greater than fully understood, particularly when considering there are at least 1000 of these chemicals on the market today, used in common, everyday products.

Improve Fertility: Remove Exposures to Endocrine Disruptors

If you and your partner are having problems conceiving consider eliminating exposures to endocrine disrupting chemicals. Research done with female infertility shows that women are equally susceptible to these hormone disruptors. Bisphenol A or BPA in plastics has been linked to egg maturation errors. If couples are lucky enough to conceive, fetal development continues to be susceptible to maternal exposures to endocrine disruptors and can wreak havoc on the health the children and grandchildren.

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Who’s in Charge of GMO Regulation?

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Lisbeth Prifolgle

We’ve all seen, and probably shouted, the catchy slogans – Say No to GMO! Keep your genes out of our meats and greens! We’ve read countless articles on the dangers of the genetically modified organisms (GMO) as well as the chemicals and foods they are sprayed and fed. We sign petitions, hit the “share” button to the various social media outlets, and get into screaming matches with friends and family members who don’t see the harm in GMOs. But do any of us really know how GMOs are approved? Do we know the best way to fight them? I’m going to guess no since it’s the eighth day of an open public commenting period about the use of DOW’s 2,4-dichlorophenoxyacetic acid (2,4-D), one of the main components of Agent Orange used in Vietnam, at the Environmental Protection Agency (EPA) and there are only a whopping 340 comments at this time. It actually didn’t occur to me that I didn’t really understand the full approval process until stumbling across the “public commenting period.” What I found was rather shocking.

Genetically modified foods and the chemicals that are sprayed on them as a result of their herbicide and pesticide resistance properties fall under the regulatory span of the United States Department of Agriculture (USDA), Food and Drug Administration (FDA), and EPA. What follows is a brief explanation how each agency works and what acts have been passed to monitor, or attempt to monitor, GMOs. Under the regulations of all three of these agencies, only the following categories of GM crops are monitored:

Plant-Incorporated Protectant (PIP) – a plant that produced pesticidal proteins or other chemicals as a result of genetic material from a bacterium into the plant. In these plants, scientists add modify the genes of corn, for example, to express a pesticidal property so that when pests digest the crop it releases a bacterial protein that will kill the pest. Yes, if we digest this plant we are also digesting this poisonous bacterial protein.

Genetically Modified Microbial Pesticides – bacteria, fungi, viruses, protozoa, or algae that has been modified to express a pesticidal properties like a PIP. In this case, the microbial pesticides are sprayed on the crop.

Herbicide-Tolerant Crops – this is the answer to the problem of weed-killer killing the crop it’s sprayed on. Like PIPs, the crop has been genetically modified to withstand the herbicides by adding the herbicide to the genetic make-up of the crop. The most commonly herbicide-tolerant crop is tolerant to glyphosate, a known carcinogen and hormone disrupter. Like most chemical substances, the weeds are becoming resistant to glyphosate in Monsanto’s Round Up. Thus Monsanto has teamed up with DOW Chemical to create crops resistant to 2, 4-D, as I mentioned before this is the main chemical ingredient for Agent Orange. Like PIPs, we are not only ingesting and breathing 2,4-D, being sprayed on our food, but it is actually part of our food.

Other GMOs that interchange DNA from one plant or animal species to another do not fall under the regulation of these agencies (and as far as I have researched, they do not seem to fall under any other regulating agency either).

usda

USDA

The USDA is the U.S. federal executive department responsible for developing and executing federal government policy on farming, agriculture, forestry, and food. It aims to meet the needs of farmers and ranchers, promote agricultural trade and production, work to assure food safety, protect natural resources, foster rural communities and end hunger in the United States and abroad. The USDA is not responsible for monitoring the safety of GMOs for human or animal consumption, but rather how it affects plant health. Within the USDA is the Animal and Plant Health Inspection Service (APHIS), which is responsible for protecting agriculture from pests and diseases. Under APHIS is the Biotechnology Regulatory Services (BRS) which is part of a science-based federal regulatory framework to protect America’s agricultural resources and the broader environment. The BRS has strict regulations for any new organism either imported, crossing state lines or being introduced, but only to ensure that it does not present a plant pest risk.

