Fluoroquinolone Antibiotic Toxicity @fqtoxicity - Tumblr Blog

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Macrolones: A New Antibiotic That is a Toxic Time Bomb

How do you combat bacterial resistance, which the World Health Organization (WHO) calls “one of the top global public health and development threats” facing humans?

One way to fix the problem is to develop drugs that bacteria can’t build resistance to. In a world where research on new antibiotics is not given a top priority, the University of Illinois Chicago (UIC) researchers came up with a novel idea that might make bacterial resistance almost impossible.

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What exactly did they do at the UIC?

They decided to combine one family of antibiotics, the macrolides, which are known to be mitochondrially toxic (1), and combine them with the most mitochondrially toxic antibiotics, the quinolones (2), to create the Macrolones.

The Macrolones are synthetic macrolide derivatives with a quinolone side chain, structurally similar to DNA topoisomerase-targeting fluoroquinolones (3).

The researchers describe how the new class of drugs can disrupt bacterial cell function in infectious diseases. First, they can kill protein production, just like macrolides, a type of antibiotics that are currently in use. Second, the macrolones can also interfere with the DNA structure of bacteria (DNA gyrase) in a similar way current fluoroquinolones act. That’s another type of widely used antibiotic.

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Over the years I have repeatedly warned against future drugs being developed that were either based on the fluoroquinolones or combined with the fluoroquinolones (4).

Researchers have confirmed time and time again that fluoroquinolones are the modern-day antibiotic equivalent of a really cool erector set. They fully admit that the quinolone’s “chemical synthesis is flexible and can be easily adapted to prepare new congeners with rationally devised structures”. You can read all about it here in the published article “Nonclassical Biological Activities of Quinolone Derivatives” (5).

The paper describes how the quinolone’s chemical synthesis is flexible and can be easily adapted to prepare new compounds and it is considered ideal for effective drug design. From the above paper “…which makes quinolones an endless source of hope and enables further development of new clinically useful drugs.”

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Despite the numerous papers, articles, and patient stories that point to the toxicity of the fluoroquinolones, it is my opinion that most scientists who work in drug development do not believe that they are very toxic. On the contrary, like a kid with who received a cool new erector set for Christmas, they see endless possibilities in synthesizing new compounds from the quinolone drug scaffold.

My research has proven to me that there is something very inherently wrong with the quinoline pharmacophore. That foundation on which new drugs are built holds a secret that is hidden in plain sight. This secret is the fluoroquinolone’s toxicity whose insidious tentacles spread throughout society causing untold worldwide health problems that routinely evade detection or documentation by separating cause and effect.

Please read this article I wrote to fully appreciate the fluoroquinolone’s long-term impact on our society:

The Fluoroquinolone’s Inconvenient Truth

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Until drug researchers fully understand and connect the fluoroquinolones to all the damage they cause, from post-viral syndromes to CFS and Fibromyalgia, from Gulf War to ALS and Parkinson’s, all avenues of development will carry with them the underlying risk of horrific adverse events for those unlucky enough to fall victim.

Do you know of a loved one, a friend, a co-worker, or someone else who suffers from a diagnosis of mysterious origin, such as peripheral neuropathy with an unidentified cause? If so, ask them to do some detective work to find out if they have used Fluoroquinolones in their past, not necessarily their immediate past. Tell them that the Fluoroquinolones are often given during surgery, often without the patient’s knowledge.

If you are faced with potential antibiotic use, for yourself or a loved one, please become informed as to your available choices. If antibiotic use is necessary, there are generally safer alternatives than the Fluoroquinolones.

If and when these Macrolones do come to the market please stay informed, especially now that they are incorporating the quinolones into other medications. And, as always, please discuss all medical concerns openly and honestly with your doctor.

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Are ICD-10 Codes for Fluoroquinolone Adverse Events on the Horizon?

A big hurdle for those who have experienced and are living with chronic illness brought about by Fluoroquinolones may have been crossed.

Talia Smith, a floxie who has been chronically impacted ever since taking Cipro for a UTI in 2021, along with Dr. Stefan Pieper, pushed for the new codes.

Smith said the CDC informed her by email that ICD-10 codes are going to be created for physicians to report patients with Fluoroquinolone poisoning.

Why are ICD-10 Codes important?

Standardized communication: ICD-10 codes provide a universal language for healthcare providers to record and share diagnoses. This allows for clear communication between doctors, hospitals, and other healthcare settings, even across different countries.

Improved data collection: With consistent coding, healthcare data can be easily collected, analyzed, and compared. This helps track disease trends, monitor public health, and identify areas where healthcare resources might be needed.

Better research: Researchers rely on ICD-10 codes to study diseases, develop treatments, and evaluate healthcare interventions. Accurate coding ensures studies have a reliable foundation.

Accurate billing and insurance: ICD-10 codes are used for medical billing and insurance purposes. Having the correct code ensures proper reimbursement for healthcare services.

Overall, ICD-10 codes play a vital role in ensuring efficient and effective healthcare on a global scale.

A CDC spokesperson told reporter Ted Daniel with 25 Investigates, “The topic of fluoroquinolones was presented at the March 2024 ICD-10 Coordination and Maintenance Committee Meeting. CDC does not publish the codes that will be implemented in advance of their official release, as we must adhere to our internal clearance processes for final posting and release. The codes scheduled for implementation on October 1, 2025, will be made available on the CDC website sometime during the latter half of 2025.”

If the CDC delivers on its promise to create the codes the fight is far from over.

Here’s why:

Focus on Diagnosis: ICD-10 codes simply classify a condition. They don’t determine its severity or urgency.

Doctor’s Discretion: Doctors use their medical judgment and expertise to decide the level of attention needed for each patient regardless of the ICD-10 code.

It will still fall back to individual doctors to recognize Fluoroquinolone Toxicity or FQAD and use the reporting code. Dr. Pieper acknowledges that “Even now, lots of doctors, I would say most of them, they do not know about the clinical picture, although there are so many patients.”

Doctors have long ignored, dismissed, and marginalized those who have reported adverse events to Fluoroquinolones over the years and this trend continues on.

As for me, besides my own person chronic battles with with FQAD, not a day goes by, when I am not contacted by someone new to this terrible plight. Their stories are all the same and each story usually involves a doctor(s) who denies that FQAD exists.

We now hope a pray that the CDC follows through with their promises and gets the codes created in a timely manner. We also hope that when these codes come out doctors start utilizing these codes which, along with the help of these tireless advocates, get additional codes that will lead to much-needed research.

A big thank you to Talia Smith, Dr. Pieper, Ted Daniels, and all those who contributed to this worthwhile endeavor. You have our profound thanks.

You can find Talia Smith of TikTok at: https://www.tiktok.com/@taliasmith2021?lang=en

Source: https://www.yahoo.com/news/advocates-cdc-approves-floxing-reportable-213159108.html

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#Advocacy #CDC #Community News

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A Drug-Free Solution for Improved Upper Respiratory Health

Having an adverse event from Fluoroquinolones means different things to different people. Many people become vulnerable to viruses and must work diligently to avoid illness.

Before COVID, the fluoroquinolone community was already a community of people where some were actively avoiding colds and flu due to the potential complications that they bring. They were constantly trying products to find new, non-drug methods for prevention.

Some if the necessary methods are making sure that vitamin D levels are optimal, along with Vitamin A, and others like Zinc, Vitamin C, etc.

Another way that has been proven to be effective for some, is airway cleansing and hydration.

Since the start of COVID a handful of previously floxed people I know have been using a product for upper airway prevention called FEND.

FEND is not a traditional nasal spray. It’s a nasal misting device designed to cleanse and hydrate your upper airways through the inhalation of a propriety mixture of salts.

From an article in Molecular Frontiers Journal. “The salts (a hypertonic mixture called FEND) associate with mucin macromolecules near the mucus surface, binding mucus molecules together, thereby increasing mucus surface tension and surface vis-coelasticity23. These effects help mucus surfaces withstand the stresses that occur on air passing over mucus during normal breathing23, resulting in fewer respiratory droplets in the airways, and fewer exhaled aerosol particles — a form of “airway hygiene.” (1)

FEND claims to capture and eliminate airborne contaminants before they reach your lungs, potentially reducing airborne virus transmission (including COVID-19) and improving overall respiratory health.

For sensitive people, FEND is gentle and comfortable with virtually no side effects or negative impacts. Unlike most nasal sprays, FEND doesn’t need insertion into the nose, making it more comfortable for some users. The mist is described as gentle and non-irritating.

FEND claims its effects last up to 6 hours after just two puffs, potentially offering sustained protection throughout the day. It was developed by scientists at Harvard University as a natural and drug-free using a saline solution with calcium and magnesium, avoiding decongestants, steroids, or antibiotics.

My experience with FEND started in the spring of 2020. I was on a phone call with a floxed person who was employed in the movie industry and was forced to work during the initial outbreak of COVID-19. This person had to be around a lot of people every day on the job site. She had discovered FEND on a recommendation from a friend and had been using Fend to protect her upper airway from viruses while around groups of people.

Initially, I was skeptical, however, she insisted that I try it and gifted me a Fend spray. Since then, I have used it along with six other people who I tracked their usage. So far, none of us have come down with COVID, and three of the five have not had any colds or flu during that time as well.

I will be the first to throw in the caveat that all the people I know who use FEND have been diligent about keeping their vitamin levels in optimal shape and taking other proactive steps such as hand washing and actively trying to avoid those who are sick with respiratory viruses as much as possible. Still, I believe there is something to keeping the upper respiratory moistened to help avoid viruses from taking hold.

Pros: FEND was developed by a Doctor at Harvard and does have studies that back its efficacy (2, 3). A non-drug alternative to help avoid upper respiratory viruses. It does have some good science behind the claims, and according to my small sample, there is some good anecdotal information showing that it works.

Cons: The vials of FEND are small and in my opinion not worth the normal cost of a single one-time purchase, however, in my experience they do last a single person about 30 days. However, there is a workaround that gives you substantial savings and makes the cost per unit reasonable if you subscribe to a monthly purchase. Fortunately, you can cancel the subscription at any time.

If you do intend to try Fend, I have secured a discount by clicking on their logo below. You will be shown a discount code where you can get $5 off and if you use the subscription model with the discount code the price is very reasonable. My motivation is not to ‘sell’ Fend, but to help keep Floxed people healthy during times of heightened respiratory illnesses. If you use Fend, please let me know what your experience is, pro or con. I will use the data to help others.

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#Colds #COVID-19 #Flu #Supplements

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Pentadecanoic Acid (C15) for Mitochondrial Health

I am starting to get good reports from people suffering from FQAD about Fatty15.

What is Fatty 15 you ask?

Fatty15 is technically pentadecanoic acid, commonly referred to as C15 or Fatty15. C15:0 is the first essential fatty acid to be discovered since the omegas—over 90 years ago. It is an odd-chain saturated fatty acid that has been garnering attention in the health and wellness communities for its potential benefits, particularly in relation to mitochondrial health. Mitochondria, the powerhouses of cells, play a crucial role in energy production and overall cellular health and are often damaged in various ways from Fluoroquinolones leading to a host of problems. From all preliminary indications Fatty15 appears to have a significant positive impact on mitochondria.

For my readers who like to geek out on the science, C15:0 is a sturdy, odd-chain, saturated fatty acid that integrates itself into cell membranes to fortify and strengthen them, giving them better protection against oxidative stress and cellular degradation than omega-3 fatty acids. Studies show that C15:0 supplementation improved cellular stability by 80% (1).

Mitochondrial dysfunction/disease is a key hallmark of Fluoroquinolone toxicity and in turn that drives, or contributes, to the onset of chronic diseases (FQAD). C15:0 increases mitochondrial function by up to 45%, keeping our cells active and ensuring they’re able to carry out cellular processes as they should. The mitochondria produce ATP, your cell’s energy currency. In studies, C15:0 was able to increase ATP by up to 350%. A pretty impressive feat!

C15:0 Long-Term Benefits

C15:0 (Fatty15) has been shown in peer-reviewed studies to:

Strengthen cellular membranes, making them more resilient against age-related breakdown. Fatty15 contains pure C15:0, which is a sturdy fatty acid that imbeds into the lipid bilayer of membranes to protect cells against lipid peroxidation. Fatty15 has been shown to improve cellular stability by 80%.

Repair mitochondrial function and restore cellular energy. Fatty15 has been shown to improve mitochondrial function by 45%. These benefits result in increased ATP energy production and reduced reactive oxygen species (ROS).

Naturally activates AMPK to support glucose control. Fatty15 activates AMPK, which supports our long-term health and is a core component of the human longevity pathway.

Lowers multiple pro-inflammatory cytokines to balance immune responses. Fatty15 lowers key cytokines, including IL-6, MCP-1 and TNF-alpha, which are responsible for aging-related breakdown.

Naturally activates PPAR-alpha and delta receptors, which regulate our metabolism and immunity. Additionally, PPAR-alpha activators have been proposed to support brain health, while PPAR-delta activators can be heart protective.

C15:0 is also helpful in assisting with clearing damaged cells. Some people FQAD suffer from an accumulation of damaged cells. C15:0 activates AMPK and inhibits mTOR, which are important mechanisms to slowing cellular senescence and clearing damaged cells. AMPK is also essential in regulatory processes, like glucose uptake (2).

C15:0 (Fatty15) near-term benefits:

Near-term roles of PPARs. Many of fatty15’s near-term benefits are due to fatty15’s role as a natural activator of two key receptors, called PPARs (pronounced pee-pars) alpha and delta, that are present throughout our body – including our brain. In addition to these long-term benefits, PPARs help to regulate our mood, stress, sleep patterns, energy, and hunger.

Near-term roles of PDC. Our bodies use C15:0 to naturally make a second molecule, called pentadecanoylcarnitine (what we refer to as PDC). PDC is the second-ever discovered full-acting endocannabinoid and has been shown to:

Activate CB1 and CB2 receptors as an endocannabinoid that can help to improve joint comfort, mood, and sleep.

Activate 5-HT1A and 5-HT1B receptors to reduce stress.

Inhibit histamine H1 and H2 receptors to calm immune responses.

Unfortunately a person can’t get C15:0 by just eating foods. The short of it is that while C15:0 is available in trace levels in food, especially whole fat dairy products, food-based C15:0 is tied up in complex lipids called triacylglycerides, which we cannot absorb. If you attempt to get large amounts of C15:0 from dairy you would have to consume an outrageous amount of dairy fats that would give you a much higher levels of ‘bad’ even-chain saturated fats (like, C16:0) and the negative effects would greatly outweigh the positives.

Another positive is that it also appears that for some people who can tolerate Omega-3’s, C15:0 seems to well tolerated and C15:0 is dosed in one small capsule per day and delivers the same benefits as Omega 3’s plus much more.

Side effects: Since C15:0 was discovered as an essential fatty acid in 2020 and introduced to the public in 2021, over 17,000 customers have taken fatty15 with very few side effects. A few minor side effects have been reported in less than 0.1% of customers: constipation, diarrhea or headache. Due to confounding factors it cannot be confirmed confirm that these side effects are directly attributable to C15:0 supplementation. One floxed person reported a minor headache that went away after a few days, and another reported a transient case of nausea.

Conclusion

Right now, Fatty15 (C15:0) is only available to purchase from the company who discovered it, and that is a the Fatty15 website. They do not sell on Amazon or in retail stores. Keep in mind that Fatty15 is not a magic cure all. It is however a substance that shows promise in the ability to heal heal or support injured mitochondria, in addition to providing other benefits. My opinion is that it might benefit those who are suffering from mitochondrial issues stemming from fluoroquinolone toxicity and I have had reports of improved energy and sleep.

One drawback is that like many new products, it is expensive, and it needs to be taken for a while to achieve full benefits. I have secured a 20% discount for those who want to try it by just clicking on the Fatty15 logo below. You will then be taken to the website for Fatty15. As usual, any benefits received for the referral link will be passed-on to other floxed people.

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#mitochondria #mitochondrial #Supplements

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Fluoroquinolone Associated Pseudotumor Cerebri

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What is pseudotumor cerebri?

Pseudotumor cerebri (PTC) literally means “false brain tumor.” Medical professionals also called PTC idiopathic intracranial hypertension (IIH). I would like to redefine PTC not only to include intracranial hypertension (IIH) but also intracranial hypotension as well. PTC occurs when there is a pressure abnormality inside the skull due to poor regulation of the cerebrospinal fluid (CSF) causing a buildup, reduction, or poor absorption of the CSF. Furthermore, I believe anecdotal data has shown that the fluoroquinolones (FQ) can induce either transient or chronic osmoregulatory dysfunction.

The IIH version of PTC is considered to be rare by medical professionals and the hypotension version of PTC is considered ‘uber’ rare. The latter being so rare that you would probably get laughed out of a doctor’s office for even suggesting it, despite the fact that it does show up in the medical literature. IIH, or the hypertension version, has more medically documented cases and causes therefore it is more known to the medical field, albeit still uncommon Intracranial hypotension, is almost always associated in the medical literature with a leak in the dura, and almost all medical professionals will not consider other causes such as osmoregulatory dysfunction.

However, one thing that has become abundantly clear to me over the last 15 years (sesquidecade) is that nothing with FQAD is actually that rare and PTC (hyper and hypo) is no exception. I have documented several anecdotal cases of PTC of both the hyper and hypo varieties.

Most cases of PTC do not get reported due to their transient nature, thus the reason for lack of awareness. Additionally, there have been patients with chronic symptoms who have gone years before getting any acknowledgement of the validity of their symptoms.

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What is Cerebrospinal Fluid?

CSF is a clear, colorless, watery fluid that flows in and around your brain and spinal cord. It is made by tissue called the choroid plexus in the ventricles (hollow spaces) in the brain.

CSF acts like a cushion that helps protect your brain and spinal cord from sudden impact or injury. The fluid also removes waste products from the brain and helps your central nervous system work properly. The CSF that is produced in the brain eventually is absorbed into the bloodstream at a rate that usually allows the pressure in your brain to remain constant in a finely balanced system that we take for granted.

If this delicate system becomes unbalanced several symptoms can appear.

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Symptoms of PTC can include:

Severe headaches and/or feelings of intense head pressure (hyper & hypo).

Abnormal pressure sensations in the ear, that can cause a whooshing sound (hyper).

Muffled hearing that may pulse with your heartbeat (hypo).

Nausea, vomiting or dizziness (hyper & hypo).

