Jerzy Tyszkowski

CEO Fluoroquinolone Toxicity Study

[Fluoroquinolone Toxicity Study @FQ_100]

Help Lauren Support FQ Advocacy!

Lauren, a former high school teacher living with disabling fluoroquinolone adverse effects, is working to bring this issue to the attention of the N. Carolina Attorney General. She is requesting a meeting with the Attorney General’s office and would be accompanied by Dr. Charles Bennett** to discuss the serious, lasting consequences and inadequate warnings, starting in her State.

Personal stories can help demonstrate that these experiences are NOT isolated. If you would like to support Lauren’s efforts, particularly if you live in North Carolina, please consider submitting a short written account of what happened to you.

✅Lauren has asked that you emphasize that the patient literature did not accurately reflect the scope of your adverse reactions

Your story could also include:

✅The adverse effects you are experiencing and for how long
✅How your health, employment, finances or family life have been affected
✅Whether you were warned about the possibility of disabling or potentially irreversible adverse effects
✅Any difficulty you experienced obtaining medical recognition, documentation, treatment or disability benefits

Even a few paragraphs can help put a human face on this issue. Each personal account adds to a clearer picture of how fluoroquinolone adverse effects can affect individuals, families and the broader healthcare and disability systems.

➥➥ Please send your story to Attorney General Jackson: [email protected]

✨✨Thank you for helping Lauren ensure that the experiences of this community are heard and taken seriously✨✨

** Dr. Bennett - is a hematologist, oncologist and professor in the Department of Clinical Pharmacy and Outcomes Sciences at the University of South Carolina College of Pharmacy. His career has focused on identifying, investigating and helping prevent serious adverse drug events. He founded the Research on Adverse Drug Events and Reports program and is affiliated with the Southern Network on Adverse Reactions, a pharmacovigilance network involving researchers from approximately 50 medical universities. He has significant knowledge on the issues surrounding FQ medications.

[Secretary Kennedy @SecKennedy]

I thank the House of Representatives for passing H.R. 4348, the Kay Hagan Tick Reauthorization Act. Tackling tick-borne illnesses like Lyme disease is a top priority for @HHSGov. Thank you to Rep. Chris Smith and everyone who championed this legislation. This bill strengthens our efforts to improve the prevention, diagnosis, and treatment of tick-borne diseases.

[Jerzy Tyszkowski @TyszkowskiJerzy]

@RobertKennedyJr My greatest concern is that fluoroquinolones, despite multiple FDA boxed warnings, are being used and will continue to be used for Lyme disease. Our Foundation has heard from thousands of patients. We’d value a meeting to share critical information. https://t.co/01inZrD0wP

[Fluoroquinolone Toxicity Study @FQ_100]

Why FQAD Patients Often Become Highly Sensitive to PVC Odors, Perfumes, Detergents, Exhaust, and “Everyday Chemicals”

A striking number of people who report fluoroquinolone-associated disability (FQAD*) also describe a second, life-shrinking problem that can feel even harder to explain to clinicians: after the antibiotic injury, ordinary smells and low-level exposures start triggering coughing, burning eyes, throat tightness, skin stinging, dizziness, tachycardia, headaches, brain fog, nausea, and a sense of “system overload.” Patients name PVC and “new vinyl” odors, perfume and fragranced personal care products, laundry detergents and fabric softeners, cleaning sprays, “new clothes smell,” plastic tubing or catheters, IV infusion sets, glues, paints, solvents, cigarette smoke, moldy buildings, gasoline fumes, diesel exhaust, and even the smell inside a new car. Many also notice that the same hypersensitivity pattern extends into food, especially additives (natural flavors/MSG etc), alcohol, caffeine, and foods that behave like triggers rather than nutrition.