As long as GMOs either introduced to American farms or imported do not present a risk to plants, the USDA does not have regulate it. The responsibility of safety for human and animal consumption is passed to the FDA.

Fda-logo

FDA

The FDA is an agency of the United States Department of Health and Human Services, one of the United States federal executive departments. The FDA is responsible for protecting and promoting public health through the regulation and supervision of food safety, tobacco products, dietary supplements, prescription and over-the-counter pharmaceutical drugs (medications), vaccines, biopharmaceuticals, blood transfusions, medical devices, electromagnetic radiation emitting devices (ERED), cosmetics and veterinary products. As far as GMOs go, under the Federal Food, Drug, and Cosmetic Act (FFDCA), as long as the bioengineered food is substantially equivalent to non-GM crops or is generally recognized as safe, it does not require pre-market approval. There are no specific regulations for GMOs and they fall under the same regulation as conventional foods. In 1992, the FDA published a policy statement titled: Food for human consumption and animal drugs, feeds, and related products: Foods derived from new plant varieties; policy statement, 22984. This policy statement specifically addresses genetically modified foods, but disturbingly there is little regulation within this policy:

Under this policy, foods, such as fruits, vegetables, grains, and their byproducts, derived from plant varieties developed by the new methods of genetic modification are regulated within the existing framework of the act, FDA’s implementing regulations, and current practice, utilizing an approach identical in principle to that applied to foods developed by traditional plant breeding. The regulatory status of a food, irrespective of the method by which it is developed, is dependent upon objective characteristics of the food and the intended use of the food (or its components).The method by which food is produced or developed may in some cases help to understand the safety or nutritional characteristics of the finished food. However, the key factors in reviewing safety concerns should be the characteristics of the food product, rather than the fact that the new methods are used.

In other words, as long as a protein remains a protein and a carb remains a carb, it doesn’t matter how it’s produced. In 1997, the FDA started a voluntary consultation process for GM crop developers, but seeing as it is voluntary, I would hardly call that legitimate legislation. In 1998, Monsanto’s then director of corporate communications, Phil Angell, stated:

“Monsanto should not have to vouchsafe the safety of biotech food. Our interest is in selling as much of it as possible. Assuring its safety is the FDA’s job.”

The FDA’s role should be to monitor the safety of these new genetically modified plants that are used both as human food and animal food, however, there are simply no regulations specifically for GMOs.

GMO Labeling

In regards to labeling, per the FFDCA, the only labeling required from the producer is the common or usual name, or in the absence thereof, an appropriate descriptive term. The only exception is if a safety or usage issue exists due to the genetic mutation and consumers must be alerted. For example, if peanut genes are added to a tomato, the tomato can no longer be called a tomato because potential allergic reactions. I’lettersizeLogom sure in cases like this, the marketing department is full of clever titles like tomatut or peanato. Currently, 25 states have introduced mandatory GMO labeling legislation.  Vermont and Connecticut have actually passed laws forcing GMO products to be labeled. The Non-GMO Verification Project is a nonprofit organization that provides third party volunteer testing and labeling for products. I always look for Non-GMO Project Verified label when I shop.

The USDA only cares about the plant, the FDA doesn’t care as long as a tomato remains a tomato. A majority of people don’t believe the various reports of cancer and infertility caused in lab mice fed GMOs and ignore the fact that there have not been any comprehensive studies on the affects of human consumption of GMOs, but even if we deny that GMOs could be dangerous, there is no denying that spraying dangerous chemicals such as glysophate and Agent Orange on fields and backyards is dangerous and should be regulated, right? That’s where the EPA comes into play.

0412epaEPA

The EPA is another regulatory agency. It has primary responsibility for enforcing many of the environmental statutes and regulations of the United States. Congress authorizes the EPA to write regulations that explain the critical details necessary to implement environmental laws and Presidential Executive Orders.