Vision loss (hyper)

Brief episodes of blindness, lasting a few seconds and affecting one or both eyes (hyper)

syncope (hyper & hypo)

Difficulty seeing to the side (hyper)

Double vision (hyper & hypo)

Seeing light flashes (hyper & hypo)

Neck, shoulder or back pain (hypo)

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PTC and Fluoroquinolones

PTC is associated with the members of the FQ family of pharmaceuticals. Although considered ‘rare’ by the medical community, anecdotal data suggests that this adverse event is not really that rare within the scope of the FQs and should probably be considered a class adverse event.

PTC was first reported in the quinolone family of drugs in 1966 when a nine-year-old girl, who was being treated by nalidixic acid, the grandfather drug of today’s fluoroquinolones, experienced the adverse event while being treated for a urinary tract infection subsequent to an automobile injury (1). In 1998 twenty cases of Nalidixic acid-induced PTC were documented in children who were being treated for acute dysentery (2).

A scholarly search will return numerous case reports of PTC associated with all members of the FQs, including the modern family members of levofloxacin, ciprofloxacin, ofloxacin, and others. The exact pathogenesis of PTC from FQs remains unclear just like many of the other adverse events from this family of antibiotics (3).

Recent studies such as “Oral fluoroquinolones and risk of secondary pseudotumor cerebri syndrome: Nested case-control study” from 2017 conclude that oral FQ usage poses a risk of PTC but it is very rare (5).

The problem with studies such as these is that they miss the non-reported cases which I believe account for the majority. Most doctors are very reluctant to report FQ-related adverse events and unfortunately, the burden falls back on the FQ community to keep track of events the best we can.

It is also unreasonable to limit the FQ’s ability to impact CSF too narrowly. Besides the more common intracranial hypertension, many cases of intracranial hypotension, and encephalopathy have been reported.

Cases of reversible encephalopathy have been reported as far back as 1966. In 2013 a 16-year boy who was being treated for pneumonia developed encephalopathy and CNS symptoms after starting Cipro. It was theorized that the pathogenesis of his adverse event was a failure of cerebral auto-regulation (6).

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Anecdotal Data

Over the years there have been numerous individuals who have experienced CSF pressure issues as just one of the many adverse event symptoms associated with FQ exposure. Thankfully, it appears that most cases of PTC seem to be of a transient nature and resolve on their own, still, there is a subset in the FQ community who are plagued with CSF pressure issues indefinitely, and some of the symptoms can be very incapacitating. Mayo Clinic’s data agree in an indirect fashion when on their website they state that PTC can resolve on its own but can also recur months or years later (4).

Over the last decade, anecdotal reports of CSF issues have included symptoms of intermittent diffuse headaches, some headaches worse in the evening or at night, and often aggravated by sudden movement. Visual disturbances include visual obscurations, blurred vision, double vision, and photophobia. Diplopia is sometimes reported as well and it is believed to be secondary to toxicity of the sixth cranial nerve.

Other symptoms reported are brain fog, lethargy, irritability, neck stiffness, tinnitus, dizziness, clumsiness, chronic fatigue, and paresthesia.

It should be noted that in anecdotal cases of FQ-induced intracranial hypertension, there have been more reports of optic disk nerve swelling (papilledema) as opposed to intracranial hypotension. It appears in FQ-induced hypertension cases visual acuity is usually preserved, helping to distinguish acute papilledema from optic neuritis, something else that can also be caused by FQ’s direct toxicity.

In FQ-induced intracranial hypotension, more noticeable auditory disturbances have been reported as opposed to FQ-induced hypertension.

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Craniocervical instability

Although not the direct subject of this article, it is necessary to mention craniocervical instability (CCI) due to the overlap and dovetailing of symptomatology between the CCI/CSF issues and the FQs.

CCI is a pathological condition of increased mobility at the craniocervical junction, the area where the skull meets the spine. In CCI the ligamentous connections of the craniocervical junction can be stretched, weakened, or ruptured impacting the brain and brainstem.

CCI is very complex and can cause a variety of serious symptoms including debilitating fatigue and weakness and is outside the diagnostic scope of most medical professionals. CCI has been implicated in certain forms of Chronic fatigue (ME). CSF pressure issues can also mimic some of these same symptoms and/or be directly related and connected to CCI. In other words, there is a large overlap in symptomatology in which pressure issues could be the result of CCI, or there could be an underlying/undiagnosed CCI condition in cases of brain pressure abnormalities.

In some cases of FQAD, symptoms of CCI are believed to be triggered by FQs causing connective tissue weakening. It has been shown in research and overwhelming anecdotal evidence that FQs upregulate matrix metalloproteinases (MMPs) and degrade collagen. This leads to increased collagen degradation and weakening of the tendons and connective tissue and could easily cause CCI (7). FQAD, CCI, and ME have overlapping symptomology and in some cases, all are present in certain cases.

In the near future, I will address CCI as it pertains to FQs.

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Choroid Plexus

Side view of head and brain showing cerebrospinal fluid.

The choroid plexus (CP) is a network of blood vessels and cells in the ventricles (fluid-filled spaces) of the brain. The blood vessels are covered by a thin layer of cells that make CSF.

Over the last decade, some conversations with FQAD-impacted individuals have led me to suspect a metabolic imbalance caused by the FQs impacting the CP. It is clearly known in academic research and in overwhelming community data that FQs negatively impact mitochondria. It is also known that without sufficient mitochondrial energy production, the active ion transporters in CP cannot operate normally and produce CSF properly (8). Researchers with Alzheimer’s disease have found that improper functioning CP cells are deficient in the mitochondrial enzyme cytochrome c oxidase and complex IV of the electron transport chain (9).

There are specific genes involved in the active transport of ions (along with the obligatory transport of H2O) from blood to the ventricular lumen of the CP. These are the final pathway of CSF production and are considered rate-limiting genes. In other words, these genes control how much or not enough CSF fluid is produced. The main genes that code for Na–K-ATPase and the Na–K–Cl cotransporter would be of interest final secretory pathway.

The work of the Na/K pump is the most fundamental process of life because it consumes 20% to 50% of the ATP produced. This regulation depends on the ability of the mitochondria to produce ATP which drives the Na/K pump. In the case of sustained oxidative stress initiated by the FQs, the NA/K pumps cannot function because ATP production is lowered. The normally operating cells switch states to a permanent stress adaptation and in turn, impact the final path of CSF production.

As I have pointed out time and time again, the FQs have the ability to reach every area of the body and the CP is no exception. Since a larger majority of PTC cases resolve on their own, it would stand to reason that these PTC cases are occurring during a spike in oxidative stress (ROS). However, the FQs can raise ROS for extended periods of time, in some cases for many years, or indefinitely. These long-term changes impact the methylation of DNA resulting in epigenetic changes. In some individuals, these changes could impact the CP.

The FQ’s ability to alter changes in CSF through impact on the CP is just one way, out of many, in which the FQs can brain physiology.

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Conclusion

If you believe you are suffering from one of these conditions options are currently limited. This is another one of those areas where there are very few experts and the patient usually becomes more well-versed in the medical condition than the doctor. There are patient groups where the members are making headway by seeing certain select doctors who specialize in these rare areas of healthcare.

Facebook Groups:

Tarlov Cysts – https://www.facebook.com/groups/971580869576257

ME/CFS+ Brain and Spine – https://www.facebook.com/groups/1353765701467793

Spinal Leak Support – https://www.facebook.com/SpinalCSFLeakSupport

Spinal Leak Foundation – https://www.facebook.com/Spinal.CSf.Leak.Foundation

Pseudotumor cerebri IIH – https://www.facebook.com/groups/247197510096871

Although I have had contact with several individuals with intracranial hypotension post FQs, there is no support group for this malady. Certain health centers like Mayo Clinic Rochester and Duke have specialists who deal with these issues, however, they will always approach the situation as if there is a CSF leak present. Intracranial hypotension caused by an mitochondrial or metabolic dysfunction is considered very, very rare, with Mayo Rochester having seen one case. That doesn’t mean they don’t exist however as logic would dictate if medical science sees cases of metabolic intracranial hypertension, then conversely cases of metabolic intracranial hypotension should exist as well, and they do.

Brain pressure abnormalities, both hyper and hypo, can sometimes be imaged with MRI and CT. Also, I will concede that a good local neurologist can probably aid with intracranial hypertension and PTC, but most cannot comprehend and/or deal with hypotension or CCI.

Let me throw in the caveat that most doctors/neurologists/surgeons only associate intracranial hypotension with trauma to the dura. Their training and experience don’t allow a differential diagnosis to include causes other than a noticeable leak in the dura such as Tarlov cysts, venous fistulae, metabolic imbalances, and especially epigenetic changes wrought by the FQs. Be careful, this is an area where an uninformed doctor can cause more harm than good, so proceed with absolute caution

PTC and the associated dovetailing conditions can be chronic or acute. Some cases can indeed be severe medical emergencies and require evaluation to rule out other causes such as tumors, acute trauma, etc. When in doubt consult with a trusted medical practitioner or advisor.

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Personal Message From David

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References

1. Boréus LO, Sundström B. Intracranial hypertension in a child during treatment with nalidixic acid. Br Med J. 1967 Jun 17;2(5554):744-5. doi: 10.1136/bmj.2.5554.744. PMID: 6025983; PMCID: PMC1841777.

2. Riyaz A, Aboobacker CM, Sreelatha PR. Nalidixic acid induced pseudotumour cerebri in children. J Indian Med Assoc. 1998 Oct;96(10):308, 314. PMID: 10063299.

3. Fernando RR, Mehta NN, Fairweather MG. Pseudotumor cerebri and ciprofloxacin: a case report. J Med Case Rep. 2011 Mar 16;5:104. doi: 10.1186/1752-1947-5-104. PMID: 21410941; PMCID: PMC3069949. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3069949/

4. https://www.mayoclinic.org/diseases-conditions/pseudotumor-cerebri/symptoms-causes/syc-20354031

5. Sodhi M, Sheldon CA, Carleton B, Etminan M. Oral fluoroquinolones and risk of secondary pseudotumor cerebri syndrome: Nested case-control study. Neurology. 2017 Aug 22;89(8):792-795. doi: 10.1212/WNL.0000000000004247. Epub 2017 Jul 28. PMID: 28754842.

6. Ali WH. Ciprofloxacin-associated posterior reversible encephalopathy. BMJ Case Rep. 2013 Apr 11;2013:bcr2013008636. doi: 10.1136/bcr-2013-008636. PMID: 23585504; PMCID: PMC3645815. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3645815/

7. Tsai WC, Hsu CC, Chen CP, Chang HN, Wong AM, Lin MS, Pang JH. Ciprofloxacin up-regulates tendon cells to express matrix metalloproteinase-2 with degradation of type I collagen. J Orthop Res. 2011 Jan;29(1):67-73. doi: 10.1002/jor.21196. PMID: 20602464. https://pubmed.ncbi.nlm.nih.gov/20602464/

8. Kant, S., Stopa, E.G., Johanson, C.E. et al. Choroid plexus genes for CSF production and brain homeostasis are altered in Alzheimer’s disease. Fluids Barriers CNS 15, 34 (2018). https://doi.org/10.1186/s12987-018-0120-7

9. Cottrell D, Blakely E, Johnson M, Ince P, Turnbull D. Mitochondrial enzyme-deficient hippocampal neurons and choroidal cells in AD. Neurology. 2001;157:260–4. https://doi.org/10.1212/wnl.57.2.260.

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#Cerebrospinal Fluid #CFS/ME #FQAD

New Post has been published on My Quin Story

New Post has been published on https://www.myquinstory.info/mitochondrial-retrograde-signaling-in-fqad-a-disease-theory/

Mitochondrial Retrograde Signaling in FQAD, A Disease Theory

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Download links are available at the bottom of this article.

Abstract

Despite warnings from regulatory agencies urging conservative usage due to the potential for major adverse events, Fluoroquinolones remains one of the most commonly prescribed antibiotics worldwide. A large number of people who take this class of antibiotics become chronically or permanently disabled suffering from what the Federal Drug Administration has observationally identified as Fluoroquinolone Associated Disability or FQAD. FQAD is an idiopathic pathological presentation of numerous, disparate, symptoms that can literally number into several hundred. FQAD, in affected individuals, can cause an intractable long-term, progressive, multi-system condition that can be severely disabling or fatal. This multisystem involvement of symptoms is usually suspected as being genetic in origin. Despite this, most clinical genetic testing fails to identify any pathological phenotypes that would explain a progressive disease. Due to the lack of further research, the exact mechanism of FQAD remains unknown, even though many disparate pieces of academic research exist documenting the genotoxicity of fluoroquinolones. Based on over ten years of anecdotal evidence by citizen scientists, and the results of some recent research findings, this paper proposes a theory that, if proven true, would elucidate the mechanism behind FQAD in an otherwise healthy population in the absence of genetic predispositions.

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Introduction

Fluoroquinolones (FQs) are a broad class of antibiotics that are one of the most commonly prescribed antibiotics within the United States. The FQs are typically prescribed for bacterial infections, however, they are very often prescribed off-label or for prophylaxis. Because this class of antibiotics brings the potential for major side effects, the FDA urges doctors not to over-use them. In fact, the agency has restricted the recommended uses for these drugs and has required several updates to the drugs’ labels to warn of life-altering risks.

The FDA has proposed the existence of a permanent disability that can come from FQ usage (Fluoroquinolone Associated Disability; FQAD). The FDA identified FQAD in a Briefing document for a joint meeting of the Antimicrobial Drugs Advisory Committee and the Drug Safety and Risk Management Advisory Committee during a formal review of the FQs on Nov. 5, 2015. FQAD is defined as a constellation of adverse event symptoms that have been identified as leading to disability. The FDA made it known that FQAD was not a formal diagnosis just an observational identification, one that is yet to be formally recognized by the medical community [1].

Despite increased awareness, the medical community still tends to dismiss patients who report symptoms of FQ toxicity. This is especially true of patients who reported being affected by FQAD. One of the main reasons for this dismissal is the great variability and severity with which the FQAD symptoms present themselves. Many of these patients are often unfairly diagnosed with umbrella diseases such as fibromyalgia, chronic fatigue, and others [2], despite the fact that symptoms often surpass those classifications and there exists both clinical and laboratory evidence that links the FQ with cellular toxicity in and of itself [3].

This article introduces a hypothesis that, if proven true, would explain the wide variety of symptoms that manifest in the condition referred to as Fluoroquinolone Toxicity or FQAD.

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Overview

The most common demographic to receive a prescription for FQs usually consists of individuals who are 45 years of age or older [4]. Although some strong exceptions exist, anecdotal evidence collected over the last decade has shown that more middle-aged and older people become permanently disabled by FQAD. It is suspected that the underlying reason for this has to do with the bioenergetic phenotype of the mitochondria of older individuals versus the young [5].

In FQAD, it is common to see a constellation of symptoms that include fatigue, weakness, muscle atrophy, neurological problems, digestive problems, cranial cervical pathologies, cardiac conduction abnormalities, and many more. These symptoms often present themselves in a puzzling array confounding many medical practitioners. Often, standard genetic sequencing does not provide any insight that would reveal a predisposed pathogenic condition or genetic variant(s) that would explain the onset and duration of FQAD. Despite this lack of a known genetic predisposition, patients manifest obvious signs of a pathophysiology that has a genetic component.

Based on the large amount of anecdotal data collected over several years, combined with recent clinical diagnostics from a few cases of FQAD, suggests a novel hypothesis.

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Mitochondrial Retrograde Signaling In FQAD

This paper puts forth a postulation that the FQs are making changes to nuclear genomic loci without altering the underlying nucleic acid sequence while still impacting gene expression and functional regulation. These pathological changes are driven by a phenomenon known as mitochondrial retrograde signaling.

In mitochondrial retrograde signaling, information flows in the opposite direction to that of the more familiar and understood anterograde regulation which is characterized by the transfer of information and material from the nucleus to mitochondria. This retrograde signaling can culminate in wide-ranging changes in nuclear gene expression.

Mitochondria play a significant role not only in energy production but also in the integration of metabolic pathways in addition to signals for apoptosis and autophagy. These semi-autonomous organelles have their own genomes, which in humans typically appear as small double-stranded closed DNA circles.

Only recently has it become apparent that mitochondria in mammalian cells play critical roles in the initiation and propagation of various novel signaling cascades [6]. Scientific research has shown that reverse or retrograde communication does exist between the nuclear and mitochondrial genomes [7,8]. This unique signaling pathway appears to influence many cellular and organismal activities under both normal and pathophysiological conditions [9].

It is now known that mitochondrial metabolic, respiratory, and genetic instability are all communicated to the nucleus as an adaptive response through retrograde signaling [6]. When mitochondria become dysfunctional, they communicate through retrograde signaling to the nucleus in an adaptive response that results in altered nuclear gene expression and cell physiology and morphology.

Again, collected anecdotal data, along with some limited clinical data, are revealing that this unique communication pathway could be the main driving factor in the complex syndrome that is known as Fluoroquinolone toxicity Syndrome (FQTS) or the more chronic sense, FQAD.

Although many theories have been put forth as to the causal mechanisms of certain aspects of FQAD, such as long-term upregulated metalloproteinase, GABA receptor inhibition, and increase ROS, it is believed these are the result of the downstream nuclear signaling cascades driven by mitochondrial retrograde signaling.

While many specific mechanisms are yet to be fully elucidated, the mitochondrial retrograde signaling cascade’s influence would explain the disordered and varied nature of FQTS and the complexity of the resulting syndrome that many medical practitioners find preposterous.

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General Discussion

Truly little was known about mitochondria themselves when the Fluoroquinolones were approved for use years ago. The fact that mitochondrial instability could directly influence disease states through retrograde signaling was also largely unknown to medical science until recently.

Evidence is emerging that points to the fact that the FQs are changing mitochondrial DNA (mtDNA) topology which in turn impacts nuclear DNA (nDNA) expression and ultimately DNA methylation.

Mitochondrial retrograde responses are initiated and sustained by metabolic pressures such as toxic exposure. The FQs have been documented to impact the normal maintenance and transcription of mitochondrial DNA (mitostasis) by changing mtDNA topology, causing impaired mitochondrial energy production and blocking cellular growth and differentiation [10].

Through this feedback loop, the mitochondria are directing the changes in nuclear gene function. This communication is happening as a direct result of the mitochondrion’s role in generating and regulating high-energy molecules, such as ATP, acetyl-CoA, AKG, etc.