This cluster of experiences overlaps with what the literature describes as multiple chemical sensitivity (MCS) or chemical intolerance:
✏️symptoms triggered by low-dose exposures that were previously tolerated, often involving multiple organ systems and common comorbidities (migraine, cough hypersensitivity, asthma-like symptoms, and pain syndromes).
Population surveys also show that fragrance sensitivity and MCS-type reactions are not rare at the population level, and that fragranced consumer products can provoke significant symptoms in susceptible people. The key point is that the “trigger list” patients give is not random: many of these exposures share chemistry that activates the same biological alarm pathways in the airways, skin, and nervous system - “sensitized sensory detection.” The nose, eyes, throat, and upper airways are wired with chemosensory nerves whose job is to detect threat. Certain receptors on these nerves - particularly TRP channels such as TRPA1 and TRPV1 - are activated by reactive chemicals, oxidants, and constituents of smoke/smog, and they can drive irritation, cough reflexes, and neurogenic inflammation when repeatedly triggered. When these pathways become hypersensitive, a small exposure that would be meaningless to most people can provoke a disproportionately large response. This idea is consistent with cough hypersensitivity syndrome research, where chronic cough is increasingly understood as a disorder of hypersensitized peripheral and central neural circuits rather than “just” a lung problem.

☑️ FQAD offers several plausible biological bridges into this hypersensitive state. Fluoroquinolones are well known for neurotoxicity patterns in susceptible situations, and mechanistic reviews describe CNS excitability via inhibition of GABAergic signaling and related pathways. Older pharmacology work also showed that quinolones can interfere with GABA receptor binding, with heightened risk when combined with other factors that lower seizure threshold (classically methylxanthines/theophylline and some NSAIDs), reinforcing the concept of a nervous system pushed toward hyperexcitability. In real life, that “excitability” is often experienced not as seizures but as exaggerated startle, sensory intolerance, sleep disruption, panic-like surges, and a lowered threshold for triggers. Once the nervous system is primed, airway and skin sensory circuits can behave similarly: smells “hit harder,” cough reflex fires earlier, and skin reacts to contact that used to be benign.

☑️ A second bridge is inflammatory amplification. Many of the exposures listed - fragrances, cleaning products, solvents, smoke, exhaust - contain volatile organic compounds (VOCs) that are documented irritants and can provoke eye/nose/throat irritation, headaches, nausea, and neurologic symptoms at sufficient exposure. Diesel exhaust is specifically described as an irritant that can trigger cough and respiratory symptoms, headaches, lightheadedness, and nausea. Gasoline vapors are similarly described as causing nose/throat irritation and systemic symptoms such as headache, dizziness, nausea, and breathing difficulties. In a sensitized person, the “dose that matters” can be far lower than typical occupational assumptions, because the limiting factor becomes the threshold of the alarm system rather than the toxicity of a single compound.

☑️ PVC and many medical plastics deserve special attention because patients frequently single them out. The “PVC smell” people describe is often not the polymer itself but the chemical ecosystem around it: plasticizers, residual solvents, stabilizers, and degradation products that off-gas or migrate. Indoor air science has a well-studied example: 2-ethyl-1-hexanol (2EH), which can appear in buildings due to hydrolysis of plasticizers and flooring adhesives and is associated with mucous membrane irritation and eye discomfort in human studies. On the medical device side, there is direct evidence that phthalates can leach from a variety of medical supplies; the 2023 analysis documenting leaching across products provides a concrete mechanistic reason why “catheters and infusion sets” can be real triggers for some individuals. Even “DEHP-free” labeling does not always mean “zero leaching,” which matters for highly reactive patients. In an FQAD/MCS-like context, this becomes part of the lived experience:

➦a chemically vulnerable system can respond to trace exposures that most bodies ignore.

☑️ Textiles are another common complaint that sounds odd until you look at the dermatology literature. Textile fibers are rarely the primary allergen; the culprits are often what’s added to fabrics - dyes, resins, finishing agents, rubber components, antimicrobials, and other performance chemicals. Reviews on textile contact dermatitis emphasize that allergic contact dermatitis from textiles is commonly due to these additives rather than the fiber itself, and patch testing often needs to include the patient’s own materials. This matches what many FQAD patients report:

➦burning, stinging, or rash from “new clothes,” certain synthetic blends, elastic bands, compression garments, or even uniforms that have strong manufacturing odors.

☑️Mold and damp buildings also belong on the core trigger list, not as a vague catch-all but because epidemiologic reviews consistently associate dampness/mold with increased respiratory and allergic health risks. Many patients describe that “moldy air” produces immediate cough, sinus burning, and brain fog; in a sensitized airway, microbial volatile organic compounds (MVOCs) and irritants can act as reliable triggers even when the visible mold is minimal.

