Is Big-Pharma Silencing You?

Every once in a while someone asks me if I’m afraid that Bayer or Johnson & Johnson will retaliate against me for speaking out about the dangers of fluoroquinolones, and specifically the fluoroquinolones they manufacture, market, and distribute–Cipro and Avelox by Bayer, and Levaquin by Johnson & Johnson.

The answer is no.

No, they haven’t done anything bad to me, and no, I don’t think or fear that they will.

Not that corporate pharmaceutical companies like Bayer and J&J haven’t been evil before–they have, and I’m sure they are currently being evil, and will continue to be evil into the future–I just don’t think that they’ll be evil or vindictive toward me.

As a patient, patient advocate, and blogger, I don’t think I’m on their radar. Perhaps I’m naive for thinking that–I just have a hard time believing that big bad Bayer actually cares what little me (Lisa) has to say. In some ways, I wish they did. If they cared, it would be because they felt threatened, and to be capable of threatening big-pharma would be pretty amazing. I don’t think I’m on that level though–for better or for worse.

When I first started this site I asked an attorney how I should protect myself. She said, “always tell the truth,” and “they can’t argue with your story – it’s yours.” Just like my story and truth are valid, your story and truth are valid too. This site has my story, and the stories of others like me who have been hurt by fluoroquinolones. Our stories are true. They are our testimonials. They are what happened to us. No one can take away our experiences, our truths, or our stories. Our stories are valuable beyond measure, and they are making a difference in how people think about fluoroquinolones specifically, antibiotics generally, and even about how pharmaceutical reactions are connected to various illnesses and symptoms.

I want everyone to be empowered to share their story. Stories of pain and injury caused by fluoroquinolones are important and they matter. So, it bothers me when people refrain from telling their stories/truths out of fear that Bayer or J&J will retaliate against them. I can’t know what will happen to anyone in the future, but I can tell you that over the past 4+ years of running this site, having my story of fluoroquinolone toxicity available, and writing about the dangers of fluoroquinolones, neither Bayer nor J&J have done anything bad to me. (And while this means that I’m not as threatening to them as I want to be, it also means that I’m not having my life ruined, and, well, that’s a good thing IMO.)

What bothers me even more than fear-based self-censorship of patients is fear-based self-censorship of scientists, researchers, and doctors. A floxed friend approached a research scientist she knew personally and professionally to ask if he would do some research into fluoroquinolone toxicity, and he declined while flippantly saying something about not wanting to jeopardize his future funding prospects. I have no idea whether or not researching fluoroquinolone toxicity would affect this research scientist’s future funding prospects, but the fact that he fears pharma reprisal, and is willing to overlook horrifying fluoroquinolone reactions in his friend and colleague just to avoid the possibility of big-pharma’s reprisal, is bothersome. Unfortunately, reluctance to take on and question pharma seems common among researchers. As the saying goes, “don’t bite the hand that feeds you,” and so much research (even academic research) is funded, at least in part, by pharmacuetical companies.

Pharma money controls the conversation. They don’t have to make overt threats. They don’t have to ruin the lives of scientists (though they do, as seen in the story of the battle between researcher Tyrone Hayes and big-ag chemical giant Syngenta or the destruction of Andrew Wakefield’s career over his questioning of the effects of the MMR vaccine on the gut biome). They just have to control the purse-strings, and many people will fall in-line.

When research scientists limit the questions that they are willing to ask in order to avoid rocking the pharma boat, they are doing us all a dis-service. There is nothing thoughtful, curious, righteous, or even scientific about failing to research adverse drug reactions out of fear of reprisal from pharma, and drugs will continue to be more and more dangerous if all incentives are for research scientists to look away. I hope that my friend’s friend is unusually timid, and that most research scientists are willing to challenge big-pharma. Though I hope that, I don’t believe it. I believe that most research scientists are falling in-line with what their funders want, either consciously or unconsciously, and that because of biases toward their funders, we, as patients and consumers, are less safe.

I have hope that individuals will get over their fear of big-pharma, and speak out about the harm that they have experienced as a result of fluoroquinolone toxicity or other adverse drug reactions. (Shout your truth – tell your story – it’s empowering – trust me, it really is!) I even have some hope that individual scientists will face their fears and confront their big-pharma funders. But I have less hope that the system of corporate, academic, and even government “science” will go against the big-pharma, big-ag, and big-chemical giants that fund and feed them. It’s too scary. Even if the fear is largely self-inflicted, it’s still too scary for most people to question and challenge paradigms.

When I got floxed, I couldn’t help but question my existing paradigms. A pharmaceutical, an ANTIBIOTIC no less, hurt me. It made me ill for a long time, and there was nothing that doctors could do to help me. I didn’t gain any acknowledgement, support, or solutions from traditional doctors (some people do though, everyone’s experience is different). It made me realize that when the medical system hurts people, they don’t know how to put them back together, and all my assumptions about the ability of the medical system to solve human health mysteries went out the window. I realized that the doctors in the Western medical system have no idea how to treat complex illnesses like fluoroquinolone toxicity (or other multi-symptom, chronic illnesses), and that the patients dealing with mysterious illnesses are largely on their own. When I realized that pharmaceuticals are hurting people and leading to chronic illness, I started to question whether or not the good done by pharmaceuticals is worth the harm. I started to see that many of the illnesses of modernity can be linked to pharmaceuticals (and antibiotics specifically, and fluoronated drugs specifically), as well as the endocrine-disrupting chemicals of big-ag and other corporate chemical companies. My paradigm shifted when I got hurt by ciprofloxacin, so it wasn’t a risk to my world-view to actively criticize Bayer, J&J, or the other pharmaceutical companies after-the-fact. There are many obvious disadvantages of getting hurt by ciprofloxacin and other pharmaceuticals, but a silver lining was that my world-view shifted, and my fear dissipated.

I’m not afraid of big-pharma. Maybe it’s because I’m naive about their power, influence, and ability to ruin my life. Maybe it’s because I’m not a threat to them, and neither of us have any reason to fear the other. But I like to think that I don’t fear them because my world-view doesn’t give them power any more. Of course they have actual power–they have money, influence, and the ability to poison and hurt me, every other human, and the earth–but they no longer have the power of me believing that they are the answer. I don’t believe that they are the answer. I believe that they are the problem. And I believe that challenging them is the right thing to do. I also believe that answers to the problems caused by pharmaceuticals are in the stories of patients who are willing to speak out about what happened to them, and in the willingness of researchers and scientists who are willing to buck-the-system and question the pharma paradigm. Some bravery is required on behalf of both patients and scientists who question and challenge big-pharma. The bravery is worth it though, and others may find, like I did, that there is nothing to fear but fear itself.