One documented way that the FQs are changing mtDNA topology is through the inhibition of isoforms of Topoisomerase 2, Top2α, and β [12]. Top2β in when exposed to an FQ has an immediate effect on mtDNA biogenesis, indicating that this isoform is involved in mtDNA maintenance [12]. Through this method, the FQs have a dramatic effect on mtDNA topology, blocking replication, reducing copy number, and inhibiting mitochondrial transcription.

Evidence of the retrograde signaling shows up when eukaryotic cells are exposed to FQs and they exhibit signs of immediate retardation of cell division that is only present in cells with functional mitochondria, implying a retrograde signal from mitochondria to nucleus either caused by oxidative stress or impaired mtDNA replication [12].

Impaired mitostasis has been suggested to induce cellular senescence [11]. Deregulation of mitochondrial homeostatic mechanisms which manifests as impaired mitochondrial biogenesis, cellular metabolism, and dynamics, has become a hallmark of cellular senescence, which is believed to be another factor in FQAD.

Dysfunctional mitochondria in a senescent cell using retrograde signaling communicate their changing metabolic and functional state to the nucleus as an adaptive response. This retrograde communication becomes a crucial factor in regulating homeostasis and translating extracellular signals into altered gene expression, altered cell physiology, and morphology. This culminates in wide-ranging changes in nuclear gene expression which in turn manifests in the wide variety of symptoms seen in the FQAD syndrome. Often, these changes are very long-lasting and/or permanent.

Changes to mtDNA have been shown to repress specific nuclear gene loci [13]. And although it appears that mitochondrial retrograde signaling can impact nDNA loci genome-wide, in some cases of FQAD, changes are occurring, at least, in part at the genomic loci of the nDNA responsible for mitochondrial mtDNA maintenance. There have been some case reports where FQAD patients have been clinically diagnosed with a mitochondrial disease after undergoing a muscle biopsy and the detected disease state would normally point to or stem from a pathological mutation in the nDNA, however, repeated genetic sequencing has failed to reveal any clinically recognized polymorphisms.

Since mtDNA lacks robust repair mechanisms, insults to the mitochondria from the FQs such as mtDNA lesions, membrane damage, insufficient O2, Top2α and β inhibition, and more can influence retrograde communication to the nDNA, which in turn alters functional regulation (anterograde) in cascading or sometimes vicious cycle.

The specific mechanisms that drive long-term or permanent changes that impact methylation in the absence of clinical genetic polymorphisms need to be fully elucidated. However, it is known that mtDNA damage is more extensive and persistent than nDNA and often these damages escape rescue mechanisms such as autophagy. During periods of chronic oxidative stress, such as those induced by Fluoroquinolone exposure, mitochondria can become extensively damaged [14]. Abnormal mitochondrial dynamics, impaired biogenesis, and defective mitophagy could be the sustaining forces that are driving the anterograde signaling altering nDNA methylation, and producing the syndrome we see in those who are severely disabled by fluoroquinolones.

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Conclusion

In a normal state, crosstalk between the mitochondrial and nuclear genomes is vital for the proper maintenance, integrity, and function of both genomes which contributes to the symbiotic relationship between them and the homeostasis of a person’s health state.

The heterogenic nature of the symptoms in those who are impacted by FQAD points to an underlying mtDNA-driven dysfunction/disease. Evidence is emerging that FQ-induced changes to the mtDNA can lead to the epigenetic modification of the nuclear genome and/or alterations to DNA methylation through retrograde signaling, thus contributing to the diverse pathophysiology observed in FQAD.

Even today, medical science is limited in its understanding of how mitochondria interact with nDNA, influence methylation, and drive disease. This is evident in the poor patient outcomes in those who have been chronically affected by FQAD.

It is hoped that the hypothesis presented in this paper will provide a foundation for future research into the role of FQs and their ability to triggering chronic illnesses by affecting the communication between the mitochondrial genome and the nuclear genome in a novel fashion, leading to severe acquired human disease.

This paper is available for download in PDF Form at:

https://figshare.com/s/ac5222ef70cf0e6fea65

https://www.myquinstory.info/wp-content/uploads/2023/04/Mito-Retrograde-Theory-in-FQAD-2023-1.pdf

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Personal Message From David

Do you shop for supplements online? If you do, you could help other floxed folks when you shop and not pay a cent more.

Click Here For More Info

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References

1. Melvin, D. (2015, November 5). FDA Briefing Information Nov. 5, 2015. Life After Levaquin. Retrieved April 12, 2023, from https://www.myquinstory.info/wp-content/uploads/2018/06/FDA-Briefing-Information-Nov-5-2015-Meeting-of-the-Antimicrobial-Drugs-Advisory-Committee-and-the-Drug-Safety-and-Risk-Management-Advisory-Committee-FQAD.pdf

2. Ganjizadeh-Zavareh S, Sodhi M, Spangehl T, Carleton B, Etminan M. Oral fluoroquinolones and risk of fibromyalgia. Br J Clin Pharmacol. 2019 Jan;85(1):236-239. doi: 10.1111/bcp.13765. Epub 2018 Oct 14. PMID: 30216492; PMCID: PMC6303210.

3. Anu Hangas, Koit Aasumets, Nina J Kekäläinen, Mika Paloheinä, Jaakko L Pohjoismäki, Joachim M Gerhold, Steffi Goffart, Ciprofloxacin impairs mitochondrial DNA replication initiation through inhibition of Topoisomerase 2, Nucleic Acids Research, Volume 46, Issue 18, 12 October 2018, Pages 9625–9636, https://doi.org/10.1093/nar/gky793

4. Baggs J, Fridkin SK, Pollack LA, Srinivasan A, Jernigan JA. Estimating National Trends in Inpatient Antibiotic Use Among US Hospitals From 2006 to 2012. JAMA Intern Med. 2016 Nov 1;176(11):1639-1648. doi: 10.1001/jamainternmed.2016.5651. PMID: 27653796.

5. Will Y, Shields JE, Wallace KB. Drug-Induced Mitochondrial Toxicity in the Geriatric Population: Challenges and Future Directions. Biology (Basel). 2019 May 11;8(2):32. doi: 10.3390/biology8020032. PMID: 31083551; PMCID: PMC6628177.

6. Guha M, Avadhani NG. Mitochondrial retrograde signaling at the crossroads of tumor bioenergetics, genetics and epigenetics. Mitochondrion. 2013 Nov;13(6):577-91. doi: 10.1016/j.mito.2013.08.007. Epub 2013 Sep 1. PMID: 24004957; PMCID: PMC3832239.

7. Butow, R. A., & Avadhani, N. G. (2004). Mitochondrial signaling. Molecular Cell, 14(1), 1–15. https://doi.org/10.1016/s1097-2765(04)00179-0

8. Mitochondria‐to‐nucleus stress signaling induces phenotypic changes … The EMBO Journal. (2001, April 17). Retrieved April 12, 2023, from https://www.embopress.org/doi/full/10.1093/emboj/20.8.1910

9. Butow RA, Avadhani NG. Mitochondrial signaling: the retrograde response. Mol Cell. 2004 Apr 9;14(1):1-15. doi: 10.1016/s1097-2765(04)00179-0. PMID: 15068799.

10. University of Eastern Finland. (2018, October 1). Ciprofloxacin has dramatic effects on the mitochondrial genome: Antibiotics should be used cautiously. ScienceDaily. Retrieved April 12, 2023 from www.sciencedaily.com/releases/2018/10/181001101943.htm

11. Vasileiou PVS, Evangelou K, Vlasis K, Fildisis G, Panayiotidis MI, Chronopoulos E, Passias PG, Kouloukoussa M, Gorgoulis VG, Havaki S. Mitochondrial Homeostasis and Cellular Senescence. Cells. 2019 Jul 6;8(7):686. doi: 10.3390/cells8070686. PMID: 31284597; PMCID: PMC6678662.

12. Anu Hangas, Koit Aasumets, Nina J Kekäläinen, Mika Paloheinä, Jaakko L Pohjoismäki, Joachim M Gerhold, Steffi Goffart, Ciprofloxacin impairs mitochondrial DNA replication initiation through inhibition of Topoisomerase 2, Nucleic Acids Research, Volume 46, Issue 18, 12 October 2018, Pages 9625–9636, https://doi.org/10.1093/nar/gky793

13. Haffner MC, Aryee MJ, Toubaji A, Esopi DM, Albadine R, Gurel B, Isaacs WB, Bova GS, Liu W, Xu J, Meeker AK, Netto G, De Marzo AM, Nelson WG, Yegnasubramanian S. Androgen-induced TOP2B-mediated double-strand breaks and prostate cancer gene rearrangements. Nat Genet. 2010 Aug;42(8):668-75. doi: 10.1038/ng.613. Epub 2010 Jul 4. PMID: 20601956; PMCID: PMC3157086.14 https://pubmed.ncbi.nlm.nih.gov/22474351/

14. Yakes, F. M., & Van Houten, B. (1997, January). Mitochondrial DNA damage is more extensive and persists longer … – PNAS. PNAS. Retrieved April 12, 2023, from https://www.pnas.org/doi/10.1073/pnas.94.2.514

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New Post has been published on My Quin Story

New Post has been published on https://www.myquinstory.info/incredible-fluoroquinolone-diagnosis-from-a-mayo-researcher/

Incredible Fluoroquinolone Diagnosis from a Mayo Researcher

Introduction

Drug-induced mitochondrial toxicity has been described over the last several years for many different drug classes and the Fluoroquinolones are at the top of the list. Unfortunately, most patients are unaware of the risks and most doctors are woefully ignorant about the long-term damage these drugs can inflict.

An overwhelming amount of anecdotal data in addition to several research articles point to an assault on the mitochondria as the underlying problem. The fluoroquinolones assault both the nuclear DNA (nDNA) and mitochondrial DNA (mtDNA) resulting in heavy epigenetic pressure and poorly understood mechanism that cause acquired pathogenic processes. I wrote a previous article titled, “Pulling The Trigger: How the Fluoroquinolones Can Cause Mutations and Disease” which explained one mechanism how Fluoroquinolones can cause mitochondrial disease without having genetic predispositions.

This assault impacts the machinery that governs all facets of DNA maintenance and biogenesis. I have, in the past, alluded as to how the Fluoroquinolones are an epigenetic monster in the way they put pressure on areas of the genome that have yet to be understood by medical science and can subsequently ‘pull the trigger’ on disease processes, which makes them very dangerous indeed.

This article discussess how a Mayo researcher discovered a Fluoroquinolone induced mitochondrial pathology in myself and one other person.

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Who Gets Severely Damaged?

I am a firm believer that no one gets out unscathed. Even in those individuals who appear to ‘handle’ a single course of Fluoroquinolones or multiple courses, there is always a certain amount of damage that takes place, and it is be cumulative. There are, however, classes of people who manifest chronic long-lasting damage more often than others, and although there are solid exceptions to any rules, my collected data over the last decade, has highlighted that a larger cohort of people who become very chronically impacted by the Fluoroquinolones tend to be middle-aged or older.

We can ‘split hairs’ on what age group defines middle aged, but for me, I was 47 when Levaquin permanently altered the course of my life, and I have seen this bandwidth run from middle to late 30’s up to late 50’s. One other person, who is referenced in this article, was in their 50’s when they became chronically impacted.

Before you point your finger at me and tell me that there are younger people that are permanently damaged, I will fully concede that fact. The point I am making is that, according to my data, there are more middle-aged and older people who become chronically disabled as opposed to younger.

I believe the reason for this has to do with the bioenergetic phenotype of the mitochondria of older individuals versus the young. This reason probably accounts for the quicker healing we tend to see in many, but not all, of the younger people who suffer from Fluoroquinolone Toxicity. The young’s ability to heal is not the product of some miraculous ‘cure’ they discovered, but has to do more with the phenotype of the mitochondria.

Environmental factors, along with the age of the individual, contribute to the decline in the ability of molecular regulation to repair mitochondrial damage. This, in my opinion, is the primary factor that impedes the ability of aging mitochondria to withstand or adapt to being hit by the Fluoroquinolone’s toxic onslaught. Basically, this is common sense, because it is probably this loss of homeostatic regulation that underlies the sometimes-greater susceptibility of older patients to have drug-induced adverse events in general.

Nevertheless, all age groups need to pay attention to the dangers that Fluoroquinolones pose, as the pathogenic process I am highlighting here poses a risk to all age groups.

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Deep Dives

Over the last fourteen years I have taken many ‘deep dives’ into various realms of my metabolism; my gut, brain, nervous system, connective tissues, genetics, and everything in between. I attended seminars, patronized various doctors (even some of the ‘so-called’ Fluoroquinolone experts), worked with some academic level researchers, and interviewed former pharmaceutical scientists. There have been many blind alleys and doors slammed shut but along the way I collected data and absorbed everything I could about the Fluoroquinolones. You’ve heard the old adage, “know your enemy as you know yourself.”

Pardon me when I tell you that despite all this time spent on researching I want to let you in on a little secret, “I hated it.” I hated having my life diverted from the way it was by a pharmaceutical that was deemed safe. I had plans that were shelved, dreams that were shattered, and limitations placed on my life in ways that I never would have dreamt. However, pragmatically speaking, Fluoroquinolone toxicity, or at least the downstream impacts from their assault on my body, wasn’t going away. So, despite many attempts to put it behind me, it stayed with me like a monkey on my back.

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Still Not Well Understood

During my long quest for answers, I kept drawing one conclusion, no one, and I mean no one, fully understands the mechanisms of these drugs and their ability to cause harm; this would even include the scientists that developed the drugs themselves. I found that a lot researchers are fully honest about their limitations on knowledge, while some clinicians, not so much, probably being driven more by profit.

The reason I briefly mention this is because I am contacted almost daily from someone seeking help trying to find a practitioner to treat them. Despite certain clinicians/practitioners claim that they can ‘treat’ Fluoroquinolone toxicity, the overall track record, according to my tally from data shared by others, is actually quite abysmal. Most of these practitioners tend to follow outdated ‘paradigms’ that were never meant to work with synthetic DNA altering pharmaceuticals, or they throw various treatments at the patient hoping one of them will stick, or, worse yet, they target what I call “low hanging fruit,” which are people whose issues are not so complex and are easier to treat and they have the means to pay the exorbitant treatment costs and fees.

The truth is, there are some cases of Fluoroquinolone toxicity that are easier to help than others. To the person experiencing these symptoms, their problems may seem quite terrible, but generally, in the scheme of things, they have fairly simple problems that many arm-chair practitioners can successfully help with, plus they were more than likely going to heal on their own either way.

The true hard-core cases of FQAD generally defy treatments and their resolution remains elusive because the mechanisms involved are elusive; these are the hard-core cases. Unfortunately, there are a lot of people impacted in this fashion and they are the ones that pique my interest, mainly because I am one of them.

In my case, traditional and alternative medical practitioners offered me little relief, but then again, I didn’t expect much. The type of damage that we are talking about in this article is usually far above the heads of most medical practitioners both standard and alternative, and for the most part is in the realm of the research scientists.

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Making Headway Isn’t Easy

Despite my forward journey through Fluoroquinolone toxicity being about as difficult as walking through waist deep snow, tantalizing clues and answers would occasionally reveal themselves along the way. Even though I would appear ‘normal’ on most standard lab tests, clues would occasionally show up in the ‘rare’ and/or ‘quirky’ health related areas that would point to the next level of investigation. Like the movie National Treasure, one clue would lead to another, each getting deeper and deeper. Despite distractions, the occasional trip down the rabbit hole, blind alleys, and taking some wrong turns, most of the clues agonizingly kept pointing to one area, the mitochondria.

I know some readers are probably going “duh, we know the mitochondria are involved, tell us something we don’t know.” While it is true that for years research as shown mitochondrial damage as a mechanism of Fluoroquinolone toxicity, I was still driven by the “why?” This question must be answered for successful treatments to be discovered. Despite this, when pressed, people in-the-know could never elucidate a satisfactory mechanism or theory. Bottom line, it wasn’t good enough to just point fingers at the mitochondria, I had to know “why” the Fluoroquinolones were causing permanent long-lasting problems in many people.

It wasn’t until I got connected with an altruistic Mayo researcher that some critical pieces of the Fluoroquinolone puzzle were revealed…at least in a few cases.

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The Researcher at Mayo Clinic

Through some friends, I was put in contact with a very curious, and like I said, altruistic PhD researcher at Mayo clinic in 2019, prior to the COVID-19 pandemic. I will call her “Dr. L.” Dr. L’s sole function at Mayo is to research difficult cases from a genetics standpoint. She does not clinically see patients but instead performs exploratory research and occasionally acts at the behest of other doctors working like a private detective looking for answers in puzzling cases.

After a brief email exchange, she became interested in my case and in early 2020 she obtained permission to retrieve the remaining residual muscle biopsy sample that was previously frozen locally at a tertiary care center. Talking tech in my interchanges with her, I was amazed at the diagnostic technology Mayo had at their disposal. This piqued my interest.

On a side note, many people have relayed their bad experiences with Mayo clinic regarding their quest to seek help for Fluoroquinolone toxicity, and I can relate. The clinical side is completely separate from the research side. I have found the clinical side very good with certain, very specific, medical problems but still the clinical side suffers from the same disconnect as other health systems. Although I have had some very good doctors at Mayo, especially dealing with intracranial hypotension, there were exceptions. I have encountered two doctors that were less than stellar. There was a clinical mitochondrial doctor that was totally incompetent, dismissive, and not worthy of the Mayo mantle, and this is saying something because in my travels I have seen some pretty incompetent doctors, but I digress.

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The Diagnosis from Mayo

Fast forward to March 2021. After a major delay caused by the COVID pandemic, I received an excited email from the Mayo researcher informing me that they completed mitochondrial studies on my muscle biopsy, and there were abnormal findings.

In an in-depth mitochondrial analysis, they had captured abnormalities that other experts had missed. Mayo uncovered an mtDNA depletion syndrome, much like a patient with an actual hereditary mtDNA depletion syndrome but fully acquired.

Understanding mitochondrial disease fairly good, I was very puzzled. I knew that I did not harbor any pathogenic variants in either the nuclear or mitochondrial genome as those would have been discovered by now. Despite this and thanks to Mayo’s diagnosis, I was able to obtain yet ‘another’ specific clinical sequencing performed by Prevention Genetics that just focused on looking for known pathogenic variants, or combinations, of variants that could cause mitochondrial depletion syndrome. Nothing was found.