☑️Home and consumer products add another layer. Fresh paint, sealants, epoxy, silicone caulk, new carpeting, and new furniture can off-gas VOC mixtures; the U.S. EPA’s indoor air guidance explicitly lists irritation of eyes/nose/throat and systemic symptoms among potential effects of VOC exposures. Memory foam mattresses are a practical example that many patients mention: measurements show VOC emissions can peak soon after installation and decay over time, which fits the anecdotal pattern of “new mattress smell” provoking symptoms early on. For a chemically intolerant person, “below typical benchmarks” may still be far above their individualized threshold, especially during the first days.

☑️Food triggers can be integrated into the same framework without making speculative claims about one single pathway. Chemical intolerance models such as toxicant-induced loss of tolerance (TILT) explicitly describe a two-step pattern: an initiating exposure (or series of exposures) followed by new triggering from small quantities of previously tolerated chemicals, drugs, foods, and combinations (classically including caffeine and alcohol). Clinically, many FQAD patients describe “cross-sensitivities” where fragrances, solvents, and exhaust flare symptoms alongside certain foods - especially those high in additives, strongly fermented products, alcohol, caffeine, or foods that provoke histamine-like reactions.

❓❓❓“How long will this last?” …..duration may be variable. In the chemical intolerance/MCS literature, symptoms may persist for years in some individuals, especially when repeated exposures keep re-triggering sensitized pathways. Others improve substantially with strict trigger reduction, careful pacing, and stabilization of sleep and autonomic symptoms, suggesting that at least part of the hypersensitivity state is plastic rather than permanently fixed. The practical implication is not that patients must fear the world forever, but that the recovery curve often depends on reducing the frequency of “alarm hits” long enough for thresholds to recalibrate.

For day-to-day living, it helps to describe mitigation as “engineering + substitution,” not willpower. According to the literature, people tend to do best when they minimize fragranced products, use unscented detergents and personal care items, avoid fabric softeners and scented boosters, ventilate aggressively after any use of paint/solvent products, choose glass/metal where possible for food and water, and avoid time in garages, gas stations, or heavy traffic corridors when symptoms are flaring. In medical settings, patients often benefit from requesting the least-odorous supplies available and discussing options for low-leaching materials; the fact that measurable leaching from medical supplies exists supports taking these requests seriously. In buildings, prompt remediation of dampness and mold is rational based on the consistent respiratory risk associations in the literature. None of this replaces medical care; it simply reduces the trigger burden so the nervous-immune-airway system has a chance to settle.

The scientific debate is not whether people can be symptomatic from low-level exposures they clearly can, but why certain bodies become so reactive, and how best to reverse that state. The MCS literature argues that this is a complex biological condition with overlapping neural and inflammatory processes, and that the field needs to “catch up to the science.”

*FQAD - Fluoroquinolone Associated Disability - see more - In  2015, after victim testimonies before the Antimicrobial Drugs Advisory  Committee and the Drug Safety and Risk Management Advisory Committee of  the FDA, a cluster of recognized symptoms became known as FQAD  (Fluoroquinolone Associated Disability).  The CDC has yet to recognize FQAD.

💊Medications in the fluoroquinolone class (incl: Cipro/ciprofloxacin, Levaquin (off market)/levofloxacin, Avelox/moxifloxacin etc) in all forms for humans and pets: https://t.co/OKH2DOWix0

Find support and resources on our sites:
🌐Find Us: https://t.co/G9NJIEKEij
▶️ YouTube: https://t.co/lWJ0LMmfeq
🔵 Facebook: https://t.co/oVDvQDnync
🐦 X/Twitter: https://t.co/Gp9ZXyhyfZ

⚠️Disclaimer: Fluoroquinolone Toxicity Study does not provide medical advice, and all videos, articles and written content are intended for informational purposes only. We do our best to provide accurate information. Such information is not a substitute for professional medical advice, diagnosis or treatment. For multiple reasons, supplements, treatments, and pharmaceutical effects and outcomes can possibly vary significantly among those affected by fluoroquinolone drugs.