 

 

 

Fluoroquinolones Increase Expression of MMPs

Fluoroquinolones degrade both the cellular matrix and collagen, and degradation of both are related to all the symptoms of fluoroquinolone toxicity. Torn tendons, nerve damage, and even memory loss and aging can be linked to cellular matrix and collagen degradation.

One theory as to how fluoroquinolones cause cellular matrix and collagen degradation (and tendon ruptures, and the hundreds of other symptoms of fluoroquinolone toxicity) is by selectively increasing expression of matrix metalloproteinases, or MMPs.

The article, “Clinical implications of matrix metalloproteinases” notes that:

“Matrix metalloproteinases (MMPs) are a family of neutral proteinases that are important for normal development, wound healing, and a wide variety of pathological processes, including the spread of metastatic cancer cells, arthritic destruction of joints, atherosclerosis, pulmonary fibrosis, emphysema and neuroinflammation. In the central nervous system (CNS), MMPs have been shown to degrade components of the basal lamina, leading to disruption of the blood brain barrier and to contribute to the neuroinflammatory responses in many neurological diseases.”

Information about the effects of fluoroquinolones on the cellular matrix, collagen, and MMPs can be found in these articles:

Though un-doing the damage caused by MMP expression from fluoroquinolones is easier said than done, there are some natural MMP inhibitors that may be helpful.

Chondroitin sulfate inhibits MMPs. Several marine animals contain chondroitin sulfate, and it can be found in shark cartilage, sea cucumbers, as well as marine heparin extracted from shrimp and sea squirt (source). According to the article, Angiogenic inhibitor protein fractions derived from shark cartilage, “Shark cartilage has been proven to have inhibitory effects on the endothelial cell angiogenesis, metastasis, cell adhesion and MMP (matrix metalloprotease) activity.”

A “floxie” friend reported that he had been helped immensely by supplementing shark cartilage. (I honestly have really mixed feelings about suggesting that shark cartilage may be healing because I like sharks, but that’s beside the point, and I don’t want to withhold information from you because I feel uncomfortable about consuming shark byproducts.)

For those who (like me) aren’t comfortable supplementing shark cartilage, some other natural supplements that are MMP inhibitors include (source):

  • Soybean Seeds
  • Citrus Fruits
  • Berries
  • Curcumin
  • Green Tea
  • Black Tea
  • Grapes

Those things certainly fall into the “worth a try” category. Unfortunately, I haven’t heard of anyone having dramatically positive results from eating berries or grapes, but they probably won’t hurt you, and are likely worth trying.

It is also worth noting that tetracycline antibiotics including doxycycline (NOT a fluoroquinolone), are also MMP inhibitors. The article, Bactericidal Antibiotics Induce Mitochondrial Dysfunction and Oxidative Damage in Mammalian Cells, notes how tetracycline antibiotics are bacteriostatic, not bactericidal, and how bacteriostatic antibiotics don’t cause the damage that bactericidal antibiotics inflict, and may even mitigate the damage caused by them. Low-dose doxycycline (or another tetracycline antibiotic) may help to inhibit MMPs and therefore mitigate damage and even promote healing. (Ask your doctor before starting this method.)

Though MMP activation is related to connective tissue breakdown, all fluoroquinolone toxicity symptoms, as well as cancer, arthritis, neuroinflammation, and more, to say that they are “bad” is overly simplistic. Everything in biology and health is complex and multifaceted. There are intricate feedback and feed-forward loops in many inputs. There are no easy or simple answers or cures.

With that said, MMP inhibitors may be helpful. Shark cartilage helped my friend, and it, or the other MMP inhibitors noted, may help you.

Though our bodies are complex, and there doesn’t seem to be a “magic bullet” that cures fluoroquinolone toxicity (or any other complex multi-symptom illness), there are things that can help push your body back to a state of health, and MMP inhibiting food and supplements are on that list.

 

 

Fluoroquinolone Toxicity Stories in the Media

It takes a tremendous amount of strength and bravery to publicly tell one’s personal story of chronic illness and iatrogenic injury, and I am so grateful to those who have told their stories of fluoroquinolone toxicity to the media.

There is often shame around chronic and mysterious illness, and that shame and desire to hide what is “wrong,” often leads people to stay silent about their illness. I commend everyone who has overcome shame associated with illness, and who has spoken out about the harm that fluoroquinolones have caused. (And I also commend those who know that there is nothing to be ashamed of, who shout about what happened as loudly as possible.)

I wanted to take this chance, and use this post, to publicly thank all of the brave and wonderful people who have reached out to the media to tell their stories. They deserve thanks. With every story that gets published in the media (whether in a newspaper, on a website, or on television) comes greater awareness of the dangers of fluoroquinolones, and more compassion for those suffering from fluoroquinolone toxicity.

There are more than 150 media stories about fluoroquinolone toxicity published on the Links & Resources page of Floxiehope.com. Each media story features a person (or two, or more) who has been hurt by Cipro/ciprofloxacin, Levaquin/levofloxacin, Avelox/moxifloxacin, or Floxin/ofloxacin. In each media story, a person got vulnerable, and opened him or herself up to risk of derision and rejection from naysayers, so that she or he can speak the truth about the harm that fluoroquinolones cause. Speaking out is not an easy thing to do, and, from the bottom of my heart, I thank everyone who has been featured in a media story.

It would be impossible for me to recognize everyone individually – without a doubt, I would leave someone out – but I want to highlight a few media stories that have been particularly impactful, and the people who made them possible.

Richard Pyne’s story was highlighted in the article “Left paralysed from Fluoroquinolone antibiotic toxicity” that was published on Al Jazeera. “Left paralysed from Fluoroquinolone antibiotic toxicity” notes that:

Richard Pyne’s health reflects a man much older than his 42 years. His world is today little more than the confines of his mother’s house, which he moved to so she could take on the role of his primary carer. Until recently, the Briton lived in his own flat and held down a job, but now, he says, he struggles to walk, to sleep and to live a day-to-day life that doesn’t involve some form of physical distress.

“My health and my life have been destroyed,” said Pyne, speaking to Al Jazeera from his home in Norwich, in England’s East Anglia.

Pyne blames his health crisis, which also includes skin and respiratory complaints, on ciprofloxacin, an antibiotic of the fluoroquinolone drug class. He was prescribed ciprofloxacin – or cipro, for short – to treat prostatitis in January 2016. Far from giving him the new start he wanted, however, the cipro, says Pyne, began to ravage his body within weeks of taking it leaving him effectively housebound.