In my genetic testing repertoire, I have genotyping (23andme), whole exome clinical sequencing performed twice (GeneDX), rare gene screening (Sequencing.com), entire genome (nDNA and mtDNA) sequencing (Dante Genomics), and an two genetic panels specifically looking for pathogenic mitochondrial genes (GeneDX). If there was a known pathogenic variant, statistically it should have been discovered. I even had a comparison exome sequencing done on my two siblings to look for any comparative clues (GeneDX).

On a side note, there are several genes involved in Mitochondrial Maintenance and Replication. Medical science knows of only ten genes that can present as depletion syndrome with the symptoms I possess. Of those ten only two can occur in adults and there are probably less than 100 cases in the entire world with even much less than that in the United States. The other eight genes are always fatal in infancy. Additionally, my life experience would rule out this rare form of depletion based on the fact that prior to being floxed I was higher functioning both physically and mentally. No, I am not self-aggrandizing here, just point out that depletion syndrome usually results in certain physical and cognitive deficits or ‘clues’ that would be present throughout life.

So, if I did not have the pathogenic genes, what else could have caused the depletion syndrome?

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Enter The Fluoroquinolones

In her email, Dr. L. went on to say, “We also had one other patient from whom we were able to get a residual muscle biopsy from the time they were acutely symptomatic from their fluoroquinolone exposure and, lo and behold, their mtDNA was abnormal, too.”

Additionally Dr. L. said, “And, like you, that patient (also seen at Mayo) had whole exome sequencing done which essentially rules out a genetic cause for this finding. “

Dr. L was convinced that I and the other floxed person did not harbor any hereditary predispositions to mtDNA depletion syndromes. Because of this, Mayo’s sent me the information on my results to share with my local doctors that my case of mtDNA depletion syndrome was a considered fully acquired.

Looking at my entire medical history, including drug exposure history, and genetic testing, Dr. L. was confident that the Fluoroquinolones were the culprit so much so that they intend to publish the results.

There are some pretty interesting theories as to how the Fluoroquinolones could interact with mitochondrial thymidine kinase or other ‘maintenance genes’ to initiate a self-sustaining depletion syndrome.

One case doesn’t necessarily signal an epidemic, however a second case lends confidence that there were probably others, maybe many others, who suffer from the chronic forms of Fluoroquinolone Toxicity. Again, Dr. L was going to publish a case study on these two cases to get the documentation in writing.

None of this should really be that surprising since drug-induced mitochondrial toxicity has been recognized to cause permanent damage to the skeletal muscle, liver, kidney, heart and the central nervous system. There have been several drugs identified that can cause mitochondrial toxicity to varying degrees and in my opinion certain anti-cancer drugs and Fluoroquinolones are at the top of the list (source).

It is important to note that most studies about drug induced mitochondrial toxicity have been conducted using isolated mitochondria and cell systems and often these systems are not of human nature. However, over the last fourteen years, I have amassed enough anecdotal data to convict the fluoroquinolones of being lethal to the mitochondria, even though most drug safety researchers refuse to look at them seriously. These drugs have truly fallen through the cracks of the pharmacovigilance system.

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Dismissing ‘Rare’ Cases

Most doctors dismiss drug toxicities by referring to the fact that safety margin for a particular drug will depend on a whole host of environmental variables as well as other contributing mechanistic toxicities. If they do acknowledge that the Fluoroquinolones caused something they usually refer to it as ‘rare’ and dismiss it.

In my case I was decidedly different. Prior to floxing I was very athletic and healthy. I had very few, if any, external environmental factors that could confound the fact that the Fluoroquinolones were to blame.

Despite the dismissive and gas lighting atmosphere that surrounds most adverse events to Fluoroquinolones in our healthcare system, I always knew that Levaquin was the “terminus ad quo,” or the instigator. It was the finger that pulled the trigger on disease processes in my body by damaging my mitochondria.

However, mitochondrial disease that is fully drug induced or acquired, one that does not involve a known pathogenic variant(s), is not well understood. Clinicians who normally deal with the standard mitochondrial diseases, like most of the rest of doctors, put people in ‘neat little boxes.’ You either have the mutation or you don’t. If you don’t have the mutation, you can’t possibly have the disease. Bottom line, they will dismiss or ignore you.

However, I believe I am living proof that the Fluoroquinolones initiated a mitochondrial disease process through mechanisms that are not well understood by medical science.

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So, What’s Next?

First, let me dispel any misunderstandings for those thinking that I can just initiate research on a dime or put you in contact with a researcher that can assist you, it is not that easy although I wish it was. Also, not to sound like a martyr, but I have had to fight every step of the way to get to this point in my journey and most of the personal discoveries were chiseled out on my own. Don’t get me wrong, I have been helped by some very incredibly talented people, many whom are much smarter than I, but nonetheless I am not rich, nor do I have a medical degree.

Having higher education has helped me understand the whole research and scientific publication game, which was very helpful given the biased nature of most of the academic research today, but it still took me a very long time just to get to this point in my understanding; too long, much longer than it should.

On a side note, I do have a very good primary care physician who has helped along the way, but I have had to educate him in certain aspects and like I mentioned earlier, this journey it is like walking in waste deep snow and doing it while you’re sick, tired, and broken; even working with Mayo clinic with this most recent diagnosis was no exception.

I will concede that COVID-19 hit Mayo Clinic hard. The research genetics lab that was working on my case lost over 50% of their staff, funding, and basic supplies that were all rechanneled to focus on COVID-19. This has hampered my forward progression, yet once again. I am pretty sure that Mayo has now directed the Dr. L to focus on more pressing issues that pursuing my case any further has fallen to the backburner. I will continue to pester them from time to time. Despite this, I am grateful for their discovery.

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There Could Be Many More

Since Mayo found this unique depletion in myself and another person suffering from FQAD, I can’t help thinking that it is occurring in other cases of FQAD. No, I am not a person who sees Fluoroquinolones hiding under every rock, but they do represent an underrecognized health crisis and over the years I have encountered a lot of people with long-term chronic cases, so I do strongly believe that there is probably a good-sized subset of individuals in the Fluoroquinolone community who are impacted similarly.

Also, keep in mind that mitochondrial depletions can be organ and system specific, meaning they can impact several organa of the body, just a few, or maybe just one, each causing a myriad of puzzling symptoms and manifesting with a wide spectrum of severity. In other words, all the symptoms do not need to ‘line up’ with everyone else’s. Also, depleted levels of mitochondria can vary greatly, impacting people differently. For instance, one person experiencing 25% depletion could have minimal symptoms, whereas someone else could be bedridden.

Although not heavily researched, it has been basically shown that Fluoroquinolones can impact mitochondrial thymidine kinase, which phosphorylates the pyrimidine nucleosides thymidine and deoxycytidine. If these nucleosides are impacted the results could be either depletions or deletions.

How can the Fluoroquinolones put in place a mechanism without having a pathogenic variant that causes the nucleosides to be diminished? I don’t know. I don’t have that answer, yet. However, this is something we have seen in the Fluoroquinolones in other areas. For example, Fluoroquinolones can cause a person to have upregulated metalloproteinases for years, without having pathogenic variants that would predispose, so this behavior is not outside the realm of possibilities.

In my case I am looking at trying to check the levels of thymidine and deoxycytidine. Dysfunction in circulating pools of these nucleosides would indicate a fault in mitochondrial biogenesis. I am trying to get connected with a doctor who is considered the world expert in depletion syndromes at Columbia in New York to consult about this, however New York has some of the most ridiculous medical regulations regarding out-of-state clinician video visits. If anyone lives in New York and has an “in” to Columbia, let me know.

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The Gold Standard To Diagnose Fluoroquinolone Toxicity

At this juncture in my long journey, I have come to the conclusion, for now, that the gold standard for testing that is needed to the get to bottom of the Fluoroquinolone problem is whole methylome analysis. This analysis will identify novel, rare, and potentially de novo epigenetic alterations made by the Fluoroquinolones that are causative of, or at least highly contributory to, the pathogenesis of FQAD.

I am convinced that the Fluoroquinolones cause epigenetic modifications impacting DNA methylation. They do so by initiating changes at the genomic loci and often these changes do not alter the underlying nucleic acid sequence but none the less, have profound effects on gene expression and functional regulation.

The equipment needed to do this ‘epigenomic profiling’ is an Illumina Infinium MethylationEPIC 850K array. This equipment allows the researchers to interrogate over 850,000 methylation sites quantitatively across the genome. If needed array scanning and next generation sequencing can be a follow-up using an Illumina NextSeq 550 system.

If I, we, had access to this level of analysis I believe we could finally unravel the Fluoroquinolone mystery once and for all by shining light on the areas of the genome that are being impacted by the Fluoroquinolones and how these changes are being sustained in the human body. This equipment would allow each person to be analyzed comprehensively. It would both case and wide net and conversely be very specific at the same time.

But alas, since I do not have millions of dollars at my disposal getting access to such equipment is currently out of my reach. If any of my readers has one of these machines lying around or has access to one, let me know. In the meantime, if my health allows, I will push on to the next clue!

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Testing For Depletions

This section is for those nerdy types of individuals who are interested in how to detect mitochondrial depletions.

While the ability to noninvasively diagnose disease or conditions involving the mitochondria has vastly improved, too many doctors are overly utilizing genetic testing just from blood or saliva. Until there are much greater improvements, tissue must still be analyzed and preferably muscle tissue.

Nonetheless, I do recommend that everyone who is getting into this level of detective work get their own genetic sequencing performed. If you can get it through insurance great, but many patients have to resort to paying for their own. In some ways this is better, because you are the master of the data and can have access to your own genome in the future.

The good news is that the prices over the last several years has come down drastically, and it is now possible to get complete genome (nDNA & mtDNA) sequencing for under $400 dollars. Once you have sequencing accomplished you can find several reputable aftermarket companies that will screen your genome for rare mutations.

For the biopsy it is very important that clinically affected tissue, such as skeletal muscle, is the tissue that is biopsied. Myopathy or myopathic changes are a common symptom with mitochondrial involvement, but it is possible to have other organs/tissue involved.

Not all neurologists are well versed in mitochondrial pathology and if they are not they often overlook many issues, basically they will screw it up and not even suspect they are screwing it up. I have firsthand experience with this. Make sure your neurologist knows what your goals are, and that he is up to the task, as it is unfortunately, up to you to determine quarterback the process. Do not hesitate to interrogate the doctor, surgeon, and pathologist, several times if you have to, to make sure they are competent. Reach out to organizations that are familiar with muscle biopsies such as the UMDF to educate yourself. You only get one chance. If the tissue is not handled correctly, it is easy to miss a diagnosis. In my case, I had a deep muscle biopsy of the vastus lateralis, but other tissues may result in better outcomes.

Mayo found abnormalities when looking at the ratio of mitochondrial DNA. More specifically copies of the RNR1 gene in mtDNA compared to nuclear DNA, specifically copies of the RPP30 gene, which is exclusively in the nucleus of the cell. They compare to the nuclear DNA because they want to control for the fact that different samples from different patients might have different total numbers of cells present.

For example, a sample that happened to have only 5 cells present is obviously going to have fewer numbers of mitochondria present than a sample with 500 cells. By dividing the quantity of mtDNA by nuclear DNA, you arrive at the quantity of mtDNA per cell rather than per sample. Effectively taking care of the issue of different numbers of cells potentially being present.

On a side note, mitochondrial depletion is not something that is ‘on the radar’ of most specialists. I was asked “why don’t doctors test for this?” The answer is simple, if you have sequencing completed and no clinical variants show up, they have no reason to pursue specialized testing such as this. Additionally, most neurologist won’t even submit muscle biopsies for mitochondrial depletion testing. It is off their radar, so to speak.

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What We Have Learned So Far

Over the last decade, I have become more and more convinced that the Fluoroquinolones cause epigenetic modifications that impact DNA methylation. An abundance of anecdotal evidence, along with peripheral scientific research, is proving this hypothesis correct. This important research finding from Mayo further bolsters this theory.

I believe the Fluoroquinolones are accomplishing these long-term devastating impacts by initiating changes at the genomic loci that is responsible for mitochondrial maintenance. These changes do not seem to alter the underlying nucleic acid sequence but somehow have profound effects on gene expression and functional regulation.

This is really not unusual behavior for the Fluoroquinolones. Like I mentioned earlier, anecdotally, we have often seen ‘unusual’ things in floxed individuals such as long-term upregulation of metalloproteinases, long term increased oxidative stress and other pathophysiology without genetic predispositions. This is what makes these drugs so very dangerous.

Again, I am confident that these mysteries can be fully explained with access to funding and the proper equipment, but for now I will have to be satisfied with the current results.

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Conclusion

There is still much more to be done before I, we, rest. However, living in the days of COVID-19 and its impact on medicine makes everything harder, not easier, especially getting answers to complex metabolic mysteries. Everything is now clouded by COVID, post-COVID syndrome, vaccine injuries and even supply issues.

The vast majority of Fluoroquinolone adverse events, if they are considered at all, are still considered rare outcomes by clinicians. Don’t expect to walk into your PCP’s office, or even your neurologist for that matter, and talk shop about depletion syndrome. If you do, most will ‘glaze over’ within a minute since this stuff is generally way over their head and more than likely they will think you have been reading too much ‘Dr. Google’ or you have some sort of psychological conversion disorder. However, if for some rare chance they believe you, 90% will go right to a genetic origin to put you in a neat little box.

Today, our medical system lacks curiosity leaving it up to the patients to purse answers. As for me, I will slowly push on, until I finally get to the very bottom of the problem or it finally gets me, whatever comes first.

In the words of Dr. Chris Martenson….” It didn’t have to be this way.”

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P.S. an additional word about the website….

I have been slowly implementing changes to the website to keep it more secure, comply with regulations, ease accessibility and incorporate some unobtrusive ads to help generate revenue for Fluoroquinolone research. I recently made changes to the registration process and now info on this site is freely available to everyone.

If you have previously ‘registered’ you will need to re-sign up to receive notifications of articles and important information.

Just simply fill in your email below. Again, I very occasionally send out a newsletter and but I do not spam. I do expect some more important information to come out in the future, so please sign up to stay informed.

Thank you.

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Personal Message From David

Do you shop for supplements online? If you do, you could help other floxed folks when you shop and not pay a cent more.

Click Here For More Info

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#Genetics #Mayo Clinic #mitochondria #Research

New Post has been published on My Quin Story

New Post has been published on https://www.myquinstory.info/the-covid-19-vaccine/

The COVID-19 Vaccine

Obviously, I am not a medical doctor, so if you decide to read beyond this point it is assumed that you agree with my disclaimer that I am not offering you medical advice.

Intro

I have to admit, I have had a very, very tough time writing this article. People have been asking me to get data about the COVID-19 vaccine up on my website for quite some time, but frankly accurate data on vaccine the experience is very hard to come by in the chronically ill population and equally hard to quantify in the Fluoroquinolone community.

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Also, I don’t want this article to take on a certain ‘tone.’ Although I am a person who was severely damaged by Fluoroquinolones and I have solidly made my own decision about the vaccine and I don’t want my personal decision to influence others. I have ingested enough science about the current vaccines and I doubt anything would come out in the foreseeable future that will change my personal decision or opinion.

Having said all that, the best I can do is to give you my opinion on the limited data I have and on more so on who I believe, in the Fluoroquinolone community, may want to exercise extreme caution when getting the vaccine. Ultimately If you have any medical questions regarding the COVID-19 vaccine and whether taking the jab is an appropriate choice for your body you should get input from a trusted medical professional that is familiar with your situation.

One more thing, getting the vaccine is an intensely personal and private decision for most everyone, so it boils down that you must ultimately be in control of your health and decide what is appropriate for your body. I recommend that you gather as much data as possible to make an informed decision and do not allow yourself to be pressured into doing anything until you are ready.

The bottom line, I do not fault people either way for either receiving the vaccination or for declining the vaccination, what I am against is overt discrimination and prejudice that plagues all sides in this argument. Although I do believe there are those who are using COVID-19, the mask, and vaccine to cause division in society, I think we must resist these divisive influences.

For those of you that want to skip all of my in-depth bloviating and go directly to the data, just click here.

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The Difficulty in Gathering Information

Most all of you reading this article know that getting accurate unbiased data about COVID-19 and the subsequent vaccines is proving very difficult. Depending on the metrics you use, both the vaccination and the COVID itself are fraught with many unknowns, especially in the long term. Since the subject of this article is the vaccination itself, I will stay focused on it. I do know that when you look ‘under the hood’ so to speak, the vaccines are not as safe as the media portrays it to be. I believe in some instances there is clear evidence that the statistics are being ‘cooked’ to show a more favorable adverse event profile.

From a social perspective, God forbid if you try to innocently inquire in many of the public social media forums to gather information. Quests for knowledge often are the impetus for firestorms of vitriolic polarization. Online exchanges have become so inflamed, and information has become so controlled that the mere mention of COVID or the vaccine can get a person booted, banned, blocked, accounts suspended, or groups shut down. On the other hand, many forums have had to resort to ‘stealth’ measures by changing their names or telling people to use coded language to avoid triggering the ‘big brother’ censors.

I personally had an incident in the large Facebook group Fluoroquinolone Toxicity Group (FTG), where a person ‘tagged’ me and asked a question about the progress of Fluoroquinolone research. Now to be fair, I never visit FTG unless I am tagged to respond to answer a question, but in a nutshell my answer was quick, very short and simple; it stated that academic research was currently on hold due to COVID, but hopefully will be back soon. That’s it, that was the entire substance of my response. Not to claim ignorance, but since I don’t spend my days scrolling through FTG’s feed in my naivete I didn’t realize that the mere mentioning of the word ‘COVID’, regardless of the context, was far worse than a F-bomb laced tirade from Samuel Jackson. I evidently had committed an unpardonable sin.

Even though my post had nothing directly to do with inflammatory nature of COVID per say, the post was deleted, and I was warned about even mentioning the word. Then, like a little kid, I was told to review the posting guidelines. Well needless to say I have always been a bit of a nonconformist and reviewing FTG’s posting guidelines was not going to happen…ever. No matter, I still had disgraced myself by mentioning the “bad” word. Welcome to George Orwell’s dystopian world. Needless to say, I personally don’t have time for being pulled into such revolving nonsense, so I left the group. On a positive note, I belong to too many groups anyway, so things like this help me ‘cull the herd’, so to speak. Anyway, I digress. I am not trying to be petulant and narcissistic but to point out that quests for knowledge or even innocent comments regarding COVID, can lead to unpredictable or unwanted inflammatory consequences.