The EPA’s role in the environmental safety of GMOs falls under the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA). According to the EPA website:

FIFRA provides for federal regulation of pesticide distribution, sale, and use. All pesticides distributed or sold in the United States must be registered (licensed) by EPA. Before EPA may register a pesticide under FIFRA, the applicant must show, among other things, that using the pesticide according to specifications “will not generally cause unreasonable adverse effects on the environment. FIFRA defines the term ”unreasonable adverse effects on the environment” to mean: “(1) any unreasonable risk to man or the environment, taking into account the economic, social, and environmental costs and benefits of the use of any pesticide, or (2) a human dietary risk from residues that result from a use of a pesticide in or on any food inconsistent with the standard under section 408 of the Federal Food, Drug, and Cosmetic Act.”

FIFRA was first passed into law in 1947, but has been amended since then. In 1972, FIFRA was essentially rewritten and amended by the Federal Environmental Pesticide Control Act. In 1996, it was again significantly amended as the Food Quality Protection Act.

While the EPA seems to hold the strictest regulations of the three agencies discussed in this article, it seems they are still coming up short. In order for a new pesticide to acquire a license from the EPA, the producer must provide more than a hundred scientific tests and studies. But, like the FDA, the producer of the pesticide provides the tests and the EPA does not actually conduct any tests on the new product. Furthermore, if it is being licensed for use on a crop less than 300,000 acres it is not considered sufficient economic incentive for registration.

EPA and GMO Regulation

Whether or not the EPA is actually regulating safe limits of pesticide aside, let’s look at their role in GMOs. Under FIFRA, the EPA provides legal requirements for registration and licensing of pesticides and therefore only monitors GMOs that are pesticidal in nature (PIP, Genetically Modified Microbial Pesticides, or Herbicide-Tolerant Crops).

The EPA also sets tolerances, and exemptions from tolerances, for the allowable residues of pesticides applied to food and animal feed under the FFDCA. However, given the pollution levels and a new study conducted by the California Department of Public Health showing a high number of California children being exposed to high level of pesticides at schools located near farms, I don’t have much faith in the EPA’s ability to safely regulate the use of pesticides.

Are GM Foods Safe?

In the end you have to ask – are GMOs safe for me and my family? Some people GMObelieve that the USDA, FDA, and EPA regulations are enough proof that they are safe, however, studies in rats fed GMO food over the course of a life time suffered premature deaths (up to 50% of males and 70% of females) and had severe organ damage (specifically liver and kidney). Also, the rats drank trace amounts of Roundup in their water (within legal limits set by these regulatory agencies) and had a 200% to 300% increase in large tumors (for more information and photos, click here).

What can YOU do?

Learn more. Do your own research on whether or not GMOs and the chemicals used on our crops are safe for consumption and the environment.

Spread the news. My friends and family are sick of hearing me telling anyone who will listen about the dangers of GMO, but I believe one person can make a difference so I keep fighting the good fight.

Buy organic, non-GMO foods. There are plenty of websites, like the Environmental Working Group, dedicated to helping families buy organic on a tight budget. Buying from local farmers can reduce cost (depending on where you live) or even buying your online. Another budget friendly tip – don’t eat out. We vote for or against GMO every time we check out at the grocery store or favorite fast food chain – make your vote count!

Get involved. I don’t mean you should quit your job to travel across the country leading protests (although if you can, go for it!). Simply watching legislation and writing in to the EPA and FDA and telling them you DON’T want Agent Orange sprayed in your backyard, is something everyone can do. We have until May 30th to tell the EPA we do not approve. Click here to add your comments. There are numerous organizations that write and submit petitions against GMOs. The Center for Food Safety is running a campaign against the use of DOW Chemical’s 2,4-D.

What do you and your family do to stop the spread of GMOs? What are your favorite NON-GMO products?