“I can’t walk properly and haven’t been able to walk properly for over a year,” said Pyne. “My elbows, knees, ankles, pelvic joints, just snap and pop – even my neck.”

Richard’s story makes the article poignant, accessible, and real to the people who read it. The article is impactful because of Richard’s story. Thank you, Richard, for telling your story.

In the PBS Newhour story “Certain Antibiotics Spur Widening Reports of Severe Side Effects” both Jenne Wilcox and John Fratti tell their stories of permanent harm done to them by fluoroquinolone antibiotics:

JENNE WILCOX, patient: I couldn’t even hold my head up. And I was bedridden for over a year. And when I say that, I mean, I couldn’t even get myself out of bed to get into my wheelchair to go use the restroom. I had to be picked up out of bed.

JOHN FRATTI: It caused nerve damage, tendon damage and central nervous system damage. Central nervous system damage is — is brain damage.

JOHN FRATTI: I have lost my job. I have lost over a quarter of a million dollars in lost wages. I have spent about $30,000 out of my own pocket in medical and insurance costs, haven’t received a dime back for this.

Certain Antibiotics Spur Widening Reports of Severe Side Effects” shows both Jenne Wilcox and John Fratti in vulnerable, deeply personal, situations, and it illustrates the pain, disability, and loss that these drugs cause. They are both appreciated for putting themselves out there, in one of the first news stories about fluoroquinolone toxicity (it was aired in 2011).

In the New York Times article, “Popular Antibiotics May Carry Serious Side Effects” the story of Lloyd Balch is featured. It is noted that:

In addition to being unable to walk uphill, climb stairs or see clearly, his symptoms included dry eyes, mouth and skin; ringing in his ears; delayed urination; uncontrollable shaking; burning pain in his eyes and feet; occasional tingling in his hands and feet; heart palpitations; and muscle spasms in his back and around his eyes. Though Mr. Balch’s reaction is unusual, doctors who have studied the side effects of fluoroquinolones say others have suffered similar symptoms.

Three and a half months after he took that second pill, these symptoms persist, and none of the many doctors of different specialties he has consulted has been able to help. Mr. Balch is now working with a physical therapist, but in a phone consultation with Dr. David Flockhart, an expert in fluoroquinolone side effects at the Indiana University School of Medicine, he was told it could take a year for his symptoms to resolve, if they ever do disappear completely.

Thank you, Lloyd, for telling your story! “Popular Antibiotics May Carry Serious Side Effects” was published in 2012, and it has been highly influential.

Roughly 100 local news stories about fluoroquinolone dangers have aired in the last couple years. Each news story features interviews with victims of fluoroquinolones, and everyone who was featured in a local news-story is brave, wonderful, and appreciated! This post would be ridiculously long if I grabbed quotes from each local news story about fluoroquinolone toxicity, and I would undoubtedly forget several people, but I want to give a broad shout-out of thanks to everyone who has been featured on a local news story about fluoroquinolone toxicity. With each of the local news stories came more awareness and compassion, and it led us closer to meaningful change in how fluoroquinolones are perceived and prescribed.

A particularly impactful local news story is “Local woman says popular antibiotic killed her husband” which aired on WSB TV 2 Atlanta. It was shared thousands of times on social media, and I heard that Levaquin prescriptions in Atlanta dropped significantly for months after it aired. You can see “Local woman says popular antibiotic killed her husband” below:

Kathy Dannelly is incredibly brave for sharing her, and Chris’s, story, and her advocacy is appreciated! Jeff Stephens is also brave and his contribution to the news story above is also appreciated!

All the stories of harm done by fluoroquinolones are valuable, important, and poignant. Without people being willing to tell their stories, no one would understand the true nature of fluoroquinolone toxicity – that it is a devastating illness. Because people have been wiling to speak out and tell their stories, more and more people realize the nature of fluoroquinolone toxicity, and many people have been warned and saved from suffering from fluoroquinolone toxicity themselves.

Humans are storytelling creatures. We understand the world through stories. Each and every story of fluoroquinolone toxicity is valuable, and the people who have told their stories to the media so that they could be amplified, are appreciated. Thank you for telling your stories. It’s not easy to do, but it’s valuable, and appreciated.

 

 

 

 

Fluoroquinolone Toxicity Mimics Benzodiazepine Withdrawal – Beware

GABA “is the chief inhibitory neurotransmitter in the mammalian central nervous system. Its principal role is reducing neuronal excitability throughout the nervous system. In humans, GABA is also directly responsible for the regulation of muscle tone” (source). Fluoroquinolones “are known to non-competitively inhibit the activity of the neurotransmitter, GABA, thus decreasing the activation threshold needed for that neuron to generate an impulse.” (sourcesourcesource) Fluoroquinolones have also been shown to have similar effects on GABA neurotransmitters as benzodiazepine withdrawal (source).

The effects of fluoroquinolones on GABA-A neurotransmitters are the exact opposite of the effects of benzodiazepines, and, on a neurotransmitter level, they are the same as the effects of benzodiazepine withdrawal.

Symptoms of benzodiazepine withdrawal, AND fluoroquinolone toxicity, include:

  • sleep disturbances
  • irritability
  • increased tension and anxiety
  • panic attacks
  • tremors
  • difficulty with concentration
  • confusion and cognitive difficulty
  • memory problems
  • nausea
  • heart palpitations
  • headaches
  • muscular pain and stiffness
  • psychosis

And many other symptoms.

Both fluoroquinolone toxicity and benzodiazepine withdrawal are multi-symptom, chronic illnesses, for which there is no cure, and, despite significant research into both, the severity and complexity of both SYNDROMES is rarely acknowledged.

The following article does a brilliant job of connecting fluoroquinolone toxicity (syndrome) and benzodiazepine withdrawal (syndrome), and it gives a thorough explanation as to why people who have gone through benzodiazepine withdrawal should NEVER be prescribed fluoroquinolones. The article was originally published on the Benzodiazepine Information Coalition web site, www.benzoinfo.com, in October, 2016. It was written by Brad Verret, and I am grateful to him for the wonderful article.

Tragically, Brad Verret has passed away. I asked the editor of benzoinfo.com if I could re-publish it on floxiehope.com, and she said yes and noted that, “Brad wrote his articles to help as many people as possible. His intentions were to sound the alarm for benzodiazepine affected people to avoid that awful class of antibiotics, and he would have been pleased to help floxies avoid getting benzodiazepine injured.” She also noted that Brad was kind and smart and that he is missed dearly. I hope that his loved-ones see the use of his wonderful article as a tribute. Brad synthesized and interpreted the data about the effects of fluroquinolones and benzodiazepines on GABA-A thoughtfully and insightfully. This is a wonderful article, and Brad’s work is greatly appreciated! Please share it (or this entire post) far and wide – thank you!!