Digging through data on COVID is both surreal, time consuming and often an exercise in futility. Most of the existing material is often propaganda that is slanted in an attempt to shape group think or reinforce a thought process. I even had to switch from the Google search engine when searching for COVID research data to a more ‘unbiased’ engine to avoid the endless stream of biased search returns. It is quite amazing the differing results between search engines on subjects such as COVID-19. Even the governmental institutions designed to give citizens unbiased information in reality only accomplish the opposite, both strengthening the social polarization and furthering confusion.

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Gathering Data

So, with all the chaos surrounding the vaccine, some people have asked me how I am gathering any accurate data on the vaccination, especially in the chronically ill population?

I belong to a specific set of health-related Facebook groups and Twitter feeds. Most of them are mainly in the realms of Mitochondrial Disease and Chronic Fatigue. I also belong to several organizations that represent the aforementioned groups. In these groups are subsets of individuals that are suffering from Fluoroquinolone Toxicity, either knowingly or unknowingly. So first, I monitor social media feeds and participate in online meetings such as Zoom to gather as much data as I can. Next, I also belong to a handful of groups and feeds that are dedicated just to reporting real-world vaccine adverse event instances both from those who are both healthy and those who have chronic illnesses. Although I will try to post a few links at the bottom of this article for those who like to do their own research.

Additionally, I look at the current science. Unfortunately, peer reviewed science has become corrupted by nefarious science experts. These PhD’s often sell their credentials to the highest bidder, let their own bias and prejudice guide their science, or succumb to governmental and/or pharmaceutical pressure. The result is that many of the papers now released on COVID-19 masquerade as science but in reality, they are designed to editorialize and propagandize. Despite this, there is still some good science coming out on COVID and the vaccines, you just must dig for it.

Finally, my favorite type of information is the real-world stories and information volunteered to me from floxies who have had first-hand experienced with the vaccine. I combine all this with the limited research data that is being released and then use it to formulate my. For me this is the best that I can do and is probably what results in the most accurate results, at least for now.

There one fundamental aspect however that is missing from the whole COVID-19 and subsequent vaccine debate, and that is a deep data pool. Unfortunately, there is no large pool of robust data from which we can draw accurate conclusions from. If someone tells you otherwise, they are lying. All data pools on COVID are shallow and it can be proven that statistics on adverse events are not reliably being captured or reported to the public.

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Example of New Data

On April 30th, 2021 some additional data was released on the Coronavirus by the prestigious Salk institute (source). This data examples why we need to proceed with caution in regard to a vaccine and how this virus and vaccine can impact those suffering from Fluoroquinolone Toxicity. Salk researchers and collaborators released studies showing how COVID’s spike protein damages cells, confirming COVID-19 as a primarily vascular disease despite the fact that it’s predominant mode of spread is via the airborne route. It is not a respiratory virus because of this holds a greater threat for some suffering from Fluoroquinolone toxicity.

If you remove the replicating capabilities of the virus, it still has a major damaging effect on the vascular cells, simply by virtue of its ability to bind to this ACE2 receptor and the S protein receptor. The S protein of the virus, the spike that forms the crown, attacks the receptor ACE2, damaging the mitochondria that generate the energy of the cells, thus damaging the endothelium, which lines the blood vessel.

The main vaccines that are widely in use today force the body to produce the spike protein so that our bodies will create antibodies to it. They do this so that when an actual virus covered with spike proteins interacts with a vaccinated person, the body will recognize it as a foreign invader attacking and neutralizing it.

However, what if the spike protein is part of the problem? For chronically ill people, let alone healthy people, what is the long-term implication of having this mitochondria damaging spike protein circulating in our bodies? Obviously, we won’t have the answer to this speculative question for quite some time until more data comes in. This is a novel complex virus and as time goes on we will learn more about it.

Since the Salk institute found out that the spike proteins are uniquely damaging the mitochondria that are in the vascular system, they are also overlapping in a metabolic sphere of influence that is impacted by the Fluoroquinolones. Although I won’t go into tall the nuts and bolts of why I believe this is crucial (this article is already way too long as it is), I believe this information further confirms that certain groups within the Fluoroquinolone community need to use caution, especially in the long term.

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How Safe is the Vaccine for Those Suffering from Fluoroquinolone Toxicity?

Again, you have to remember that the data on the vaccine’s long-term impact is very limited, especially in the chronically ill population and that the Fluoroquinolone community is very diverse or heterogenous in nature. So, coming up with a one size fits all recommendation on whether people should get the vaccine is impossible.

For me to tell you whether the vaccine is safe for your body, is about as accurate as me predicting the exact date for the end of the world as we know it, and in all seriousness the latter would probably be easier, given the daily newsfeed.

Seriously, I do know some severely chronically floxed people that have taken the vaccine and have surprisingly fared pretty well with little or no negative symptoms to show for it, at least in the short term. While I know this is very encouraging for those who wish to take the vaccine, at the same time I need to warn you that on the flip side I know some floxies who greatly regretted getting the vaccine.

Also, how do you define ‘toleration’ of the vaccine. Some people have had no symptoms at all, whole others got their ‘but kicked’ for several days, then started feeling better. Again, suffering is subjective as to what people consider ‘worth it’ or not. So, for the sake of clarification, I am including those who had a tough time with the vaccine but recovered in the ‘Yes’ category.

The following graphics are based on my observational data so far.

The first two circle graphs show the overall trend of toleration of ALL vaccines combined and then averaged from the data I have received so far. I realize that there are different vaccines that use different mechanisms of action but for now, until more deeper data comes in and I have time to tabulate it, this is the best I can do. I do not have enough data to extrapolate if one type of vaccine is safer than the other.

The second group of pie charts attempts to capture observational toleration of the vaccine based on the ‘type’ of floxed person who received the vaccine. Please note that I have separate Fluoroquinolone toxicity into two camps: FQTS (acute) and FQAD (chronic).

The third group is a crude attempt to correlate observational data according to predominant FQ based symptoms. It seems, on the very surface, that those who complain only of musculoskeletal symptoms (no neurological, mitochondrial, psychological, etc…) seem to fair better with the vaccine.

Although my non-medical advice would be to think real hard about getting a COVID vaccine if you are in the throes of a severe acute FQ adverse event, those that are recovering or have significantly recovered from FQTS, seem to overall tolerate the vaccine better than those chronically impacted. Toleration of the vaccine in the FQAD camp appears to be lower than the FQTS. I believe this has to do with the long term impact on mitochondrial mechanisms, which are hit hard by both COVID and/or the vaccines.

General COVID-19 Overall Vaccine Toleration

60 %

Toleration COVID-19 Vaccine

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40 %

Non-toleration COVID-19 Vaccination

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COVID-19 Vaccine Toleration Among FQTS & FQAD

Yes = Tolerated | No = Did Not Tolerate

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FQTS - Mild Cases

Mild to moderate cases of FQTS.

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FQTS - Moderate

Moderate to more severe cases of FQTS.

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FQAD

Chronic FQAD.

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COVID-19 Vaccine Toleration According to FQ Symptom Type

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Musculoskeletal

Cases whose predominate FQ symptoms are musculoskeletal only.

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Neurological

Cases whose predominate FQ symptoms are neurological only.

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Mitochondrial

Cases whose predominate FQ symptoms are mitochondrial.

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Multifocal

Cases whose FQ symptoms are broadly multifocal.

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Again, data changes almost frequently, so please consider these as observational trends only, they are definitely not set in stone. Also, they definitely do not encompass all variables or possibilities, which means that you may not personally fall into any of these categories. Mark Twain said, “Facts are stubborn things, but statistics are pliable.” Trying to categorize floxed people is very ‘pliable’ and tenuous indeed.

In some ways I believe that it is easier to list groups of people who I believe should exercise caution in getting the vaccine than it is to try and correlate vaccine response to varying levels of Fluoroquinolone toxicity due to its heterogeneity. Because of this I have listed below groups of people that I think should exercise caution when receiving the vaccine. Before we look at those, let’s see an example of bad advice.

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Bad Advice

The various social media groups that are gathering points for those suffering from Fluoroquinolone toxicity is a melting pot of advice. Some of this advice is good, and some of it is frankly, terrible.

I happened to visit one of the larger groups where I act as a back-up admin. The first post I saw was in relation to the COVID vaccine. A man was telling people in a comment, “a year ago I couldn’t walk because of Levaquin. Now I am almost recovered. I had the vaccine, and I am fine.” He went on to encourage a young woman, who supposedly was dealing with a recent adverse event to Cipro, to get the vaccine. I had to face palm,

Obviously, this man’s opinion is based on his lived reality, but it is both myopic and frankly…wrong. Flippant remarks like can be dangerous, unfortunately policing remarks such as this in a large forum takes a small army.

His is a common mistake that I see people make all the time; they extrapolate their own experience as being universal. Remember, the level of suffering is subjective and true comparisons are difficult to make. One thing that I have learned by studying Fluoroquinolone toxicity for the last fourteen years is that floxing, again, is very, very diverse, and so is each person’s response to drugs, supplements, vaccines, etc…

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Who Should Use Caution in Receiving the COVID-19 Vaccine?

Whether you decide to get the vaccine or not make sure your decision is not based on someone’s misguided comments. You can’t undo the injection once it is done, but you can always do it later after more data comes in and after you have had time to research. One more thing, I would ask you, “what is your gut telling you?” You know your body better than anyone else.

In general, those whose adverse events to the Fluoroquinolones that were mild and limited to mild or moderate musculoskeletal symptoms seem to be tolerating the vaccine the best. However, those who had severe neurological, immunological, and mitochondrial pathologies do not seem to be tolerating the vaccine as good. However there are always exception to any rule.

Like I mentioned earlier, coming up with a one-size-fits-all universal statement is both irresponsible and difficult, so instead I will list my opinion on those who I believe should exercise caution in taking the vaccine.

It is my opinion that anyone…

…who is still suffering from an acute adverse event to the Fluoroquinolones should use extreme caution. These would be people that are newer active cases with rapidly changing symptoms. These individuals don’t fully know what body systems are going to be impacted by floxing in the long term.

…who has a confirmed mitochondrial pathology post Fluoroquinolones should use extreme caution. Fluoroquinolone’s can initiate mitochondrial disease and COVID-19 and the vaccines hit the mitochondria hard.

…who has myopathy, muscle weakness, chronic fatigue, or severe energy issues post Fluoroquinolones should use extreme caution. Many individuals suffering these symptoms again, have moderate to severe mitochondrial involvement. Some floxies have reported new, worsening or long-term fatigue and weakness after receiving the vaccine.

…who has vascular problems post Fluoroquinolones, especially those who have been floxed and have Ehlers Danlos Syndrome should use caution. We do know that the FQ’s can impact connective tissues long term, however at this time we do not know the long-term impact of the spike protein on endothelial and connective tissues.

…who has developed a blood pathology, such as a clotting disorder, post Fluoroquinolones should use extreme caution. Many of the fatalities with the vaccines have to do with blood clots.

…who has moderate to severe neurological problems post Fluoroquinolones, especially severe peripheral or sensory neuropathy should use extreme. Many people who have these issues especially severe ganglionopathies are sensitive souls and I have received reports of increases in sensory neuropathy symptoms from the vaccines.

…who has immune mediated inflammatory conditions post Fluoroquinolones should use caution. This virus and the vaccines do initiate a body-wide inflammatory state.

…who have a known allergy to any of the vaccine ingredients such as polyethylene glycol (PEG). Strangely enough, I have seen several people develop an intolerance to PEG post Fluoroquinolones and when they take it, it exacerbates neurological symptoms.

Obviously this is not an all inclusive list of cautions. I will update this as more data comes out.

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My Decision

I am not taking the vaccine. Why? My primary care physician, who is pro vaccine in general, who is very familiar with my health history, has adamantly advised me against getting the vaccine. I have a confirmed mitochondrial pathology that involves muscle myopathy and muscle weakness that was initiated by the Fluoroquinolones. My doctor believes that the vaccine poses a risk that is equal to me as the virus and told me that exercising safety measures would be more effective. I agree with him 100%. I want to make it clear that I do not live in fear of the virus, I simply keep my vitamin levels optimized and take responsible precautions and do not violate the four D’s.

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Conclusion

Data is slowly trickling on COVID-19 vaccine use in the chronically ill, however most of it is still short-term data. To help you understand this let me tell you this analogy:

My largest demographic of readers and followers are those who have been impacted long-term by the Fluoroquinolones. Many, if not all, of these individuals did not know years ago that they were going to by impacted long-term by the Fluoroquinolones. Many, if not most, thought they would only be impacted short-term and some even thought they would heal quickly and completely. It wasn’t until several years later they realized Fluoroquinolone Toxicity had become a chronic health problem, plus it contributed to other health issues as well.

This same issue applies to COVID-19 and the subsequent vaccines. We do not know the long-term impact of the vaccines on floxed individuals. We do know that COVID-19 is causing a ‘long-haul’ pathology in many people and in those there are a large subset of people who have Fluoroquinolone toxicity intricately woven into their long-haul case. Unfortunately, I have seen both a re-emergence of floxing symptoms and long haul health issues from the vaccine in a limited number of people.

Only time will tell us the true long-term impact the vaccines have on the floxed. I understand that living under the thumb of COVID-19 is not pleasant and causes a great deal of stress. However, there is no going back if you regret taking the vaccine, so make sure you make the best-informed decision you can.

Again, as more data comes in, I will refine this article to reflect that data.

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Facebook: COVID19 Vaccine victims and Families (over 4.8 Thousand members):

https://www.facebook.com/groups/616637409732910/

Facebook: ME/CFS and the COVID VACCINES (6.3 Thousand members):

https://www.facebook.com/groups/226441995768222/

Facebook: COVID-19 Vaccine Side Effects (146 thousand members):

https://www.facebook.com/groups/allvaccinesarefake/

Facebook: C & V Floxie Group:

https://www.facebook.com/groups/456988725441400/

Frontline Critical Care Alliance

I am a fan of Dr. Pierre Kory and the Frontline doctors that are working with COVID. https://covid19criticalcare.com

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Personal Message From David

Do you shop for supplements online? If you do, you could help other floxed folks when you shop and not pay a cent more.

Click Here For More Info

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#COVID-19 #Medications #vaccines

New Post has been published on My Quin Story

New Post has been published on https://www.myquinstory.info/qui-tam-lawsuit-filed-by-dr-bennett-against-johnson-johnson-bayer-merck/

Qui Tam Lawsuit Filed by Dr. Bennett against Johnson & Johnson, Bayer, Merck

A Qui Tam whistleblower lawsuit has been filed against pharmaceutical giants Johnson & Johnson, Bayer and Merck by Charles Bennett, M.D., Ph.D., M.P.P., SmartState Chair, Director of the Center for Medication Safety and Efficacy at the University of South Carolina. The lawsuit was recently unsealed in the United States District Court for the Southern District of New Jersey district court.

The Qui Tam lawsuit filed against Johnson & Johnson, Bayer and Merck claims fraud against Medicaid, Medicare, and other government programs related to a class of drugs manufactured and marketed by these drug companies, referred to as fluoroquinolone (FQ) antibiotics. FQ antibiotics manufactured and marketed by these drug companies include Johnson’s Levaquin and Bayer and Merck’s Cipro. Johnson & Johnson manufactured Levaquin from 1997 to 2018; Bayer and/or Merck have manufactured Cipro since 1988.

The Qui Tam accuses Johnson & Johnson, Bayer, and Merck of making false statements and misbranding their FQ antibiotics which resulted in fraudulent claims to be filed against the United States government for Medicaid and Medicare patients and for other government programs in violations of 31 U.S. Code § 3729-33 the False Claims Act.

Since the 1990s, hundreds of millions of prescriptions have been written for FQ antibiotics used to treat pneumonia, sinusitis, bronchitis, skin infections, prostatitis, urinary tract infections, and kidney infections. It is estimated that at least 60% of these prescriptions were for Medicaid and Medicare patients.

The lawsuit, in part, accuses Johnson & Johnson, Bayer and Merck of committing fraud by misbranding, marketing, promoting, and introducing through interstate commerce, their FQ antibiotics without any warning on the drug labels that consuming these antibiotics may result in Fluoroquinolone-associated Disability (“FQAD”) and mitochondrial toxicity.

The Qui Tam argues that decisions by Johnson & Johnson, Bayer, and Merck to misbrand Levaquin and Cipro are particularly troubling because the drug makers are fully aware and are on full notice of the very serious adverse events based on Dr. Bennett’s extensive research; Levaquin’s and Cipro’s FDA Adverse Events Reporting System (FAERS) reports; other FQ research; FDA pharmacovigilance review reports; FDA advisory committee meeting discussions; and two Citizen Petitions submitted to the FDA by Dr. Bennett.

Specifically, the Qui Tam charges that Johnson & Johnson, Bayer, and Merck ignored information contained in the Citizen Petitions Dr. Bennett filed in June 2014 and September 2014; an April 17, 2013 FDA pharmacovigilance review “Department of Health and Human Services, Public Health Service, Food and Drug Administration, Center for Drug Evaluation and Research, Office of Surveillance and Epidemiology,” with the subject line, “Disabling Peripheral Neuropathy Associated with Systemic Fluoroquinolone Exposure;” an FDA report presented at the November 5, 2015 FDA Joint Meeting of the Antimicrobial Drugs Advisory Committee and Drug Safety and Risk Management Advisory Committee; a January 31, 2016 study authored by Dr. Bennett and others which replicated certain adverse reactions using mice treated with Cipro; and hundreds of patient reports submitted to the FDA.

The lawsuit further argues that Johnson & Johnson, Bayer, and Merck ignored the science and continued to stand by Levaquin and Cipro as labeled. As a result, the Qui Tam claims that healthcare providers continued to prescribe Levaquin and Cipro without warning patients—the majority of whom were Medicaid, Medicare, or other Government program beneficiaries—of the risks of FQAD and of the risks of possible mitochondrial toxicity.

The Qui Tam charges that the lack of adequate warnings resulted in the government healthcare programs and other government programs providing reimbursements and making payments that should not have been provided or made.

Johnson & Johnson, Bayer, and Merck knowingly disregarded federal laws and FDA regulations relating to prohibitions on suppressing the harmful effects of the fluoroquinolone antibiotics Levaquin and Cipro, according to the lawsuit.