References

[1] Molot J, Sears M, Anisman H. Multiple chemical sensitivity: It’s time to catch up to the science. Neuroscience & Biobehavioral Reviews. 2023.
[2] Miller CS. Toxicant-induced loss of tolerance—an emerging theory of disease? Environmental Health Perspectives. 1997;105(Suppl 2):445–453.
[3] Miller CS. Toxicant-induced loss of tolerance (TILT). 2001.
[4] Bessac BF, Jordt S-E. TRPA1 and TRPV1 in airway chemosensation and reflex control. Physiology. 2008.
[5] Song WJ, et al. Cough hypersensitivity syndrome: a few more steps forward. 2017.
[6] Wakayama T, et al. Comprehensive review of 2-ethyl-1-hexanol as an indoor air pollutant. 2019.
[7] Wang W, Kannan K, et al. Leaching of phthalates from medical supplies and their implications for exposure. 2023.
[8] U.S. EPA. Volatile Organic Compounds’ Impact on Indoor Air Quality. Updated 2025.
[9] OEHHA (California). Health Effects of Diesel Exhaust. 2001.
[10] Illinois Department of Public Health. Gasoline: health effects.
[11] Svedman C, et al. Textile contact dermatitis: how fabrics can induce dermatitis. 2019.
[12] Mendell MJ, et al. Respiratory and allergic health effects of dampness, mold, and dampness-related agents: a review of the epidemiologic evidence. 2011.
[13] Beckett EM, et al. Evaluation of VOC emissions from memory foam mattresses and potential implications for consumer health risk. 2022.
[14] Anwar AI, et al. Fluoroquinolones: Neurological complications and side effects in clinical practice. 2024.
[15] Segev S, et al. Quinolones, theophylline, and diclofenac interactions with the GABA receptor. 1988.
[16] Steinemann A. National prevalence and effects of multiple chemical sensitivities and fragrance sensitivity. 2018.
#FQAwareness #Fluoroquinolones #MitochondrialHealth #AntibioticSideEffects #Floxed #Cipro #Levaquin #FQAD #mcs

[Jerzy Tyszkowski @TyszkowskiJerzy]

@PiotrWitczak_ to co chcieli zrobić w roku pięćdziesiątym pierwszym zrobili w osiemdziesiątym szóstym. niestety stałem się ofiarą tego systemu,

[Fluoroquinolone Toxicity Study @FQ_100]

Because we are seeing people having adverse effects after Lasik and cataract surgery we frequently like to provide this information:

🧿Eye Surgery, Antibiotics and Post-Op Drops: What Patients Should Know

Laser vision correction procedures such as LASIK, PRK, as well as cataract surgery are typically followed by a post-operative drop regimen designed to prevent infection, control inflammation, and support surface healing. During cataract surgery, your doctor may utilize an intracameral antibiotic (injected into the eye at the end of surgery) - which is often a fluoroquinolone antibiotic. In many clinics, patients receive an antibiotic eye drop together with a steroid drop, plus frequent artificial tears, especially during the first days after surgery [1]. The goal is straightforward: reduce bacterial risk during the early healing window and dampen inflammation that can drive pain, haze, light sensitivity, and delayed recovery [1].

In everyday practice, the antibiotic chosen is often a fluoroquinolone. Moxifloxacin is frequently referenced in post-LASIK care discussions and instructions, and ofloxacin is also used in some settings, largely because these agents offer broad antibacterial coverage and convenient dosing that supports adherence when patients are managing several drops at once [1].

➥What is less commonly emphasized to patients is that “topical” eye drops are not always purely local. Part of each dose can drain through the nasolacrimal system into the nasal mucosa, where absorption into the bloodstream can occur. For this reason, clinical drug monographs describe techniques such as gentle pressure over the tear duct region (nasolacrimal occlusion) or keeping the eyelids closed briefly after instillation to reduce systemic exposure [2]. Product monographs for ofloxacin ophthalmic solutions similarly note that a small amount may be systemically absorbed after topical use [3].

➥➥This distinction matters because fluoroquinolones, as a drug class, are associated with systemic adverse effects that come with Black Box warnings including tendon disorders and neurologic symptoms, which are well documented for oral and injectable formulations. Even if the probability is lower with eye drops, the possibility of systemic-type reactions is not conceptually “impossible,” particularly in susceptible individuals, and is discussed in drug monographs that acknowledge systemic absorption from ophthalmic use [3]. Separately, post-operative regimens often include a topical corticosteroid (for example, prednisolone acetate) alongside the antibiotic. Systemic literature on fluoroquinolones notes that corticosteroid exposure is a risk modifier for tendon injury, which is relevant when a fluoroquinolone and a steroid are used together, even if both are prescribed as drops [4].