Hidden Dangers of Fluoroquinolone Antibiotics in the Benzodiazepine-Dependent Population

By Brad Verret

Whether it was for a sinus infection or bronchitis, most people have taken an antibiotic at some point in their lives. Antibiotics can be lifesaving medications but, like all other drugs, they come with risks. In particular, one specific class of antibiotic drugs called the fluoroquinolones carry serious risks that few people are aware of. In light of the growing epidemic of antibiotic resistance, each new generation of antibiotics has bolstered an enhanced degree of potency which can be viewed as both an asset and a liability. The fluoroquinolone class features a robust, broad-spectrum antibiotic effect and includes many popular drugs such as ciprofloxacin (Cipro), ofloxacin (Floxin), norfloxacin (Noroxin), levofloxacin (Levaquin), moxifloxacin (Avelox), and gemifloxacin (Factive).

Chemically speaking, the mechanism of action of the fluoroquinolones closely mirrors that of certain chemotherapy drugs, so it is rather unsettling that these powerful agents are sometimes prescribed for relatively benign infections that would probably resolve on their own or with a milder drug. One notable and unique risk of the fluoroquinolones is that, unlike most other antibiotics, they are neurologically active at commonly prescribed dosages. As an action secondary to their primary antimicrobial effect, they are capable of binding to certain receptors in the brain, spinal cord, and peripheral nervous system. The primary receptor type affected is the GABA-A receptor, which is the exact same receptor that benzodiazepines act on.[1]

When a fluoroquinolone binds to a GABA receptor, the result is the polar opposite of the effect of CNS depressants like benzodiazepines. Fluoroquinolones are antagonists of the GABA-A receptor, meaning that they prevent the binding of GABA and can displace other molecules bound to the receptor, such as benzodiazepines.[1] GABA is an inhibitory neurotransmitter and drugs which enhance its action, like benzodiazepines, cause sedation. The GABA receptor blockade caused by a fluoroquinolone results in a CNS stimulant effect, with neurological manifestations ranging from mild insomnia and agitation to hallucinations and seizures.[2] Anyone can suffer these side effects, but individuals prescribed benzodiazepines are notably much more prone to experiencing these adverse neuropsychiatric reactions.

The culprit is the GABA receptor downregulation imposed by benzodiazepine tolerance. When a benzodiazepine is given chronically (beyond 10 days) there are a series of downward compensatory mechanisms which seek to restore a neurological equilibrium in light of the overstimulation of GABA receptors by the drug. This results in GABA receptors becoming progressively less receptive to GABA over time following prolonged exposure to benzodiazepines.[3] Over time, the brain’s GABA-dependent systems are weakened and there is a heightened vulnerability to external influences which decrease the action of GABA.

A storm neural excitation ensues when a fluoroquinolone “unmasks” the GABA receptor downregulation associated with benzodiazepine tolerance. In addition, since they share the same target, fluoroquinolones are capable of competing with benzodiazepines for GABA receptor binding in a concentration-dependent manner. Studies have shown a complex interaction when a fluoroquinolone and a benzodiazepine are simultaneously bound to a GABA receptor. At high concentrations, fluoroquinolones are capable of displacing a portion of the benzodiazepine molecules bound to GABA receptors.[4]This displacement can precipitate an acute benzodiazepine withdrawal syndrome which is identical to that which would normally happen if an individual were to suddenly reduce their benzodiazepine dosage.

Imagine each GABA receptor as having a gas pedal and a brake pedal. The entire GABA receptor, with its imaginary gas and brake pedals, is anchored into the neuron whose pace it controls. GABA agonists like benzodiazepines act on the brake pedal and GABA antagonists like fluoroquinolones act on the gas pedal. When an agonist acts on the brake pedal, chloride ions flow through the receptor into the neuron. Chloride ions are like an electrostatic glue which slows the neuron down. When an antagonist acts on the gas pedal, the flow of chloride stops and the neuron speeds up.

When an agonist is present for a prolonged period of time, the brake pedal gradually becomes worn out. Additionally, the neuron will recruit chemical messengers to tune up the gas pedal so that the neuron can continue to move along at its desired pace. It might be a pace that provokes anxiety, but it is the precise pace which will allow the neuron to fulfill its purpose within the unique neural circuit it belongs to. After being chronically slowed down by benzodiazepines, neurons want to break free but are held back by the presence of the drug. They will progressively fight back harder and harder to overcome this pharmacological oppression. Fluoroquinolones unleash neurons from their chemical bondage by disengaging the brake and stepping on the gas pedal, causing a sort of neural short-circuit as the freed neurons begin to race out of control.

It has been shown that certain non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen are capable of enhancing the GABA receptor blockade cause by fluoroquinolones, potentiating their neurotoxicity and exacerbating their CNS side effects.[5] NSAIDs are frequently co-prescribed with fluoroquinolone antibiotics for painful infections like sinusitis and urinary tract infections. Adding further insult to injury, some fluoroquinolones including ciprofloxacin (Cipro) are inhibitors of the CYP1A2 liver enzyme which is responsible for metabolizing caffeine and other xanthine alkaloids found in coffee, tea, and chocolate.[6] This commonly results in an increased sensitivity to the stimulating effects of caffeine when ciprofloxacin is taken. Hence, it is hardly a surprise that coffee drinkers who are prescribed a benzodiazepine are at an even higher risk for fluoroquinolone-induced seizures and neuropsychiatric disturbances.