The Qui Tam claims that Johnson & Johnson, Bayer, and Merck fraudulently obtained billions of dollars from the federal government, thereby unjustly enriching themselves at the expense of taxpayers and at the risk of patient health.

Moreover, the lawsuit claims that by continuing with its fraudulent, misbranded labeling and by neglecting their own duty, Johnson & Johnson, Bayer, and Merck exposed—and continue to expose—many individuals who could have been spared FQAD and mitochondrial toxicity if they had acted in accordance with the law and with FDA regulations.

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#Community News #Dr. Bennett #Lawsuit

New Post has been published on My Quin Story

New Post has been published on https://www.myquinstory.info/covid-19-fluoroquinolones-and-the-long-haulers/

COVID-19, Fluoroquinolones and the Long Haulers

We knew it was inevitable. With COVID-19 viral infections on the rise in many places of the world, the much touted ‘second wave’ of the COVID-19 pandemic has proven itself a reality, especially in some areas. Regardless of your opinion on COVID-19, one thing is abundantly clear, it is a real boon for the pharmaceutical industry.

While the contentious political debate rages around various aspects of COVID-19, one fact has become apparent, many patients with COVID-19 , especially those who develop infections or are at risk for developing co-infections, are being given Fluoroquinolone antibiotics (1).

Fluoroquinolone Use

Statistics are showing on average that seriously ill adult patients with COVID-19 are being prescribed antibiotics between 87-94% of the time. Depending on the country, Fluoroquinolone antibiotic usage varies around the globe from 50% to 92% (1). Preliminary observations show that levofloxacin, ciprofloxacin, and moxifloxacin seem to be the Fluoroquinolones of choice when they are used.

This usage has market analysts predicting increased sales, with the generic levofloxacin tablets market expecting tremendous growth in the very near future (2).

Steroids

If the risk of receiving a Fluoroquinolone antibiotic alone was great enough, another fact surrounding COVID-19 is that a majority of COVID patients are given some form of strong steroid therapy to combat the devastating inflammation that COVID is so known for causing (3).

It has been found that dexamethasone and other corticosteroid drugs are effective treatments for treating from of COVID-19 inflammation in patients, especially those who are critically ill. That demographic of patient would also likely need antibiotic therapy (4).

The Proverbial Oil and Water

Anecdotally, we (the Fluoroquinolone community) have known for decades that Fluoroquinolones and steroids do not mix. Many severely impacted individuals were damaged by combinations of these drugs and, at the very least, many individuals had their adverse event amplified by the addition of a steroid to the mix.

The ‘official’ medical opinion regarding Fluoroquinolone and steroid concomitant use remains dubious. Some authorities see it as a dangerous combination (5), while others hold to plausible deniability and believe that a potential interaction between Fluoroquinolones and steroids may be unlikely, making them more apt to prescribe the combination (6).

Despite the disagreement in modern medicine as to the danger of using Fluoroquinolones and steroids in clinical use, the truth is that many individuals have been and are being treated with these possible lethal combinations. Now, due to COVID-19, they are being used together on a regular basis, especially in those with moderate to severe cases of COVID-19 (3).

That brings me to my central point, and one that directly affects the Fluoroquinolone community.

While the whole world is focused on COVID-19 mortality, survival rates, mask usage and vaccines, there is an entire element of the COVID-19 illness that is missing from the discussion sphere.

The “Long Haulers”

The medical landscape is already littered with the people who have adverse events to the Fluoroquinolones. They are the “walking wounded” as I call them. As we know, Fluoroquinolone victims permeate other chronic illness communities such as fibromyalgia, chronic fatigue/ME, mitochondrial diseases and so on. I have found that, in these communities, a large subset has had exposure to Fluoroquinolones. Some of them have connected the dots and made the connection, while many others remain clueless buying into the medical paradigms that deny the Fluoroquinolones are the instigators of their adverse health symptoms.

Now we have long-haul COVID-19 added to the mix.

In a scenario so familiar with individuals damaged by Fluoroquinolones, Long Haulers are being ignored amongst all the ‘noise’ that is being generated by the political clamor in the world. Long haulers are defined as people who are experiencing extended post-viral sequelae. Sequelae is pathological condition resulting from a disease, injury, therapy, or other trauma.

Post-viral Sequelae

Post-viral sequelae are nothing new. It accounts for a large portion of people in health communities such as mitochondrial, fibromyalgia, chronic fatigue and many more.

For many, the problem has always been, “what is the root cause?” Was it the illness itself, a toxic pharmaceutical treatment, or a combination of the two that cause the chronic illness?

Many COVID-19 patients, even people who were never sick enough to go to a hospital, much less lie in an ICU bed with a ventilator, are reporting a laundry list of ill-defined symptoms that I would include under the umbrella of mitochondrial dysfunction. Long Haulers are reporting neuropsychiatric symptoms such as brain fog, numbed limbs, exhaustion, fumbling for words, depression, anxiety, and PTSD. Still others are reporting symptoms including headaches, dizziness, lingering loss of smell or taste, and deep cognitive impairment.

Mayo clinic says that they are seeing a number of cases of people who report long-term fatigue, headaches, vertigo (and), interestingly enough, difficulties with cognition, hair loss, cardiac and cardio-respiratory fitness concerns, and gastrointestinal issues.

Dr. Gregory Poland, Mayo Clinic’s COVID expert says “I think what we’re going to find out is that a large portion ― not all, but a large portion of that ― is likely to relate to the significant cellular-level damage that this virus can cause,” referring to those who are asymptomatic or have mild cases of COVID-19.

“I think it’s an argument for why we take this disease so seriously,” says Dr. Poland. “People who are thinking, especially young people: ‘(It’s a) mild disease, you know. I might not even have any symptoms, and I’m over it.’ Whoa. The data is suggesting otherwise. There’s evidence of myocardial damage, cardiomyopathy, arrhythmias, decreased ejection fractions, pulmonary scarring and strokes.”

“We’re going to see more and more of the longer-term consequences come out, and we’re going to need to study those as vigorously as we did the acute symptoms. Catalog them, understand them and then do clinical trials to figure out how best to treat them,” says Dr. Poland (7).

Whether you believe COVID-19 is a serious health threat to society or not, one thing we all can agree on is that there is no long-term health information available. We do not have the luxury of historical data. Will those who seemingly had no initial reaction to the virus, come down with something serious, months or years down the road? Only time will tell.

What is the percentage rate of those experiencing extended post-viral sequelae? Well, in contrast, to more than 90% of flu patients who recover fully within two weeks, only 65% COVID-19 are recovering fully in the same time frame. That means that 35% of all patients not hospitalized are not returning to normal quickly and many are complaining of lingering symptoms, some indefinitely.

It wasn’t until late July that the US Centers for Disease Control published a paper recognizing that as many as one-third of coronavirus patients not sick enough to be admitted to the hospital don’t fully recover (8).

It does appear that SAR-COV2 hits the mitochondria hard, but let’s get back to the Fluoroquinolones.

Complexity

Now before someone accuses me of being Chicken Little or at the very least looking at the world through rose colored glasses, I will be the first to admit that not every person who gets COVID is prescribed a Fluoroquinolone. So no, I don’t see Fluoroquinolones under every rock. But the truth is that many are being prescribed Fluoroquinolones, so much so that market analysts are expecting an increase in Fluoroquinolone manufacturing. Also, as I mentioned earlier, many COVID patients are also being prescribed a steroid as a common adjunct.

Most of my readers know that once the Fluoroquinolone enters the mix, the complications of diagnosing go up exponentially. After being exposed to a Fluoroquinolone, no one really knows if the post-viral sequelae are being cause by, or at least influenced by, the Fluoroquinolone that was tossed into the mix. One thing is for certain, you can never rule it out, ever.

They’re Here

Although I have not had many contacts from post COVID patients, I have had a few. I am anticipating that this will go up in the future as more and more individuals are given a combination of drugs to battle COVID that included a Fluoroquinolone, and possibly a steroid as well.

Additionally, I’m afraid, that this will be another area where the Fluoroquinolones fall through the cracks in the medical system, where they will get a pass. They will cause their damage and then hide, remaining blameless while the medical authorities look in another direction. After all, who would suspect a commonly prescribed antibiotic that has been around for decades, that has a wonderful safety record, as causing any lingering problems? (Sarcasm)

Conclusion

These are truly challenging times we live in. I hope it never becomes reality, but the chances are good that one of our loved ones could be faced with the potential for antibiotic use to treat COVID. During times of crisis most people don’t think of questioning the treatment regimen. If you haven’t, do your loved ones a favor and let them know that there are usually safer options if they are ever faced with this choice.

During a recent COVID study the authors observed that administration of antibiotics, especially multiple antibiotics, did not seem to change the disease outcome, so they recommended the rational use of antibiotics (1).

Again, if antibiotic use is necessary, there are generally safer alternatives than the Fluoroquinolones. The risk/rewards and any other concerns should be discussed with the treating doctor so as to choose the safest treatment for the particular situation.

Stay safe everyone.

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Personal Message From David

Do you shop for supplements online? If you do, you could help floxed individuals when you shop and not pay a cent more.

Click Here For More Info

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#Advocacy #Coronavirus #COVID-19 #Steroids

New Post has been published on My Quin Story

New Post has been published on https://www.myquinstory.info/the-fluoroquinolones-an-epigenetic-monster/

The Fluoroquinolones: An Epigenetic Monster

Introduction

The fluoroquinolones are frighteningly epigenetic. I am of the opinion that the Fluoroquinolone Antibiotics are one of the most epigenetic impactful pharmaceuticals that has ever been unleashed on society and the reasons for this are very simple.

If you combine the molecule’s broad spectrum of influence that permits it to penetrate deep hitting an untold number of points in a person’s metabolic environment greatly influencing epigenetic machinery, and then you add the sheer number of historical worldwide prescriptions, you have the recipe for disaster.

Epigenetic Intrusion

A real-world analogy is its similarity to brute force hacking software. In a simple brute force attack the hacker attempts to gain access by literally trying something over and over. There are no limits to the number of access attempts. The higher the scale of the attack, the more successful the chances are of entry.

In our bodies, the Fluoroquinolone molecule attempts access to every aspect of our biological system. It uses excessive metabolic influence to gain access to areas, such as the brain, spinal cord, bone, etc… No area is off limits. Any weakness in any area of access and the greater the chance of a negative outcome.

This tremendous broad-spectrum activity has the ability to change the genetic phenotype without changing the genotype. In other words, it affects gene expression, or the ability to activate or deactivate genes. For many people, this can carry with it the possibility of a pathogenic process that can manifest quickly or, for some, …many years later.

This creates a frightening dilemma……currently the Fluoroquinolones are way ahead of us.

A Step Ahead

Modern genomics is progressing at breathtaking speed, defining hundreds or thousands of rare pathogenic genetic variants that each person harbors inside their genome. The potential associations between these variants and a possible disease state that they can manifest are enormous. While it is true that the vast majority of the yet to be discovered variants are likely to be inconsequential, at present, we do not have a complete picture.

Regardless, the Fluoroquinolones are reaching these yet to be discovered pathogenic variants ahead of us. It is reaching them before we have had a chance to discover these variants and research their ability to cause us harm.

The Fluoroquinolones have the ability, that we know of, to initiate and sustain genetic change via at least three systems, DNA methylation, histone modification and non-coding RNAs, and it would appear that they have the ability to induce global epigenetic changes under both normal and pathological conditions (1, 2).

It is shocking to think that this monster has impacting society for decades and I am afraid, no, I am confident, that we will be dealing with the tremendous pathological outcomes unleashed by it for many years.

Profound Ignorance

Right now, we are living in an age of profound ignorance. Those that we trust with our medical safekeeping are ignorant to the fact that a monster that they unleashed years ago is causing a tremendous amount of disease right before their very eyes, and yet they cannot see it and in some cases they choose to turn a blind eye.

The Fluoroquinolones have been implicated in later onset Mitochondrial Disease, Chronic Fatigue, Fibromyalgia, dementia, Parkinson’s, various neuropathies, cognitive dysfunction, neuropsychiatric illnesses, and much more. The symptoms of their adverse event profile can reach into the hundreds and defy differential diagnoses by many doctors (3).

Yes, there are several other pharmaceuticals that have a penchant for harm, but the Fluoroquinolones are at the very top of the list when you consider their wide-ranging adverse event profile in conjunction with the sheer amount of prescriptions written, the ability to create delayed adverse events, and a medical system that does not include them in differential diagnosis algorithms. The Fluoroquinolones truly hide in plain sight and have slipped through the cracks our pharmacovigilance system.

Conclusion

Do you know of a loved one, a friend, a co-worker, who suffers from a medical condition that defies diagnoses or is of unknown origin? If so, do some detective work and search their medical history. Don’t necessarily look in the immediate past and also remember that Fluoroquinolones are routinely given during surgery, often without the patient’s knowledge.

If you are faced with potential antibiotic use, for yourself or a loved one, please become informed as to the choices that you have available. If antibiotic use is necessary, there are generally safer alternatives than the Fluoroquinolones. Discuss all these concerns with your doctor so as to choose the safest method for your particular situation.

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#Adverse Events #Advocacy #Genetics

New Post has been published on My Quin Story

New Post has been published on https://www.myquinstory.info/fluoroquinolone-herbicides/

Fluoroquinolone Herbicides

Introduction

Over the years I have outlined several times in the past how the quinolones (fluoroquinolones) will be part of our society for many years to come, for several reasons.

In the publication, Nonclassical Biological Activities of Quinolone Derivatives published in Journal of Pharmacy & Pharmaceutical Sciences Vol 15, No 1 2012, it outlines why the quinolones are an excellent platform (scaffold) for modification to create new pharmaceutical products.

The Journal states “Quinolones as “privileged building blocks” with simple and flexible synthetic routes allow the production of large libraries of bioactive molecules. Because of their diversity, drug-like properties and similarities to specific targets, they are considered a central scaffold to build chemical libraries with promising bioactivity potential.”

The quinolones are very effective at what they do….kill.

Because of this, I alerted my readers to watch for development in three areas:

Antibacterial

Anti-cancer

Antiviral

Well now you can add a fourth area to the development:

Herbicides

Fluoroquinolone Herbicides

Recently, while I was lying in bed winding down getting ready to go to sleep, I was thinking about an article I recently read how scientists are trying to re-purpose fluoroquinolones as herbicides. The article “Antibiotic analogue puts researchers on path to ending herbicide drought” was published in 2018 and it really didn’t garner much attention at the time.

In a nutshell, some mad scientists in Australia and the United Kingdom have found a new herbicidal mode of action by modifying the antibiotic ciprofloxacin. Finding a new herbicidal mode of action has evaded scientists for 20 years.

Like kids with an erector set, scientists have been tinkering with the fluoroquinolone scaffold and found a ciprofloxacin analogue that selectively targets an enzyme required for plant growth yet has decreased antibacterial activity.

Joshua Mylne and Keith Stubbs, from the University of Western Australia, and their colleagues, target DNA gyrase in their new system. In their literature they state that DNA gyrase is a type of enzyme that helps control DNA unwinding during replication. “It is essential for plant growth but not present in humans, and therefore a prime herbicidal target.”

DNA gyrase not present in humans? Well maybe, but you would think that researchers would delve deeper in the complete profile of the drug they are tinkering with, wouldn’t you?

As far back as 1993, research showed that Ciprofloxacin targeted DNA gyrase AND toposiomerase II (1). DNA gyrase is the prokaryotic equivalent of DNA topoisomerase II.

Anyway, I digress. Why would we need newer herbicides when we have the world’s most (in)famous herbicide, glyphosate?

Glysophate Replacement?

Peter Andreana, an expert in small molecule synthesis and drug design from the University of Toledo Ohio, who was not involved in this study said that, “glyphosate is now susceptible to resistance in many different plants, so there is a substantial amount of concern.” Andreana is concerned that we need to come up with viable alternatives to replace glyphosate.

We have literally drenched the world in glyphosate and now nature is fighting back by naturally selecting plants that are glyphosate resistant. This usually happens when humans over do it and scientists, unfortunately, appear to be search for replacements in all the wrong places.

Concerns About Developing Herbicides from Antibiotics

Since ciprofloxacin is an antibiotic and using it directly in agriculture would greatly contribute to the ever-growing antibiotic resistance problems facing the world, the team (Mylne, Stubbs and colleagues) decided to develop analogues of ciprofloxacin with reduced antibacterial activity.

In chemistry, an analogue is a compound with a molecular structure closely similar to that of another.

To do this, they produced a basic fluoroquinolone scaffold then added chemical moieties differing in size, shape and hydrophobicity at the N-1 and C-7 positions. After some experimentation they found an analogue with sufficiently decreased antibacterial properties and increased herbicidal properties. This confirmed to the researchers that targeting the pant’s DNA gyrase was a realistic new mode of action for herbicides.

What Could Possibly Go Wrong?

Despite the reduced antibiotic abilities of the new fluoroquinolone compounds, some scientists are still concerned about the idea of modifying antibiotics for use in agriculture, and the precedent that this will set for future research.

Jack Heinemann, an expert in antibiotic resistance and genetic engineering at the University of Canterbury, New Zealand says, “we are pushing both our medical and food systems to such extremes that we have to threaten one to temporarily relieve stress on the other.” He feels that this poses a great threat to one of humankind’s greatest medical resource, our antibiotics.

Researcher Stubbs counters saying, “Our study is not saying that people should start putting ciprofloxacin directly onto their weeds … if you do that, you will be contributing to antimicrobial resistance.” He continues, “We have shown that this [inhibition of plant DNA gyrase] is possible, which is really cool, but huge amounts of work will be necessary to achieve it completely.”

The team plan to extend their study by evaluating different types of fluoroquinolones that act in a similar manner and tweaking these structures accordingly to see if they can get similar results.

Conclusion

It has always held true that reality is often stranger than fiction. Just like the fluoroquinolones, there are researchers and scientists who see toxic products like glyphosate as benign. Despite being implicated in a whole host of health maladies, saturating our land, water, and food, they view glyphosate as useful product that has reached its life expectancy and needs to be replaced. Unfortunately, instead of searching out safer alternatives, their thinking is shaped by an academic educational system that is likewise saturated with pressure from the pharmaceutical industry. An industry that controls their every thought through textbooks, funding, and peer reviewed research.

I see herbicides as the next unfortunate step in the ever progressing evolution of the fluoroquinolones.