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Poor Nutrition Stress: The Enemy of Health

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Stress and Diet

In previous posts, I have indicated that stress can initiate or exacerbate disease and medication or vaccine adverse reactions. Read that statement, you might think I am attributing the onset of serious disease and adverse reactions to a psychosocial cause. That is not the case. Stress comes in a myriad of forms, some external, some internal, and although much of what we call stress relates to psychosocial responses to perceived threats, I think stress encapsulates so much more. At its most fundamental level, stress represents a physical state where the body is performing less than optimally. Let me explain.

What is Stress?

I define the word “stress” as a physical or mental force that is acting upon you. An example of mental or psychosocial stress might be an insult from a person, meaning that the stress comes from a source outside the body. On the other hand, it might be the realization that a deadline has to be met, a mental source from within. Any form of injury is an obvious source of physical stress. Physical action such as shoveling snow is another form of stress, demanding energy consumption imposed by the individual who wishes to get rid of the snow. Being infected with a virus or by bacteria is a form of stress that demands a defensive reaction. In each of these instances, the body reacts to the inflicting stressor. Sometimes, when the resources are available, it reacts efficiently. Other times, when the resources are not available or when additional factors intercede, the body’s response to the stress is ill-adapted.

Your Body is Your Fortress, Your Immune System the Soldiers

Perhaps an analogy might help to provide an explanation for the remarks that follow. I imagine the body as being like an old fashioned fortress. The people living within it go into action when the fortress is attacked by an enemy from outside. It would be of little use if the defense soldiers went to the eastern battlements if the attack came from the west and so there had to be a central figure that would coordinate the defensive reaction. The nature of the attack would be spotted by a guard on duty and the central figure informed by messenger.

The body represents the fortress and the lower part of the brain represents the central figure that coordinates the defense. The cells in the blood known as white cells can be thought of as soldiers, armed with the necessary weapons to meet the nature of the enemy. Suppose, for example, a person’s finger is stuck by a splinter carrying a disease bearing germ. The pain, felt in the brain, recognizes its source and interprets it as a signal that an attack has occurred. White cells in the area can be regarded as the “militia under local command” and a “beachhead” is formed to wall off the attack. The white cells sacrifice themselves and as they die, they form what we call pus. If the beachhead is broken and the germs manage to get into the bloodstream, it is then called septicemia and the brain/body goes into a full defensive reaction where high fever is the most obvious result. Such an illness is an attack/defense battle.

The symptoms that develop from such an infection represent the evidence for this defense, feeling ill, pain and developing a fever are excellent examples. Micro-organisms are most efficient at 37° C, the normal body temperature. The rise in body temperature, initiated by the brain, makes the microorganisms less efficient and may kill some of them. One therefore has to question the time honored method of reducing the fever, during illness, as being an example of good treatment. While reducing fever improves the symptoms caused by the infection, it also reduces the efficiency of the immune battle raging within.

The outcome against the stressor is death or recovery; although it is possible sometimes to end up in a kind of stalemate, represented by prolonged symptoms of ill health. Chronic illness may be viewed as the immune system’s inability to eradicate fully the stressor.

Poor Nutrition and Stress

As I have emphasized in previous posts, the autonomic (automatic) nervous and endocrine systems are used to carry the messages between the body and the brain that enable the defense to be coordinated. This demands a colossal amount of cellular energy, no matter the nature of the stress. That energy to fight stress comes from oxidation of the fuel that is provided from nutrition. Of course, the greater the stress the greater the energy demand, but in the end the equation is quite simple. If the energy required to meet the stress is greater than the energy that is supplied, there must be a variable degree of collapse within the defensive system. That collapse presents as intractable symptoms, where the body is unable provide the energy needed to sustain health. This is the secret of the autonomic dysfunction in the vitamin B1 deficiency disease, beriberi. It is also the secret behind the initiation of POTS because both conditions are examples of defective oxidation. You can read more details regarding thiamine deficiency, beriberi, POTS and other health issues from previous posts on this website

High Energy Demands Equal High Nutritional Demands

Nutrient density of diet might appear to be perfectly adequate for a given individual, but inadequate to meet the self-initiated energy demands of a superior brain/body combination in a highly active individual such as an actively engaged student or athlete. Our genetic characteristics, the quality of nutrition and the nature of life stresses each represent a factor that all combine together to give us a profile for understanding health and its potential breakdown.