The practical takeaway for patients is not to self-diagnose, but to recognize patterns and act early. If unusual tendon pain, tendon swelling, weakness, or new tingling and burning sensations develop after starting post-op drops, patients should promptly contact the treating clinician, describe the timing clearly, and ask whether the regimen should be adjusted, including whether a non-fluoroquinolone alternative is appropriate in that specific case. Patients can also ask the clinician to confirm the correct instillation technique to reduce systemic absorption, since this is explicitly discussed in pediatric and ophthalmic drug guidance [2]. For broader context, regulators have repeatedly highlighted the seriousness of certain fluoroquinolone adverse effects for systemic use, reinforcing why symptom-triggered reassessment is prudent when unexpected reactions occur [5].

Ask the surgeon’s office for the exact names in writing of:

❌Anything placed in the eye during surgery (intracameral injection or “dropless” injection)

❌Any drops or medications you will use before or after surgery

You always have the right to ask for alternatives, or find a doctor that will respect your requests. Always research any medication for possible adverse effects before taking.

✅ A complete list of fluoroquinolones in all forms: https://t.co/OKH2DOWix0

🧿🧿🧿🧿🧿🧿🧿🧿🧿🧿🧿🧿🧿🧿🧿

References

[1] Cataract & Refractive Surgery Today (CRSToday). “Simplifying Postoperative LASIK Care.”
https://t.co/itFgN4In4p

[2] American Academy of Pediatrics (AAP) Pediatric Care Online. Drug Monograph: Ofloxacin (Ophthalmic) — includes guidance on minimizing systemic absorption (e.g., nasolacrimal occlusion/eyelid closure).
https://t.co/qy5Sop4k5F

[3] Health Canada / Drug Product Database PDF (example product monograph). Ofloxacin ophthalmic solution monograph noting systemic absorption after topical ocular use and related safety information.
https://t.co/j8QqlJJrfY

[4] StatPearls (NCBI Bookshelf). Fluoroquinolone-associated tendinopathy and risk modifiers including corticosteroid exposure.
https://t.co/PFJ6vLjewY

[5] U.S. FDA. Drug Safety Communication: updated warnings for oral and injectable fluoroquinolones regarding disabling side effects.
https://t.co/di9iw1yPff

✏️Disclaimer:
Fluoroquinolone Toxicity Study does not provide medical advice, and all articles and written content are intended for informational purposes only. We do our best to provide accurate information. Such information is not a substitute for professional medical advice, diagnosis or treatment. For multiple reasons, supplements, treatments, and pharmaceutical effects and outcomes can possibly vary significantly among those affected by fluoroquinolone drugs.

Find support and resources on our sites:

🌐 Medical resources: https://t.co/gjkZgGyJ0V
🧭 Help & Misc resources: https://t.co/a63hkPq4Mv
▶️ YouTube: https://t.co/lWJ0LMmfeq
🐦 X/Twitter: https://t.co/Gp9ZXyhyfZ

#FQAwareness #Fluoroquinolones #MitochondrialHealth #AntibioticSideEffects #Floxed #Cipro #Levaquin #FQAD #LASIK

[Jerzy Tyszkowski @TyszkowskiJerzy]

@FQ_100 Thank you for mention me ❤️

[Fluoroquinolone Toxicity Study @FQ_100]

💖🌈 A message of hope for those hit the hardest by these antibiotics. A comeback story of survival and fighting your way back, by one of the foundation's founders- Jerzy Tyszkowski

✨✨✨ From 9% to 60% — my story, in plain words ✨✨✨
I won’t dress this up. My trouble with fluoroquinolones* started long ago. The first big hit was in 2003, when I took 170 tablets of ciprofloxacin in a single treatment. Later came multiple therapies with levofloxacin. The last time I took levofloxacin was in 2010 — just 5 tablets — and that was enough to break me. After that exposure, I was bedridden for almost two years, from 2010 to 2012.

My life fell apart. Acumen testing showed my mitochondria working at only about 9%. I had more than 150 side effects, I was completely bedridden, and honestly, I thought I might not survive.
Don’t forget the delayed reaction — symptoms can appear months after exposure. That’s why at first I had no idea what was happening to me. I was poisoned by fluoroquinolone toxicity.
I visited dozens of doctors. Most didn’t understand. Some suspected multiple sclerosis, others simply gave up. Out of many physicians, only a few finally gave me the right diagnosis: mitochondrial dysfunction. That diagnosis changed everything. Doctors stopped doing things that were making me worse and began focusing on protecting what little energy production I had left.