You can’t make this stuff up, and with Halloween in close proximity I, tongue-in-cheek, have various titles swirling through my head; one of them is “The Antibiotic That Took Over The World.” Soon it seems, the fluoroquinolones, or their derivatives, will invade every aspect of our lives.

I close this article with my thoughts I had before drifting off to sleep. New herbicide brand names were swirling in my head, Levacide, Floxicide, ….well you get the idea. What could possibly go wrong?

Or better yet, maybe they’ll develop a new human antibiotic based on glyphosate, or a glyphosate fluoroquinolone combination.

Needless to say, I didn’t sleep well.

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The FDA Fails Again With Fluoroquinolone Psychiatric Labeling Changes

“More and more people are having psychiatric problems as a result of these drugs,” said Dr. Charles Bennett referring to adverse events caused by the Fluoroquinolones, a commonly prescribed family of powerful antibiotics.

Bennett’s group SONAR (The Southern Network on Adverse Reaction project) based out of University of South Carolina School of Medicine provides a systematic approach to pharmacovigilance and drug safety. Wherever necessary, SONAR seeks to make global policy changes that reflect the true dangers that certain drugs could pose to the general public.

Dr. Bennett and Sonar have been tireless advocates in their pursuit to bring the dangers of the Fluoroquinolones into the public eye.

In regard to their penchant for causing psychiatric problems, amongst other life-altering adverse events, Bennett says, “It’s just a hidden secret. It should not be a hidden secret.”

Dr. Bennett’s words ring true. The mental health adverse events caused by the Fluoroquinolones such as levofloxacin (Levaquin), ciprofloxacin (Cipro), moxifloxacin (Avelox), ofloxacin and gemifloxacin (Factive) to name a few, have long been a hidden secret; a secret too easily dismissed and relegated to the fringes of medicine.

The Petition

The psychiatric adverse events needed to be brought into the light. So much so that on June 17, 2019, SONAR and Dr. Bennett submitted a citizen petition to the FDA requesting a black box warning to specifically identify psychiatric adverse events, including suicide and suicide-related adverse events.

The citizen petition also requested the FDA add Fluoroquinolone-Associated Disability (FQAD) to the black box warning and implement a risk evaluation and mitigation strategy for the drugs. FQAD was a termed coined by the FDA in 2015 during its formal review identification for a constellation of symptoms that have been identified in the FDA’s Adverse Event Reporting System (FAERS) in review of data in the fluoroquinolone safety reports.

Bennett’s petition was the last in a series of proposed labels changes highlighting the inherent dangers of the Fluoroquinolone.

Not Safe

The Fluoroquinolones have slipped through the cracks of the medical establishment. Personally, I hear from hundreds of individuals each year who have been permanently damaged harmed in one way or another by these drugs and whose pleas for help and justice fall on deaf ears.

I have also worked with Dr. Bennett on several occasions and contributed to his “Fluoroquinolone-associated Suicide” paper published in the European Journal of Medicine on July 20, 2018, that highlights the neuro-psych dangers of these drugs.

Many medical practitioners believe that these drugs have a proven safety and efficacy record, when in fact the opposite is true. The spectrum of damages that one can experience, including psychiatric problems, along with their documented ability to cause delayed adverse events, falls outside the diagnostic paradigm of most medical practitioners who in-turn view these claims as preposterous.

Many practitioners either miss these adverse events or attribute them to something else. Either way, this perpetuates the false safety record of the drug and the suffering experienced by an untold number of individuals.

Disappointing Response

The FDA’s response to the latest label change petition confirms what Dr Bennett and other advocates like me, have said. On August 28, 2020, more than a year after the citizen petition was submitted, the FDA denied their request saying the drug had already undergone numerous label updates to inform prescribers and patients of the drug’s risk.

“Such risks are adequately communicated in Levaquin’s approved labeling,” the FDA said in their denial letter. What the FDA is saying is that basically the drug family has enough warnings already, we don’t need to add more.

What the FDA fails to recognize is that although there are strict warnings on the labels, practitioners are still not heeding the warnings, with an estimated 22 million people in the United States use the generics of Levaquin and Cipro alone.

Recently, more doctors across the country have been prescribing Fluoroquinolones to treat COVID-19 related pneumonia.

In a news article ABC’s WRTV investigative news team reached out to Janssen, the maker of Levaquin, for a response to Bennett’s petition.

“At Janssen, our first priority is the well-being of the people who use our medicines. Janssen is reviewing the Safety Labeling Change Notification and working with the FDA to ensure labeling will be updated appropriately to facilitate the safe and appropriate use of LEVAQUIN®,” said Kelsey Buckholtz, Janssen spokesperson in a statement to RTV6. “LEVAQUIN® (levofloxacin) has been used for nearly 20 years to treat bacterial infections, including those that may be serious or life-threatening. LEVAQUIN® is part of the important fluoroquinolone class of anti-infective prescription medications, and its safety profile remains well-known and established.”

To reiterate, Janssen says that Levaquin’s safety profile “remains well-known and established.”

Levaquin’s True Safety Profile

Although it is hard to exactly quantify Levaquin’s true lethality because the FDA admits that only between 1% and 10% of all adverse events to pharmaceuticals ever get reported (1). Figuring conservatively at 10% reporting, between 1997 and 2020 Levaquin alone (not including other drugs in this family) has caused upwards of over 29,000 deaths and 461,000 adverse events. If you go with the 1% reporting percentage, the deaths go up to 290,000 and the adverse events to 4,000,000.

Levaquin Adverse Events 10% Reporting

Adverse Events 461,000 Death Cases 29,000

Levaquin Adverse Events 1% Reporting

Adverse Events 4,610,000 Death Cases 290,000

The true numbers of deaths, permanent disabilities, and walking wounded is much higher than what is assumed, which is horrifying.

Walking Wounded

The role of the Food and Drug Administration should be one of watchdog, watching out for the safety of the general public, but they fail appallingly. Instead, like a general that sends thousand of soldiers to their certain death just to erode the the enemy, the FDA does likewise. For the Food and Drug Administration it doesn’t matter how many people’s lives are utterly destroyed, just as long as some lives are saved and a disproportionate profit is earned.

For each live saved, how many lives are destroyed? Yes, the deaths are tragic but so are what I call the “walking wounded.” In first aid and triage the walking wounded are injured persons who are of a relatively low priority. The Fluoroquinolone walking wounded are much like the COVID-19 Long Haulers; those invisible people who are permanently maimed in the battle, but not counted as a tragic statistic. Thye are not the focus of the battle, but should be. I believe the true number of walking wounded that are associated with the Fluoroquinolones is incalculable.

Conclusion

If policy makers, like the FDA, continued to dismiss the alarms that are raised, it lessens the amount of energy put towards drug safety, curbing the use of these drugs, and researching academic medical solutions for the toxicity. Their repeated refusals to strengthen warnings on these dangerous drugs, reinforces bad practices by doctors and alienates the multitudes that become damaged and disabled from these medications. Thanks to the FDA and pressure from the pharmaceutical industry, Fluoroquinolone Toxicity does not have legitimate recognition. In other words, the problem continues on, relegated to the dark fringes of medicine, and it remains like what Dr. Bennett said, “a hidden secret.“

I have been in this for almost fourteen years and I have no idea the exact count of disenfranchised and damaged people wandering about like battle weary survivors of an apocalypse, and I probably never will. All I know is that they are there, and there many more than I had even begun to imagine when I started this dubious endeavor.

There is something inherently wrong with all the drugs that are based on the quinoline substrate. There is a thread of poorly understood idiosyncratic toxicity that spreads out like a crack in the foundation and affects all of the drugs based off of this platform.

There is enough evidence that the FDA knows about the fluoroquinolone toxicity epidemic that is happening, but their true client is the the industry and the FDA exists, first and foremost, towards protecting the interests of the manufacturers.

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So, You Want to Take A Fluoroquinolone Antibiotic?

Every once in a great while I am contacted by someone who, for one reason or another, insists that they must take a fluoroquinolone antibiotic. Because of this quandary, they inquire if there are ways to mitigate the risk of having an adverse event. If this describes you, then this article is for written for you.

Caveats

First, I have to throw in the disclaimer that I am not a doctor and any concerns regarding prescription medication needs to be discussed with your doctor. Second, you also agree to the obligatory disclaimer list on this site.

A Word of Warning

Now that we have the legal caveats out of the way I need to add one of my own. In my opinion, I would do everything I could to NOT take a fluoroquinolone antibiotic and try to opt for a safer alternative.

Obviously, my opinion is biased, but you need to know that taking the fluoroquinolones is much like playing Russian Roulette. Many people when they pull the trigger are fine, but you never know when the hammer is going to contact a loaded chamber and disaster will strike.

Another Warning

One thing is for certain, apart from a few exceptions, most individuals have no way of knowing ahead of time if they are going to have an adverse event to this family of drugs. Also, these drugs are cross-reactive, meaning if you have an adverse event to one member in this family of drugs, you will have an adverse event to another. There have also been cases of cross reaction between the quinolones and certain antimalarials (quinolines) which are chemical cousins so-to -speak. Additionally, once an adverse event ensues, there is no turning back the clock and reversing what has been done.

And Another Warning

Also, if you have already taken previous courses of fluoroquinolone antibiotics and believed you have been fine, cumulative toxicity is another factor that you must consider. Please read the article, Cumulative Toxicity of The Fluoroquinolones. Many people have taken multiple courses of the fluoroquinolones with seemingly no problems, however cumulative toxicity is a very real threat with these drugs that can rear its ugly head.

Hedging Your Bet Against An Adverse Event

Having covered the warnings, I realize that there are many different scenarios that could arise that would lead to your doctor recommending a fluoroquinolone. Far be it from me, or anyone else for that matter, to contradict what your doctor has deemed necessary for your medical care. My goal is to inform.

There are many, many variables that go into a person having an adverse event. Perhaps your genetics and environment make you an unlikely candidate for an adverse event because you are a genetically good metabolizer of chemicals and you live a fairly clean life with low toxic exposure. Also, short doses may well be tolerable for your body if your metabolism is favorable.

So if you are required to take a fluoroquinolone, or have made the personal choice to take a fluoroquinolone and have been educating in the risk/reward ratio, there are certain steps you can consider during a treatment to reduce the risk (not eliminate) of an adverse event.

1 Adjusting the treatment

Make sure that the dose is adjusted according to your weight. In other words, makes sure the doctor is not giving you a dose that is strong enough to treat an elephant. We have had many reports of people receiving much larger doses than would normally be deemed correct for their weight. Bottom line, why take more than what is needed (1).

2Take Magnesium

There is good scientific literature that Magnesium (or the lack thereof) can set the stage for an adverse event. Conversely, magnesium taken at the same time as taking a fluoroquinolone, interferes with the absorption. So, to keep your intracellular magnesium levels optimized and to avoid interfering with the fluoroquinolone dose, take magnesium at a separate time during the day. Many people in our society are deficient on magnesium and this is believed to play a part in adverse events in some people, plus magnesium has a protective role over many tissues (2).

3Drink Water During Treatment

It helps to maintain an adequate hydration of the tissues and facilitate the elimination of the drug and the metabolites through the kidneys, so drink plenty of water to remain properly hydrated.

4Avoid Steroids

Steroid use while taking fluoroquinolones is contraindicated. In other words, do not take any steroids during the treatment with the quinolone family of antibiotics, unless your doctor has deemed it completely necessary. There is research literature and plenty of anecdotal information that steroids dramatically increase the risk of adverse events. I understand that in certain circumstances your physician may have determined that taking a steroid while taking a fluoroquinolone is necessary (combined therapy). If this is the case, this advice is not to contradict your doctor’s medical advice. So, disregard this advice if you cannot avoid steroids but maybe discuss this concern with your doctor (4).

5Avoid Non-steroidal Anti-inflammatories (NSAIDs)

They amplify the negative effects of fluoroquinolones, specially the risk of central nervous system occurrences, and neuropathies. Many people unwittingly take these two together and combining these two dramatically increases the risk of an adverse event (5). You can also click here to read about Dr. Mark Noble of the University of Rochester, NY who had disturbing findings when researching Levaquin and NSAIDS.

6Watch for other Drug Interactions

Some drugs cause dangerous interactions with quinolones. All are included in the package insert so read the insert, check with a reputable website, or check with your pharmacist. There is quite a great chance that your doctor does not know or has not read it, seriously. (Levaquin, Cipro)

7Avoid Grapefruit

Grapefruit inhibits the actions of the liver enzymes that degrade the fluoroquinolones, so these antibiotics can reach very high concentrations in the blood. As a good preventive measure, eliminate grapefruit from your life, especially if you take other drugs on a regular basis.

8Watch Out for the Effects of Coffee (Caffeine)

Caffeine is a canary in a coal mine forewarning of danger. If caffeine starts to cause you problems such as restlessness, nervousness, disturbed sleep, etc… then it is time to consider that your liver is becoming overwhelmed by the fluoroquinolone you are taking. Some people have used this poor man’s test: Drink some coffee during treatment and watching out for changes. This supposes that you drank coffee before the treatment and were familiar with the normal effects that caffeine has on your body.

9Ask for Some Tests During Treatment (Especially Long Treatments)

Although what would consider long treatments is kind of subjective, for sake of discussion we will consider in this instance, those that last more than two weeks. You could discuss concerns with your doctor and ask for the normal tests plus the following:

Liver panel, especially bilirubin

Pancreas panel

Muscular enzymes (CPK, aldolase)

Immunological markers (sedimentation rate and ANA specially, and also IgE to the drug)

Cholesterol and triglycerides

Coenzyme Q10

Thyroid panel, TSH, free T3, free T4, PTH

Obviously not all doctors would be copacetic to allowing such tests to be run during the course of treatment, but in an ideal world it would be wise to monitor for subtle (and not so subtle) changes to your metabolism that would indicate a larger problem.

10Avoid Strong Sunlight (Ultraviolet Radiation)

Wear appropriate clothing and sunglasses to protect yourself against the photocarcinogenic action of fluoroquinolones.

11Perform Daily Provoking Tests

For example, do some repetitions of raising a weight like a box with the tips of your toes (resting the heels on the floor), or raising a bottle of water with the arm extended. If in a few days a strong tendinitis develops, it is time to bring the concern to stop the fluoroquinolone treatment to your doctor, right away.

Detoxing – After the Fact, Yet Another Warning

In order to bring complete gravity to the decision to take a fluoroquinolone antibiotic I would be remiss if I did not bring up one more point. I have also had people contact me who have taken a fluoroquinolone and started having an adverse event or a negative set of symptoms. They have contacted their doctor and he/she has told them to stop the medication and switch to something else. Their next question is, “how do I get the fluoroquinolone out of my system?”, “Can I detox it out?” Well unfortunately the answer is no.

While it is true that there are several substances that can interfere with the absorption of fluoroquinolones such as such as aluminum, magnesium, calcium, iron, and zinc (6), they must be present while the drug is being taken, which would defeat the purpose if you were taking it for its antibiotic properties. There is nothing that I am aware of that can chelate fluoroquinolones, or their metabolites, from the body if you want them removed in haste.

Fluoroquinolones are widely distributed throughout the body with high tissue penetration; that is what they do, and that is what the are good at. They are a synthetic product that does not ‘detox,’ at least according to the detoxing paradigms of both allopathic or alternative medicine. I have more about detoxing fluoroquinolones list in my FAQ section, you can read it here.

Since the fluoroquinolones are manly eliminated by the renal route (non-renal routes to a much lesser extent), staying well hydrated as to flush the remaining drug and its metabolites our of the body though the natural process of elimination, is about the only thing you can do, besides wait and see.

Conclusion

Obviously if you got this far you certainly read my warnings near the beginning of this article, so there is no reason to rehash them again. The main purpose of this website is to inform. Many people in our world today do not have enough information to make informed decisions when taking pharmaceuticals. It is best to have all the information available so that it spurs meaningful discussions with your doctor about the risk/rewards and safer alternatives.

The choice to take or not no take a fluoroquinolone antibiotic is a personal decision that is based on many factors. I, nor anyone else, can make the decision for you. The only thing I can do is to tell you that many, many people have taken these drugs and have regretted the decision. Many were not informed beforehand. Knowledge is power, use it wisely.

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Avoid These Four Psychological Pitfalls After Floxing

Unlike many of the articles on this website, this article is specifically directed to those who are newly floxed, although veteran floxies may also relate to some of the issues discussed.

For the person that is starting to become aware, or at least suspecting, that their health issues could be the result of damage by the Fluoroquinolones (Levaquin Cipro, Avelox, Floxin, etc…), the amount of data that you can be faced with is often overwhelming, frustrating, and just downright depressing.

When trying to assimilate information about a subject that is often dismissed by the medical community and that is scattered over a broad playing field, a person can be faced with several disadvantages. Some of these disadvantages can become psychological pitfalls and if you are not careful and they, in-turn, can hamper your progress.

The first pitfall: Separating Facts from codswallop, also known as poppycock, balderdash, hog wash, and the like.

There nothing like starting out with a hard and sensitive subject. This pitfall is one of the most difficult pitfalls for many people and a subject that I could write volumes on: The sorting of facts from opinions and personal belief.

For some, this pitfall arises because of the ambiguity between real medical research and personal opinion. These opinions, which are often well-meaning, can range all over the place from the practical to the downright bizarre, and they can come from various sources, some of them seemingly quite credible. These sources encompass countless floxed ‘experts’ that you find populating online forums and groups (myself included) to doctors who, although they have the moniker of M.D. by their name, wouldn’t know a floxed person if the surgeon general himself came up and put their arm around them.

Bottom line, the task of discerning good data from bad data can be overwhelming.

If you are a data driven person, the ugly truth is, when it comes to Fluoroquinolone toxicity, there are actually very few officially documented facts. Some folks, especially those with a science background, are often shocked by the paucity of research that has been done, despite the many years that have gone by and the sheer amount of people affected. Many times these well-meaning newcomers will march off, disgusted that I and others haven’t done more, hoping to change the world, that is, until they run into the FDA, AMA, and the whole “for-profit” medical industry.

In a nutshell, there are many reasons that explain the lack of robust medical research that has gone into Fluoroquinolone toxicity, but the nitty-gritty is that the drug companies control our “for profit” medical industry through funding and data. Even now, in many medical circles, Fluoroquinolone toxicity, is much like the Bermuda Triangle or Bigfoot, completely relegated to the lunatic fringe.