Epigenetics and Mitochondria: The Stress of Our Parents

Epigenetics, the science of how our genes are influenced by diet and lifestyle, is relatively new. Epigenetics considers the possibility that genes can be activated and deactivated by nutrition and lifestyle. Stress can come in many forms, from psychosocial trauma, poor nutrition, environmental and medical toxin exposures, to infections. Stress impacts how our genes behave. Even though one may inherit a hard-coded genetic mutation from a parent, that mutation may not be activated unless exposed to a particular type of stress. Similarly, an individual who may have no obvious illness-causing genetic abnormalities but stress, in the form of nutritional depletion, exposures or trauma, can turn on or turn off a set of genes that induce illness. What is remarkable about epigenetics is the transgenerational nature of the stressors. The memories of stressors affecting our parents and even our grandparents can affect our health by activating or deactivating gene programs.

We also have to consider the state of our mitochondria, the “engines” in each of our cells that produce the energy for cellular function (to learn more about mitochondria and health, see previous posts on this website). Mitochondria have their own genes that are inherited only from the mother. Damage to the DNA that makes up these genes sometimes explains the similarity of symptoms that affect a given mother and any or all of her children. For example, although this damage may be inherited, we also have scientific evidence that thiamine deficiency, known to be the result of poor diet, can damage mitochondria. A bad gene might be the solitary cause of a given disease, but even where this is known as the cause, the symptoms of the disease are sometimes delayed for many years, suggesting that other variables must play a part. A minor change in cellular genetic DNA might be alright to meet the demands of normal living, but impose a risk factor that could be impacted by prolonged stress or poor nutrition, and disease emerges.

Nutrition is the Only Factor that We can Control

The imposition of stress on any given individual is variable, most of which is accidental and out of our control. Therefore, if we represent these three factors, genetics, stress and nutrition as three interlocking circles, all of which overlap at the center of such a figure, there is actually only one circle over which we have control and that is nutrition. We now know from the science of epigenetics that nutritional inadequacy can affect our genes. By examining the mechanism by which we defend ourselves against stress, we can also see the effect of poor nutrition.

Poor Nutrition Equals a Poor Stress Response

Using these three variables, perhaps we can begin to understand several unanswered questions. Why does a vaccination negatively affect a relatively small percentage of the total population vaccinated? Or why do some medications negatively impact only some individuals? It might be because of a genetic risk factor or because of a collapse of the coordinated stress response related to quality of nutrition or a combination of both. Why does a vaccination tend to “pick off” the higher quality students and athletes? Again, the same kind of answer; high quality machinery demands high quality fuel. Since the limbic system of the brain has a high energy demand and represents the computer that coordinates a stress response we can understand the appearance of beriberi or POTS and cerebellar ataxia, all examples of a deviant response to stress. Nutrition, therefore, should not be looked at as supplement to good health, but as the foundation of health. When disease or medication and vaccine reactions emerge, efforts to identify and then restore nutritional deficiencies must be the first line of immune system health. Without critical nutrients, the body simply cannot mount a successful stress response and the battlefield will expand and eventually fall.

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Don’t Let Your Babies Grow Up to be Floxies

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Lisa Bloomquist

Moms and Dads, as your children get bacterial infections and are prescribed antibiotics, please be careful and note what kind of antibiotics are given to them. Not all antibiotics are benign. Truthfully, none of them are completely benign, even though they are thought of as such – but some are significantly more dangerous than others.