It is an unfortunate truth that many healthcare practitioners outside the realm of neuroscience are unaware of these lesser-known facts about fluoroquinolone antibiotics. The fluoroquinolone-caffeine interaction is well documented but the fluoroquinolone-benzodiazepine interaction is not currently recognized in any of the current web-based drug interaction cross checking systems commonly used by healthcare consumers. Most pharmacists are not aware of the issue either, and will readily dispense fluoroquinolone prescriptions to benzodiazepine-dependent patients. This interaction is not consistently recognized yet it very consistently gets benzodiazepine-tolerant individuals into deep trouble. Studies have found that benzodiazepine-dependent individuals frequently experience depression, anxiety, psychosis, paranoia, severe insomnia, paraesthesia, tinnitus, hypersensitivity to light and sound, tremors, seizures, and suicidal thoughts upon exposure to fluoroquinolone antibiotics.[7] 

These symptoms are all consistent with acute benzodiazepine withdrawal syndrome. Furthermore, it may take several weeks or even months after discontinuing the fluoroquinolone for the affected individual to become symptom-free. This may be due to the long-term potentiation that occurs when excitatory glutamate-containing synapses are overstimulated by a deficit of GABA activity. Some individuals never return to their pre-fluoroquinolone state and they are commonly referred to as having been “floxed”. They are left with conditions including peripheral neuropathy, muscle weakness, cognitive dysfunction, new or worsened mental illness, and even paralysis which are all consistent with excitatory neurotoxicity (excitotoxicity) and brain damage.[8][9][10]

Taking all this into account, it is imperative that moving forward more healthcare professionals will become aware of and publicly acknowledge this dangerous interaction which has rendered normal, healthy people disabled. However, this alone is not enough. It is equally important that benzodiazepine-dependent individuals become aware of this interaction so that they can better advocate for themselves. It is well known that chronic benzodiazepine usage often creates chemical sensitivities which require the affected individuals to avoid a variety of foreign substances which most normal people can tolerate, and fluoroquinolones probably fall at the very top of that list.

All doctors should be aware that prescribing a fluoroquinolone to a benzodiazepine-dependent individual carries a serious risk for disability which could potentially be permanent. Fluoroquinolones should be contraindicated with chronic benzodiazepine exposure in nearly every scenario, including nonmedical benzodiazepine abuse. Clinicians should explore all alternatives before fluoroquinolones are considered. In rare cases where it has been determined that failing to administer a fluoroquinolone could result in death, benzodiazepine-dependent individuals should have their benzodiazepine dosages increased for the entire duration of fluoroquinolone therapy and until the drug is completely cleared from their system.

 

 

Autonomic Nervous System Dysfunction from Cipro, Levaquin, and other Fluoroquinolones

Many symptoms of fluoroquinolone toxicity involve autonomic nervous system dysfunction.

The autonomic nervous system (ANS) regulates bodily functions such as the heart rate, digestion, sweating, salivating, respiratory rate, pupillary response, urination, sexual arousal, and certain reflex actions such as coughing, sneezing, swallowing and vomiting. The ANS also controls the balance between the parasympathetic (the “rest and digest” or “feed and breed” system) and the sympathetic (fight or flight system) nervous systems.

Many fluoroquinolone toxicity victims/”floxies” (those who have been poisoned by Cipro/ciprofloxacin, Levaquin/levofloxacin, Avelox/moxifloxacin, Floxin/ofloxacin or other fluoroquinolone antibiotics) struggle with:

  • Digestive dysmotility
  • Either sweating too much or too little
  • Increased heart rate / racing heart
  • Breathing difficulty / air hunger
  • Increased frequency, urgency, and pain with urination
  • Sexual dysfunction
  • Loss of libido
  • Dry mouth and dental problems
  • Dry eyes and vision problems
  • Adrenal dysfunction and fatigue
  • Lightheadedness
  • Loss of balance
  • Anxiety
  • Difficulty regulating blood-sugar levels

ANS dysfunction is also common among those with POTS/Postural orthostatic tachycardia syndrome (“The hallmark sign of POTS is a measured increase in heart rate by at least 30 beats per minute within 10 minutes of assuming an upright position”), EDS/Ehlers–Danlos syndrome (a grouping of genetic connective tissue disorders), and MCAS/Mast cell activation syndrome or MCAD/mast cell activation disorder (an inflammatory immune system disorder that leads to many multi-symptom, chronic illness). ANS dysfunction is also a symptom of each of these illnesses.

Fluoroquinolone toxicity symptoms mimic and overlap with those of POTS, EDS, and MCAS/MCAD. All these disorders are multi-symptom, chronic illnesses for which there is no cure. In addition to causing ANS dysfunction, fluoroquinolone toxicity, like EDS, causes connective tissue damage, and like MCAS/MCAD, fluoroquinolone toxicity involves immune system dysfunction. There is significant overlap in symptoms, and maybe pathology, between fluoroquinolone toxicity, POTS, EDS, and MCAS/MCAD.

You can find many examples of ANS dysfunction (and other symptoms of fluoroquinolone toxicity that overlap with symptoms of POTS, EDS, and MCAS/MCAD) in the stories of fluoroquinolone toxicity on https://fqwallofpain.com/, http://www.fluoroquinolonestories.com/, https://www.facebook.com/groups/floxies/ and here on https://floxiehope.com/. Personally, I experienced several ANS dysfunction symptoms, including digestive dysmotility, increased heart rate, dry eyes, loss of balance, anxiety, adrenal fatigue, difficulty regulating blood-sugar levels, and I didn’t sweat for years after I was hurt by ciprofloxacin.

Most of my ANS dysfunction symptoms, along with all my other fluoroquinolone toxicity symptoms, have improved.

The thing that helped to improve my digestive motility most was supplementing hydrochloric acid (HCL). I think that probiotic supplements and foods, meditation, and time also helped to heal my digestive tract.

A Chinese herbal supplement called suxiao jiuxin wan helped to calm my racing heart. I think that acupuncture, stress reduction, and time also helped.

I can’t pinpoint anything specific that cured my dry eyes, inability to sweat, or loss of balance, but those symptoms have all subsided with time.

Anxiety is common among “floxies,” and it can be severe. The post, Treating Fluoroquinolone Anxiety, goes over some suggestions as to how to deal with it. Magnesium and uridine supplements helped me to get through fluoroquinolone-induced anxiety, and those supplements have helped others too. In addition to reading Treating Fluoroquinolone Anxiety, I also suggest reading some of the recovery stories from people who have recovered from fluoroquinolone toxicity anxiety, especially Marcela’s Story, Ruth’s Story, and Nick’s Story.

I still struggle with adrenal fatigue and difficulty regulating my blood-sugar. I tend to feel better when I reduce my stress levels, avoid caffeine, avoid alcohol, and cut out sugar. I’m imperfect about those things though.

ANS dysfunction, and the diseases associated with it (fluoroquinolone toxicity, as well as POTS, EDS, MCAS/MCAD, etc.) are serious, and often the symptoms of these diseases are severe and life-altering. They are not trivial, and there is no easy or simple “cure” for ANS dysfunction or any related diseases.

With the severity of ANS dysfunction and related diseases noted, I’m going to make a suggestion that I hope doesn’t seem too trite:

Love, connection, community, laughter, and peace can all help to heal the autonomic nervous system. Meditation and breathing exercises are helpful too. Anything that you can do to bring love, connection, community, laughter, and peace into your life will be helpful in healing your autonomic nervous system.