Getting back to facts. There are good facts that bolster our case against the Fluoroquinolones. Much of it is spread out across a large playing field and it is not connected together and this can be a daunting task that requires hours of research. Also, of the existing Fluoroquinolone facts that are available, we do have some good facts, but conversely we also have questionable facts despite having authors with seemingly impeccable credentials.

An example of a good simple documented fact about Fluoroquinolones is that they are Topoisomerase 2 Inhibitors. Again, this is a known and documented fact. Another fact is that they are chemotherapeutic agents that exhibit anti-cancer or anti-tumor tendencies. Again, both of these facts have been documented well in research.

However, just because the research has a supposed authoritative source, doesn’t mean the facts are actually good facts. An example of a questionable fact is that Fluoroquinolones have a good safety record. Although the science proving Fluoroquinolone safety is readily accepted by doctors, much of the science that supports Fluoroquinolone safety it is fraught with drug interference and author bias. These supposed documented safety facts, are also contradicted by the lived experience of thousands of individuals who have become disabled over the last several decades and is backed up by the FDA’s own data.

Tip: Always look at author bias or author motives in the data that is being presented. Is the author representing the pharmaceutical industry? Or, is the author selling something? (Hint: I am not in this for the notoriety, fame or money).

So how do I filter out truth? I look at the data (medical science, research, current medical practices) and then compare it with the truckload of anecdotal information and form my opinions. I have to admit that I am in the unique position of having access to a lot of anecdotal information. But let me say one more thing about this point.

Many, many people in the floxed community, who are mostly well-meaning, incorporate personal opinions about the Fluoroquinolones into their personal belief system and these belief systems exist at the sub-conscious level. Again, although well meaning, these beliefs can be incorrect but because of lived experiences or other influences this erroneous data is often believed to be correct. Let me give you an example:

There is a belief that circulates around the Fluoroquinolones community that NSAIDS are bad for floxed people, despite the paucity of data that backs up the belief. While it is true that NSAIDS are contraindicated and should not be taken WHILE a person is currently taking an Fluoroquinolones, there really is no hard science to show that they cannot be taken later, after an adverse event. The truth is, some people find out they can take them with no problem, while others cannot. Still, you have die-hard individuals telling the newly floxed, “You can never take another NSAID again!” or “NSAIDS will always cause a bad reaction post floxing.” These statements are coming from a belief system, albeit an erroneous one.

On a side note, do you know what happens when you question a belief system? You usually get anger as a response. If you question a person and get anger in response, you have tapped into their belief system. Social media is fraught with belief centered confrontations, especially during the COVID-19 pandemic.

Bottom line: Always be proactive and question medical knowledge that will be applied to your personal situation, regardless of the source. It doesn’t matter if it is safe for others, the question is, is it safe for you?

The second pitfall: Putting all your eggs in one basket.

Some people may think that my website (as great as it may be), or another website dealing with Fluoroquinolone toxicity, or a certain Facebook forum, or a certain floxed solution ebook sold elsewhere on the internet, are great authoritative compendiums of information. So much so, that they do not have the need to look for information elsewhere. Avoid this pitfall by looking at all sources of information that you glean from other sources, with a critical, detached attitude. Use the all information for your personal benefit by adjusting it to your own expanding awareness and your lived reality. For example, because of your own unique physiology you may get very ill taking a supplement that everyone else finds perfectly safe.

Don’t go overboard, but look at data from other sources? Do they agree with one another? Is there a general consensus?

Basing your decisions on one fact or piece of data can be very dangerous.

Mark Twain once said, “Be careful about reading health books. You may die of a misprint.”

The third pitfall: Watch out for Hypochondria.

Please do not read this website, the Flox report, listen to other ‘experts’ in Facebook groups or discussion forums and start believing that you have all the symptoms of any Fluoroquinolone Toxicity. Doing this you will end up convinced that you are suffering a far worse reaction than it really is, and that will make you suffer unnecessarily.

Recently, I believed I could have some symptoms from heavy metal poisoning, which can be real concern post floxing. To gather more information, I joined a Gadolinium forum to search out some specific information on various detoxing regimens from heavy metals. Boy was that a mistake! It was like taking an adventure into an alternative parallel universe. If I had not compiled the learned experienced of over 14 years in the flox community, I would have walked away devastated. I literally saw many of people with symptoms who were in search of a cause. Hear me…. I am not saying that Gadolinium deposition disease is not real, nor am I saying that people don’t suffer greatly from it, I am just using this to make a point.

I have seen this very exact thing play out in the floxed community hundreds of times over the last decade; some floxed individuals want, at all costs, to match their reactions against data and experiences of others in order to create an instrument to rate their adverse event (AE) or symptoms. They look for a precise timetable of recovery from others, who are eager to give it out, and then try to make plans to foresee every event that is going to happen to them during their recovery. Let me let you in on a little hint…no one can do that. Predicting the future, is not its objective of this website and it should not be the objective of any other source of data either.

While it is true, I and maybe some others, can give you a general idea of what floxing is and the suffering that is caused by Fluoroquinolones, I cannot, and neither can others, evaluate your individual case and determine its outcome or course of progression.

Bottom line: There are no prophets in the Fluoroquinolone community.

There was a person, who, in one of the Facebook forums, was handing out timeline advice like candy that was based on their own personal experience. They would tell people, “your digestive issues should clear up by the 6-month mark” or “an average reaction takes about two years to complete,” etc…

If after being told this information by someone who seems well respected, you try to establish at all costs the predicted recovery date for that symptom of yours, you will surely get very anxious and depressed when your digestion is not normal by month 12.

If you attempt to use the opinions of others as a complete guide for your illness, you will become frustrated and you will lose the necessary perspective and strength to handle your intoxication from the proper perspective.

Floxing is a life altering experience that does not resemble any normal illness process that you have experienced before in your life or have come to learn about, like post-surgery recovery, healing an infection, or post-traumatic recuperation. Most likely, all health issues that you had prior to the floxing started to heal as soon as the offending agent was removed. This is not the case with quinolones. They are synthetic DNA damaging/altering chemotherapeutic agent.

The hard truth is, some floxed folks will feel progressively worse for months or maybe years before returning to a normal functional life achieved. Most people are programmed under our current medical system, that there is something that can be done such as take a prescription medication, put a Band-Aid on the wound, or perform some rehabilitation exercises. Fluoroquinolones toxicity is different.

For most nothing can be done to halt or reverse an AE from Fluoroquinolones after the end of treatment. It is very much like suffering from a chronic degenerative illness and has many overlaps with gulf war syndrome, lyme, lupus, multiple sclerosis and others.

However, if you have one or even several symptoms of a severe AE, that does NOT mean that you are destined for a severe AE, and no one can predict its outcome. It truly is the whole complete picture that counts. I have seen too many floxed persons that have mild AE’s become hypochondriacs worrying about the possibility of having a severe AE and magnifying real or imaginary symptoms to match those of a severe AE.

Tip: Never, I mean never, take healing advice or timeline advice from someone who claimed to have been healed from Fluoroquinolone Toxicity in six month or less. The overwhelming chances are, they were never floxed in the first place.

The fourth pitfall: Becoming Overzealous.

Having partially fallen into this overzealous trap myself early on in my floxing, it is another extremely common mistake to be overcome overzealous in your search for exact answers, explanations, cures, treatments, timetables and protocols for every minor symptom that shows up.

Even people considered extremely healthy have negligible physical changes or events that take place in their life that are totally ignorable. Overreaction to the Fluoroquinolone AE can cause floxies to become worried and look for Fluoroquinolones lying in wait at every corner of their lives, or extremely afraid and obsessive about potential negative influences of normal habits, like taking a shower with tap water tainted with fluoride.

At the same time, this does not mean that you should not adhere to good medical practice and have new or unusual symptoms evaluated by a competent medical professional. About eight years into my floxing I kept getting some abdominal pain in my lower right abdomen. I assumed that it was a muscle spasm, and due to my medical knowledge, I even convinced my doctor that it was muscle spasms as well. Wrong, it ended up being my gallbladder that was displaying atypical symptoms.

Bottom line: Be proactive and advocate for your health, but please do not look at your entire life through the Fluoroquinolone lens. This only adds anxiety and despair to the already intense impact of being floxed.

Conclusion

Above all else keep in mind that your floxing experience is unique one that centers around your physiology. Floxing experiences are novel, probably more novel than the coronavirus SARSCOV2. No person (not even me), no report, no Facebook group, no Twitter post can substitute for your own personal knowledge about your symptoms, your recovery and all your health aspects.

Our medical system today has its strengths and weaknesses. It is very good at triage and very bad at pharmaceutical interventions. No one wants to go through the terrible experience of floxing, as floxing represents the darker side of our medical system. Most floxies end up here through no fault of their own. Instead, they trusted the advice of someone who was suppose to be an expert.

If you are new to this plight, do yourself a favor, first be kind to yourself, and the try not to fall into these four psychological pitfalls.

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COVID-19 Preventative and Critical Care Management Protocol

Introduction

The entire world is currently on hold due to the coronavirus and I realize that it affects everyone’s lives in a negative fashion. For me, the effects have been far ranging. Personally, we have been isolated from loved ones and have even had someone in our extended family die, due to the virus. It has put current FQ research on hold, as the researchers that I was working with have had to refocus their efforts.

As most of my readers know, FQ Toxicity is a devastating syndrome that impacts each person in various ways. It changes a person’s perception on life, and it adjusts how they approach life in general. One of these ways is to do everything in one’s power to mitigate further risk from medications and diseases.

Floxed people are some of the most health conscious people I know, and with good reason. Many have bodies who are now in a more fragile state of health, so they do what they can to stay healthy and try to avoid getting any further illness or disease.

Prevention

One of the more common questions I get asked is, “what can I do to increase my chances to prevent from getting COVID-19?”

If you have searched the internet you know it is a confusing place. As the old saying goes, the opinions on COVID-19 are like belly buttons, everyone has one. And to listen to all those opinions, even ‘so-called’ expert ones, is an exercise in futility and confusion. It is like the weather in Illinois, give it a moment and it will change. Also, try this experiment, post an opinion on COVID-19 and see what happens. If you have been seeing the same things that I have, you will get numerous ‘expert’ opinions.

The internet has one big fault, well, actually two, but who is counting. Anyway, there is too much information, and it overwhelms the senses. Also, anyone can find any numbers of so-called expert sources to bolster their prejudices.

Recently the East Virginia Medical School’s (EVMS) released the Critical Care COVID-19 Management Protocol. This protocol is updated periodically to reflect current critical care knowledge. This is one of the better COVID-19 critical care management guidelines (even includes Vitamin C IV’s and other supplements) that I have seen.

Their motto is “If what you are doing ain’t working, change what you are doing.”

That is a motto that I can relate to.

As part of their Critical Care COVID-19 Management Protocol, they have preventative (prophylaxis) guidelines for supplements you can take at home. Let me throw in the caveat that I know that some Floxed people cannot take some of these supplements for various reasons, so you should use common sense and consult your trusted health care professional to tailor this list for your situation.

Prophylaxis

While there is very limited data (and none specific for COVID-19), the following “cocktail” may have a role in the prevention/mitigation of COVID-19 disease. While there is no high-level evidence that this cocktail is effective; it is cheap, safe and widely available.

Vitamin C 500 mg BID and Quercetin 250-500 mg BID

Zinc 75-100 mg/day (acetate, gluconate or picolinate). Zinc lozenges are preferred. After 1 month, reduce the dose to 30-50 mg/day.

Melatonin (slow release): Begin with 0.3mg and increase as tolerated to 2 mg at night

Vitamin D3 1000-4000 u/day

On a side note I want to give Selenium, Vitamin A, and S-acetyl-glutathione a strong consideration for addition.

Critical Care COVID-19 Management Protocol.

Those that know me, know that I am no friend of governmental medical agencies, however I will give credit where credit is due.

For the most part I believe that good COVID-19 emergency protocols, unfortunately, are still not being used here in Illinois (at least in the area I live in). We had an extended relative die of COVID recently who was older with no comorbidities and lived near Chicago. I am pretty sure after talking with family that something like this wasn’t followed.

The PDF version of this Critical Care COVID-19 Management Protocol would be good to have available. God forbid, if you would have to go to the ER for COVID-19, it would be a time of turmoil so having something to use as a guideline would be extremely helpful. I am not fully endorsing all the drugs listed, but this document could be used to facilitate conversations with your doctors to formulate an action plan or to determine if the facility you are at is competent enough to offer you the best medical care.

Here is the link to the PDF.

In Summary

My advice for floxies is still to try and do everything humanely possible to avoid getting COVID-19. I won’t go into the lengthy details but it can easily be proven that it is much more serious than the flu and should not be compared to the flu, it can have long term health impacts, even in healthy people, and can be very deadly for those in certain demographics. Don’t live in fear, but don’t take any unnecessary chanced. Humankind has been dealing with this for too short a period of time to fully know all the implications, and because of this we must err on the side of caution.

Having said all that, I still understand that people need to live and survive in this imperfect world.

I currently do not have any data about any chronically ill floxies who have contracted COVID-19. When I have some credible data to share from reliable sources about floxed COVID-19 cases, I will get that data out as soon as possible.

Please, be safe everyone.

#Advocacy #Coronavirus #COVID-19 #Supplements

New Post has been published on My Quin Story

New Post has been published on http://www.myquinstory.info/what-everyone-must-know-about-using-antimalarials-for-the-coronavirus/

What Everyone Must Know About using Antimalarials for the Coronavirus

As a drug safety advocate specializing in quinolone antibiotics, namely the fluoroquinolones (FQ’s), I have learned about both the history and the chemical compositions of this drug family. Because of this, I am very familiar with the chemical links to the quinoline pharmacophore including the anti-malarial drugs in this class.

Based on everything I have learned over that time and have seen other’s personal experiences, I am not a proponent of any pharmaceutical that is based on the quinoline pharmacophore.

My research has led me to believe there is something inherently wrong with the all drugs that are based on this substrate. It can be shown, going all the way back to the natural alkaloid from the cinchona tree, that there is a thread of idiosyncratic toxicity that is poorly understood that spreads out like a crack in the foundation. This idiosyncratic toxicity loosely affects all of the drugs based off of this platform. Again, this includes all the quinolone antibiotics and the quinoline antimalarials, more specifically chloroquine, hydroxychloroquine, and mefloquine.

Antimalarials, COVID-19, and Safety Concerns

Recently, chloroquine and a similar drug, hydroxychloroquine (plaquenil), showed encouraging signs in small, early tests against the coronavirus, COVID-19. Yet those preliminary studies sparked intense interest after President Donald Trump tweeted that hydroxychloroquine plus an antibiotic could be “one of the biggest game changers in the history of medicine” and should “be put in use immediately.” He cited a French study that gave the combo to only six patients.

Dr Eric Topol

“It is a very weak study … leaving us in suspension of whether the combination strategy has any merit,” said Dr. Eric Topol, a cardiologist and head of the Scripps Research Translational Institute in San Diego.

But the drugs have do have major side effects, one reason scientists that know about them don’t want to give them without evidence of their value, even in this emergency.

Meghan May

“Chloroquine is an extremely toxic drug with a terrible side effect profile. Hydroxychloroquine is far safer, but its side effects are still significant,” Meghan May, a microbiologist at the University of New England College of Osteopathic Medicine in Biddeford, Maine, wrote recently in an email.

Nevertheless, excitement about treating the new coronavirus with malaria drugs has garnered massive media attention after the mention from President Trump.

Chloroquine seems to work by acting as an “ionophore” and helping zinc to enter the cell to inhibit viral replication. Something I wrote about here.

Right now, the evidence that they may help the broad population is thin, and a run on the drugs is complicating access for a select group of people who need them for rheumatoid arthritis or lupus.

Sounding the Alarm About Antimalarial Use

Dr. Remington Nevin

The Quinism Foundation has warned of a risk of sudden and lasting neuropsychiatric effects from the use of antimalarial quinolines against COVID‑19, and has urged policy makers, physicians, and members of the public to be alert to such effects.

“The same endosomotropic properties that likely underlie the effectiveness of quinoline antimalarial drugs such as chloroquine and hydroxychloroquine against the virus may also underlie their dangers, ” said Dr. Remington Nevin, MD, MPH, DrPH, a Johns-Hopkins trained psychiatric epidemiologist and drug safety expert and former U.S. Army public health physician, who now serves as Executive Director of The Quinism Foundation. “These are not safe drugs.”

Read their official press release here: The Quinism Foundation Warns of Dangers from Use of Antimalarial Quinolines Against COVID‑19

Safer Way of Dealing with COVID-19

On such safer way to deal with COVD-19 is outlined in this article from Italy.

It is the asymptomatic carriers that are mainly responsible for spreading the disease. If you successfully locate them via readily available testing and subsequently quarantine them for a reasonable period of time, you can stop the spread of this virus in its tracks.

Deadly Assumption

Driven by media hype, the general public and even medical researchers, often make the assumption that because a drug has been around for a long time it has an acceptable toxicity profile. In other words, if it has passed the test of time, it is acceptable for use. In reality, nothing could be further from the truth, especially with quinoline based pharmaceuticals.

Antimalarial quinolines have been commonly prescribed in the past, but it is important to note that a substantial number of patients need to discontinue the drugs early owing to the development of serious adverse events.

Like quinolone antibiotics, quinoline antimalarials display idiosyncratic adverse events that can cause irreversible adverse events even when used at relatively low doses. It is usually never known ahead of time who is susceptible to these adverse events and often when a patient experiences them, it is too late, and the adverse events do not stop after discontinuation.

“During any outbreaks of epidemic and pandemic levels, there is hardly any time left for new drug development and clinical trials,” said Sunit K. Singh, PhD, a professor of molecular immunology & virology and head of the molecular biology unit at Banaras Hindu University’s Institute of Medical Sciences in Varanasi, India. Therefore clinicians will turn to trying existing drugs, known as “repurposing.”

The CVOID-19 presents society with a desperate situation. In desperate times humans often resorts to desperate measures. History is replete with lessons that caution against resorting to haste in times of desperation because during these times well-meaning cures can become the cure that kills instead.

Sources:

NCBI: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6149725/

AP News: https://apnews.com/2f3dd1099c6054bb5015391b9a6f3b0c

The Guardian: https://www.theguardian.com/commentisfree/2020/mar/20/eradicated-coronavirus-mass-testing-covid-19-italy-vo

The Quinism Foundation: https://quinism.org/press-releases/dangers-of-antimalarial-quinolines-against-covid-19/

#Advocacy #Antimalarials #Coronavirus #COVID-19

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