Not all Antibiotics are Created Equally

Most people are aware of the fact that many antibiotics (especially penicillin and sulfa antibiotics) can cause allergic reactions – some of which are serious and potentially deadly.  Many people are also aware of diarrhea, upset stomach and even c-difficile as potential side-effects of antibiotics. But most people aren’t aware that the side-effects of some antibiotics include destruction of cartilage and tendons throughout the body, seizures, hallucinations, depression, peripheral neuropathy, urticaria and many other severe reactions for which there are few treatments; and when they occur simultaneously make up a multi-symptom, chronic illness. Not all antibiotics can cause a multi-symptom, difficult to treat, chronic syndrome that includes the frightening side-effects listed (and more). Unfortunately, and frighteningly, some can though. The kind of antibiotics that can hurt children (and adults) by causing those symptoms are fluoroquinolone antibiotics – Cipro/Ciprofloxacin, Levaquin/Levofloxacin, Avelox/Moxifloxacin and Floxin/Ofloxacin.

The 43 page warning label for Cipro goes over some of the adverse effects of fluoroquinolones noted – but it fails to mention that many of the side-effects listed can happen simultaneously, that they don’t go away after administration of the drug has stopped, or that the drug can convert an acute health problem – an infection, into a chronic multi-symptom illness – fluoroquinolone toxicity syndrome – an illness that can last months, years, or a lifetime.

To put it as simply as possible, fluoroquinolone toxicity syndrome involves damage to connective tissue (tendons, ligaments, cartilage, fascia, etc.) throughout the body, damage to the nervous systems (central, peripheral and autonomic), and more.  An article going over the basics of fluoroquinolone toxicity can be found HERE, links and resources, including 100+ peer-reviewed journal articles about fluoroquinolone toxicity can be found HERE, and stories of pain and suffering experienced by those who are going through fluoroquinolone toxicity can be found HERE.

If you look through the stories of pain and suffering linked to above, you will note that these drugs brought strong, healthy adults to their knees. Some of the people hurt by fluoroquinolones are in their 20s and 30s, many of them are athletes. If these drugs can leave an athletic 25 year old unable to walk or think, can you imagine what it might do to a small child?

Fluoroquinolones are Given to Children – Despite Contraindications

Fluoroquinolones are contraindicated in the pediatric population because they have been shown to damage the cartilage and joints of juvenile animals (source).  A review in U.S. Pharmacist noted that:

“Fluoroquinolones have demonstrated adverse effects on cartilage development in juvenile animals through the inflammation and destruction of weight-bearing joints.  These arthropathies were often irreversible, and their potential occurrence in children limited the use of fluoroquinolones in this population.  In one pediatric study, ciprofloxacin had a 3.3% (9.3% vs. 6.0%) absolute risk increase in musculoskeletal events within 6 weeks of treatment compared with control agents used to treat complicated UTIs or pyelonephritis. Adefurin and colleagues found a 57% increased relative risk of arthropathy in children given ciprofloxacin (21% overall) versus those in a non-fluoroquinolone comparator arm. In contrast to animal models, neither dose nor duration had an effect on the rate or severity of arthropathy.  A 2007 study by Noel and colleagues determined the incidence of musculoskeletal events (primarily arthralgias) to be greater in children treated with levofloxacin compared with nonfluoroquinolone-treated children at 2 months (2.1% vs. 0.9%; P = .04) and 12 months (3.4% vs. 1.8%; P = .03).  These results and the severity of the effects should be weighed heavily when initiation of fluoroquinolones is being contemplated in pediatric patients.” (source)

To summarize, fluoroquinolones can cause irreversible musculoskeletal harm and in doing so, they can put an end to your child’s days of running, jumping, playing soccer, skiing, dancing, etc. Think about that for a second – a drug – an antibiotic no less – can cause permanent damage to the musculoskeletal system of a child.

In addition to the horrible musculoskeletal adverse effects of fluoroquinolones, they also have multiple mental side-effects. Just a small sample of the mental side-effects of fluoroquinolones listed on the FDA warning label for cipro/ciprofloxacin are, “dizziness, confusion, tremors, hallucinations, depression, and, rarely, psychotic reactions have progressed to suicidal ideations/thoughts and self-injurious behavior such as attempted or completed suicide.”  No loving parent would want their child to experience any of those things.