Before you accuse me of being too hippy-dippy, hear me out on the logic behind suggesting that love and peace are healing. When you are stressed, or when you feel unsafe or threatened, your sympathetic nervous system–the fight-or-flight system–is activated, and subsequently, your digestive system shuts down, you either sweat profusely or stop sweating, your heart races, your breathing becomes shallow, etc. You have an acute moment of ANS dysfunction. For most people, this situation resolves itself as soon as the stressful moment passes, and the parasympathetic nervous system is re-activated. However, people with ANS dysfunction (whether it is caused by fluoroquinolone toxicity, POTS, EDS, MCAS/MCAD, or something else), get “stuck” in a state of sympathetic nervous system activation and parasympathetic nervous system disengagement. Love, connection, safety, community, laughter, peace, meditation, and more, activate the parasympathetic nervous system, and shut off the sympathetic nervous system that is shutting down your ability to digest food, have sex, see clearly, etc. Activation of the parasympathetic nervous system helps to relieve symptoms of sympathetic nervous system overdrive, and helps to relieve symptoms of ANS dysfunction.

Exercises and practices that activate and heal the vagus nerve–the long nerve that connects your brain to your digestive tract and various organs, and controls your autonomic nervous system–can also help to heal your ANS, and relieve symptoms of ANS dysfunction. The post, Hacking Fluoroquinolone Toxicity via the Nervous System, goes over the connections between the vagus nerve and fluoroquinolone toxicity, and the post, 32 Ways to Stimulate Your Vagus Nerve (and Symptoms of Vagal Dysfunction), goes over some ways that you can stimulate your vagus nerve, which activates the parasympathetic nervous system, and reduces symptoms of ANS dysfunction. Love, laughter, connection, breathing exercises, acupuncture, etc. help to activate and stimulate the vagus nerve.

ANS dysfunction is complex, and it is not an easy thing to fix or “cure,” and I hope that my suggestion of love and stress-reduction as helpful in symptom alleviation isn’t seen as trite or dismissive.

I wish that ANS dysfunction, and the symptoms associated with it, were more acknowledged as symptoms of fluoroquinolone toxicity. They are serious, severe, and cause significant pain and suffering. Even though I am suggesting that peace, love, and meditation are helpful (they are), they are not simple cures that can be implemented in a short period of time. They are processes and practices, and despite doing their best to meditate regularly, love heartily, etc. many people are still very ill with fluoroquinolone toxicity, and other ANS dysfunction diseases. Neither peace nor love are cures for multi-symptom, chronic, illnesses like fluoroquinolone toxicity. Of course love and stress-reduction are helpful, but they’re not cures. We need more cures… and love… and acknowledgement.

 

 

Fluoroquinolone Toxicity Article – Treatment of the Fluoroquinolone Associated Disability – the pathobiochemical implications

I’m so excited to share this article, “Treatment of the Fluoroquinolone Associated Disability – the pathobiochemical implications” by Krzysztof Michalak, Aleksandra Sobolewska-Wlodarczyk, Marcin Włodarczyk, Justyna Sobolewska, Piotr Woźniak, and Bogusław Sobolewski, with you! It is the first article of its kind that I’ve seen. While there are thousands of articles about fluoroquinolones, many of which focus on the damaging effects of fluoroquinolones, and many case-studies that note the adverse-effects of fluoroquinolones (hundreds of articles about fluoroquinolones are linked HERE), this is the first article that acknowledges that fluoroquinolone toxicity (referred to as both Fluoroquinolone Associated Disability (FQAD) and fluoroquinolone toxicity throughout the article) is a disabling syndrome, that also goes over the mechanisms by which fluoroquinolones can cause fluoroquinolone toxicity/FQAD, and even gives recommendations on how to treat fluoroquinolone toxicity/FQAD (while also acknowledging that there are no cures or verified treatments). The article even calls for more extensive research to be done into fluoroquinolone toxicity, and the various mechanisms through which fluoroquinolones hurt people.

It is an enlightening article, and I encourage you to print it out and give it to your doctors, family members, and anyone else who is interested in what fluoroquinolones do and how they hurt people. In this post, I’m going to go over some highlights from the article, but I recommend that you read it yourself (you can access it through THIS LINK, after clicking on the “provisional pdf” link).

The first paragraph of the abstract to the article states:

“Long term Fluoroquinolone Associated Disability (FQAD) after fluoroquinolone (FQ) antibiotic therapy appears in recent years a significant medical and social problem, because patients suffer for many years after prescribed antimicrobial FQ-treatment from tiredness, concentration problems, neuropathies, tendinopathies and other symptoms. The knowledge about the molecular activity of FQs in the cells remains unclear in many details. The effective treatment of this chronic state remains difficult and not effective. The current paper reviews the pathobiochemical properties of FQs, hints the directions for further research and reviews the research concerning the proposed treatment of patients.”

To see that in writing, in an academic article, is incredibly validating.

Adverse Effects of Fluoroquinolones

Treatment of the Fluoroquinolone Associated Disability – the pathobiochemical implications, goes over the documented effects of fluoroquinolones. For tendinopathies and tendon ruptures, researchers have found that:

“FQs are associated with an increased risk of tendinitis and tendon rupture. This risk is further increased in those over age 60, in kidney, heart, and lung transplant recipients, and with use of concomitant steroid therapy.”

Fluoroquinolones cause neurotoxicity, as well as central and peripheral nervous system ailments:

“Taking FQs is associated with their neurotoxicity, as well [5-8]. The main symptoms being correlated to FQ treatment include insomnia, restlessness, and rarely, seizure, convulsions, and psychosis [9-11]. Many reports point to chronic persistent peripheral neuropathy to be generated by FQs [12-18]. Cohen et al. [19] showed that a possible association between FQ and severe, long-term adverse effects involving the peripheral nervous system as well as other organ systems are observed.

Fluoroquinolones also cause cardiotoxicity and an elongation of the QT interval, as well as hepatotoxicity and nephrotoxicity. Fluoroquinolone use has even been linked to type-2 diabetes onset.

Fluoroquinolone toxicity / FQAD is a multi-symptom, chronic illness that affects all body systems. Fluoroquinolones deleteriously affect every muscle, tendon, ligament, nerve, and even bone, in the body. They damage every cell in the body.

Fluoroquinolone Damage Mechanisms

Treatment of the Fluoroquinolone Associated Disability – the pathobiochemical implications, notes the various mechanisms by which fluoroquinolones cause cellular (mitochondrial) damage, including oxidative stress, and the downstream effects of oxidative stress, including disruptions in the mitochondrial Permeability Transition Pore (PTP) (and the article authors state, “The influence of FQs on the detailed regulation of PTP is the urgent topic for further research.”), Calcium and magnesium homeostasis, lowered ATP production, and more.