If Cipro Can Tear Down a 32 Year Old, Imagine What it Can Do to a 3 Year Old

FDA warning labels are official and credible, but people tend to assume that what is listed on the warning label won’t happen to them or their children. So, to make things a bit more personal, I’ll tell you what happened to me when I was a strong and healthy (other than a urinary tract infection) 32 year old.  After taking Cipro, I could barely walk. My feet and hands were swollen to the point that it hurt to use them. My legs became weak and my muscles simply didn’t work.  I lost my flexibility and balance. My tendons were inflamed and painful.  I was exhausted and if felt as if I had a constant flu. I had hives/urticaria all over my body.  I was anxious, depressed and scared. I lost cognitive skills – my memory, reading comprehension, concentration, motivation and ability to connect with other people in a conversation. This went on, to varying degrees (I got worse for a period of time, then I slowly got better – with some bumps in the road) for 18 long and frightening months.

I dealt with the ordeal of having my body and mind fall apart quite badly, despite having 32 years of coping skills built up. Children haven’t built up the capacity to deal with pain, fear, depression, anxiety, loss of motivation, loss of physical capacity, etc. I can only imagine how frightening it would be for a child to go through even a portion of what I went through and, believe it or not, my reaction was not as severe as many.

Under-recognition of Adverse Effects: Delayed Reactions,Tolerance Thresholds and More

Adverse reactions to fluoroquinolones are often delayed (they can occur weeks or months after administration of the drug has stopped) and there is a tolerance threshold for them (meaning that people can tolerate fluoroquinolones up to their personal threshold and only fall ill after their threshold is crossed).  Because of these features of fluoroquinolone toxicity, and because of the absurdity of a prescription antibiotic causing a multi-symptom chronic illness, adverse effects of fluoroquinolones are under-recognized. No one really knows how common adverse reactions are.  People say that adverse reactions are rare; but if delayed effects, tolerance thresholds, multiple exposures and even individual genetic profiles aren’t being taken into consideration, how would they know?  And how is a parent (or doctor) supposed to know how much of a risk these drugs pose to a child?  These variables are too hard to know enough about, so I suggest that every parent reading this err on the side of caution and avoid Cipro/Ciprofloxacin, Levaquin/Levofloxacin, Avelox/Moxifloxacin and Floxin/Ofloxacin in all situations that are not life-threatening.

If you have a child who has a mysterious multi-symptom illness (which can, admittedly, have many causes), I suggest that you look through his or her medical records. Despite the official contraindication in the pediatric population, children are given fluoroquinolones all the time. They often come as ear and eye drops, in addition to pills and IVs.

Protecting Your Children

Please be careful with your babies. Know that there are some dangerous drugs out there.  One category of dangerous drugs is fluoroquinolone antibiotics – again, Cipro/Ciprofloxacin, Levaquin/Levofloxacin, Avelox/Moxifloxacin and Floxin/Ofloxacin (they have different names in different countries and ear and eye drops also often have different names – please ask a pharmacist if a drug is a fluoroquinolone before taking it). Iatrogenic multi-symptom chronic illness is not something that you want inflicted on your child and, as absurd as it may be, multi-symptom chronic illness can be the result of taking a fluoroquinolone antibiotic.

As someone who has experienced fluoroquinolone toxicity, I cannot begin to express the horror of thinking of a child going through what I experienced.  It was as if a bomb had gone off in my body and mind. Everything fell apart at once. It was terrifying. The thought of a child going through what I went through is even more terrifying though. I hope that Moms and Dads who read this heed my warning and keep their children far, far away from these drugs. They are too harsh and too dangerous for children.

I wish all parents the best of luck in keeping their babies safe. Staying away from fluoroquinolone antibiotics is one thing that can be done. There are safer antibiotics available. Please use them, and keep your children away from fluoroquinolones if at all possible.

Information about Fluoroquinolone Toxicity

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

Participate in Research

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

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

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What Else Can I Do To Help?

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

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Related posts:

beyond the ER with FQWhen Investigating Fluoroquinolone Reactions, Move Beyond the ER

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