Here is a diagram of the mechanisms of fluoroquinolone toxicity (published in the article):

Figure 2. The main ways of FQ toxicity. The positive regulatory loops magnifying the toxicity of FQs are marked with ‘+’. The ‘?’ signs denote the possible but not confirmed effects of FQ toxicity.

The article also notes the epigenetic effects of fluoroquinolones and oxidative stress:

“Beside OS (oxidative stress), epigenetic effects of FQs are of high importance, as well. The epigenetic effects may depend on the methylation of DNA and/or histones, however, ROS contribute also to epigenetic changes [42]. Some authors point also to the similarity of bacterial and mitochondrial DNA, both existing in circular super-twisted helices and gyrase-like enzymes being postulated to be responsible for the organization of mitochondrial DNA, suggesting the possible direct effect of FQs to mitochondrial DNA leading to the disturbed mitochondria regeneration and division [43, 44]. The changes in the cytoskeleton were observed also after FQ treatment [45] and cytoskeleton has been demonstrated to be strictly connected with energy dissipation and organization in mitochondria [46-49].”

Treatment of the Fluoroquinolone Associated Disability – the pathobiochemical implications, also notes that fluoroquinolones chelate various minerals and metals. The article notes that, “Seedher’s results indicate that chelation formation with bivalent metals can cause significant alterations in the human serum-FQ binding affinity.” The article also describes how fluoroquinolones chelate iron, zinc, magnesium, and other minerals, and how this chelation can have enzymatic and even epigenetic adverse effects.

Fluoroquinolones are GABA antagonists, and the effects of fluoroquinolones are similar to those of benzodiazepine withdrawal. The authors of Treatment of the Fluoroquinolone Associated Disability – the pathobiochemical implications, describe a potential mechanism through which GABA is depleted by fluoroquinolones:

“One of the proteins which can support PTP opening is Translator Protein (TSPO), called also peripheral-type benzodiazepine receptor or isoquinoline binding protein. TSPO is predominantly located on the surface of the mitochondria where it is postulated to physically associate with VDAC-ANT. It has been suggested that TSPO may activate PTP opening, causing ∆Ψm reduction and leading to apoptosis [80, 81]. Some authors suggest that epileptogenic activity of FQs possibly relates to GABA-like structure of some FQs which may allow them to act as GABA antagonists [82, 83]. Since TSPO is also a benzodiazepine receptor, similar interaction may maybe also take place between FQs and TSPO leading to opening PTP.”

I have always wondered how GABA inhibition is connected to mitochondrial destruction. The article excerpt above answers that question for me.

Fluoroquinolones can lead to chronic illness and permanent disability, which has led many people to question whether or not they remain in the body for an extended period of time (or, if they do damage while they’re in the body that continues long after the drug has left the body). The authors of Treatment of the Fluoroquinolone Associated Disability – the pathobiochemical implications note that:

“The other important feature of FQs has been presented by V.T. Andrioleet al. [55]. Namely, they estimated the minimum solubility of FQs in neutral pH. They pointed that this class of molecules is characterized by very high melting point, generally >200°C, which indicates that the crystal forms are very stable. All these FQ features strongly support the thesis that FQs can survive in the cell for a long time contributing to chronic, long-term adverse reaction in patients treated with FQs. The question, to what extent takes this phenomenon place and if it contributes to chronic symptoms of FQAD, remains unclear.”

It is acknowledged throughout the article that it is unknown whether or not fluoroquinolones stay in the body for an extended period of time. It is possible, through the mechanism noted above, but no hypotheses about fluoroquinolones remaining in the body after they “should” have been metabolized and fully excreted, have been explored. It’s both possible that they remain in cells, and that they don’t – no one really knows.

The article authors repeatedly call for additional research into the various mechanisms by which fluoroquinolones lead to pain, disability, and chronic illness:

“Summing up, the number of enzymes possessing reduced activity due to their ion-cofactor chelation is probably long and it is the important topic for further research. The separate problem consists the chronicity of ion-chelation by FQs. The presented research does not describe the chronic state of FQAD but the phenomena taking place during FQ application. It must be analyzed, to which degree persistent ion chelation takes place at FQAD patients.”

Fluoroquinolone Toxicity Treatment

Treatment of the Fluoroquinolone Associated Disability – the pathobiochemical implications is the first article I’ve seen that discusses the treatment of fluoroquinolone toxicity as a multi-symptom, chronic illness. The authors note that the first step in approaching a treatment is to discover why fluoroquinolones are causing chronic illness in the first place. Effective treatment, of course, depends on effective identification of the problem. With that noted, the article authors have enough knowledge to make a few suggestions:

“Until detailed knowledge concerning FQ toxicity would be recognized, the following directions in supporting FQAD patients are proposed according to the known and probable mechanisms of FQ toxicity: A. reduction of the oxidative stress; B. restoring reduced mitochondrial potential ∆Ψm; C. supplementation of uni- and bivalent cations that are chelated by FQs;D. supporting the mitochondrial replication in the cell – pulling the more destroyed to apoptosis and proliferation of the more healthy ones; E. removing FQs permanently accumulated in the cells (if this phenomenon takes place); F. regulating the disturbed epigenetics and enzyme activities”

The article authors note that antioxidant supplementation is a broad topic and that fixing the damage done by fluoroquinolones and oxidative stress is not as simple as just ingesting an antioxidant pill. However, antioxidant supplements that specifically target the mitochondria have shown some promising results:

“The antioxidants which enter easily the mitochondria are the most interesting ones. Lowes et al. [79] shows that the mitochondria targeted antioxidant MitoQ protects against fluoroquinolone-induced oxidative stress and mitochondrial membrane damage in human Achilles tendon cells. In cells treated with MitoQ the oxidative stress was lower and mitochondrial membrane potential was maintained.”

Other antioxidants have also had promising results in repairing fluoroquinolone treated cells. Some of the antioxidants with promising results include N-acetylcysteine, resveratrol, as well as Vitamins C and E. Supplementation of the trace minerals that are important cofactors for antioxidants is also important.

Conclusion

I greatly appreciate the authors of Treatment of the Fluoroquinolone Associated Disability – the pathobiochemical implications. They approach fluoroquinolone toxicity/FQAD as a complex and multifaceted illness. It IS a complex and multifaceted illness, and it is refreshing to read an article that doesn’t over-simplify or downplay the illness. I also appreciate the exploration of what is currently known about fluoroquinolone toxicity/FQAD, and the assertions that more research into fluoroquinolone toxicity is needed (it is!). I think that everyone who is going through fluoroquinolone toxicity/FQAD should read it, and share it as widely as possible.

 

 

 

Floxie Hope Podcast Episode 23 – Tara

Tara shared her journey through Levaquin-induced fluoroquinolone toxicity in Episode 23 of The Floxie Hope Podcast. Please check it out!

http://www.floxiehopepodcast.com/episode-023-tara/

and

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

You can also read more about Tara’s journey in her story:

https://floxiehope.com/taras-story-healing-from-levaquin-effects/

Tara has noted several times that she was not as far along in her journey as she thought she was when she wrote her story. Please listen to the podcast for more information about Tara’s journey. It is not a repeat of her story above.

Also, here is a different podcast that she did with her doctor:

https://floxiehope.com/2016/03/12/true-health-made-simple-podcast-featuring-tara/

Tara gives a wealth of information about her journey, and how complete avoidance of fluoride, along with various homeopathic methods, supplements, and other things, have helped her through the last two years.

Also, here are some notes and resources from Tara to accompany the information she gives in the podcast:

“What I’m told by fluoride experts is that it matters how much fluoride was already accumulated in your system if you get fluoride poisoned or if you are already sensitive to it by genetics or be because of other chemicals or stressors. Also, whether or not a person becomes hypersensitive does not seem to correlate with how badly they are injured. Ex: People who are hurt much worse than me, still may not become hypersensitive. The spectrum of sensitivity may not have anything to do with the amount of injury from what I can tell through research or peoples’ stories.”

“Also, Im not sure if I was clear about the Fluoride Poisoning symptoms – a person does not usually “feel” anything after ingesting fluoride or coming in contact with fluoride – only a hypersensitive person like myself, which is rare -most people who are poisoned because of fluoride just develop symptoms/diseases/disorders due to the enzymes, tissues, and structures that are poisoned. Most people discover they are poisoned from fluoride by getting completely off of it and symptoms get better (damage has to be repaired over time, some damage is not repairable for all people – but there is always hope of better).”

“Coffee – I forgot to mention this most important topic! 🙂 I was not able to drink anything caffeinated – not even a sip – for 20 months – using the SCIO to heal neurotransmitters (Adenosine is neurotransmitter associated with caffeine receptor site – also used SCIO to heal neurotransmitters in general helped immensely, to heal nerves, healing mitochondria DNA, food allergies, and attempting to desensitize from fluoride).

I am more than happy to report I can now drink a small cup of Bulletproof coffee (free of mold), and put Brain Octane (distilled coconut oil  – helps mitochondria for brain energy), butter (also good for brain), and when my fluoride is low enough, I can handle also putting in the Collagelatin powder in the coffee (good way to replace collagen and gelatin) for me. This is all mixed in a food processor together to combine – according to his book, there is a scientific reason why stirring doesn’t have same effects so needs to be blended.  I really like the taste and that it’s mold free. The founder of Bulletproof used to have Chronic Fatigue Syndrome, mold allergies, I think also Lyme, etc – so his story is good to read for inspiration – it brought him to a lot of research on mitochondria and health and building this very successful company.
bulletproof.com
(This is also the coffee I use for coffee enemas – it does matter that the coffee is pesticide and toxin free as possible – helped with small intestinal bacteria overgrowth SIBO)”

Resources:

Homeopathy – company name White Dove – Vitamin C, Bone Support, Pitui Liquitrophic, Fem Liquitrophic (I get these from my chiropractor’s office)
Solutions 4 supplements (chiropractor’s office)
MitoQ – mitoq.com
Pelican brimac bone char filtration system to remove fluoride – https://www.pelicanwater.com/whole-house-fluoride-filters
Allerphase (allergy/asthma herbal supplement – https://www.tangoherbs.com/allerphase60.html (side note: My son, 10-years-old, was able to get off his allergy and asthma medications – he has been on them since age 3, with the addition of Allerphase and MSM (from mercola.com), as well as getting off dairy/gluten and switching to an organic diet)
Harmless Harvest Coconut Water from Whole Foods (all coconut water is not made equal – some are highly processed – good idea to do some research – this is the one I use)
Infrared sauna – http://www.sunlighten.com/
Hyperbaric Oxygen Chamber Treatment – http://www.oxygenunderpressure.com/ – This is the HBOT Institute I went to – it’s a stand alone chamber by the Kansas City, MO airport – people from all over the United States come here for treatment – sessions were $125-$175 per session, 40 sessions is what was recommended. Expensive but worth getting my brain back.
Books:
Diagnosis and Treatment of Chronic Fatigue Syndrome and Myalgic Encephalitis by Dr Sarah Myhill
Eat Dirt by Dr. Josh Axe –
The Thyroid Connection by Dr. Amy Myers
The Wahl’s Protocol by Dr. Terry Wahls
The Devil’s Poison: How Fluoride is Killing You by Dean Murphy, DDS
Letting Go by Dr. David Hawkins
The Fluoride Toxicity Research Collaborative – http://www.slweb.org/ftrcfluoroquinolone.html
The Truth About Water Fluoridation by Charles Eliot Perkins (1952)
SpectraCell test – for minerals/vitamins/antioxidants/etc – also get test for iron and copper
Dr. David Gulledge, chiropractor for homeopathy, SCIO
Supplements suggested by the Fluoride Toxicity Research Collaborative (FTRC) for fluoride/fluoroquinolone toxicity (they lab tested to find good/cheap brands):
Calcium – solutions 4 brand or FTRC said Standard Process (can get from a chiropractor or naturopath) – fluoride binds to calcium and leaves the body in large quantities
Vitamin C with flavanoids- detoxes fluoride – they said Trader Joes brand with the lemon flavanoids. I do better with homeopath Vitamin C.
B-vitamins – fluoride disrupts synthesis of B-vitamins – (FTRC said Trader Joes brand)
Magnesium – fluoride chelates this mineral as well (FTRC said Kal brand – found at whole foods is good). I use Epsom Salt. If I wasn’t as sensitive to fluoride, I would choose Ancient Minerals magnesium lotion – loved it.
This article was sent to me by my chiropractor- it’s is by Dr. Jack Kruse – about being floxed and what to do about it – good information on staying away from EMFs, fluoride, etc. (I am very sensitive to EMFs since being floxed/fluoride poisoned)
Blue-blocking glasses I use to watch TV, look at my phone or computer – needed since being fluoride poisoned
Thank you for listening!