At that time, I couldn’t tolerate normal doses of supplements. When mitochondria are at 9%, every vitamin or amino acid is not just nutrition — it’s work. The cell needs ATP and enzymes to process it. Giving big doses then was like asking a broken engine to run flat out. So I used micro-doses, transdermal and sublingual forms. If a sublingual product contained sugar, I rinsed my mouth after one minute to avoid swallowing carbs and breaking ketosis.
Oxygen therapy became a necessity. After FQ toxicity, my oxygen saturation at night would drop below 90%, sometimes down to 84–85%. I developed severe sleep apnea and had to use both CPAP and supplemental oxygen. Oxygen wasn’t a cure, but it kept me alive — helping my cells survive low-oxygen states long enough to start repairing.

For the first years I couldn’t fast because my blood sugar was unstable. I had to be careful — eating very little, very often, while constantly monitoring glucose. Only years later, when my when my mito results was more then 60% and glucose stabilized, I could safely introduce fasting. That became a turning point. Ketones give cleaner fuel, lower oxidative stress, and fasting activates autophagy and mitophagy — clearing out the most damaged mitochondria so the healthier ones can survive. With time, fasting also activates PGC-1α, which drives the creation of new mitochondria. Slowly, the system began to turn.

In the second phase of diet, I could only tolerate selected foods — I had to carefully choose and test what I ate, step by step. It was part of stabilizing and rebuilding.
I also developed a special therapy for myself, aimed at speeding up cell renewal. It supported cell division and accelerated the formation of new mitochondria — a process naturally linked to tissue regeneration. I won’t describe it here in detail, but it was another piece of the puzzle that helped my body restart its regenerative capacity. My protocol also helped several other people I trusted — and they, too, began to improve.

There’s one more thing I want to mention — the work we did in Poland. In our studies, I was the only person who went through every stage of the stem-cell renewal protocols we tested. My body began to produce stem cells, which later contributed to forming cell lines across different tissues. We documented these stages in the study. For me, this was a breakthrough: proof that regenerative processes can be reactivated, even after heavy damage.
As my mitochondrial function improved, the chronic low-grade inflammation that had followed me for years started to fade.

Damaged mitochondria release alarm signals — fragments of mtDNA, ROS, abnormal metabolites — and the immune system stays in constant alert mode. When mitochondria stopped leaking those signals, inflammatory markers dropped, pain and brain fog eased, and life became quieter. This isn’t poetry — it’s biology: less ROS, fewer alarm signals, better cellular balance.

It took me two long years just to get out of bed, and many more to rebuild a life that could be called living. After several years and three Acumen tests, mitochondrial function rose from about 9% to over 60%. I haven’t returned to the man I was before, but I’m here. I walk, I work, I meet people. If you are lying in bed now, in pain and without hope, listen to me: I was there too. If I could climb out of that hole, you can too. It’s a slow process. Often boring. But possible.

Now my goal is to publish case study — based on my mitochondrial tests and other testing in comparison with several other cases, including that of a close friend — to show the huge progress that is possible with proper treatment. I want to do this together with doctors and scientists who are willing to collaborate, not for profit, but for truth and for patients.

To everyone reading this who is suffering: don’t give up. Take one small step today — measure, rest, keep your meals steady, and try to reduce the noise around you. Recovery doesn’t happen in a single day, but it can happen in days that add up. You are not a lost cause.

🌀My protocol had three phases:

Phase 1: I was bedridden. I couldn’t even turn by myself. My weight dropped to almost nothing — just skin and bones. Because of glucose swings, fasting was impossible then. Instead, I ate very little, very often, constantly checking blood sugar.

Phase 2: When I began to tolerate food again and slowly gain weight, I stabilized supplementation. In this phase, I could only manage certain foods, and I very cautiously raised supplement doses where it was safe.

Phase 3: When glucose instability calmed and my body was stronger, digestion improved and I could use supplements more easily. This is when I introduced intermittent fasting as part of my routine.

What made me worse was not only being “refloxed.” The decline came from many directions — other medications, anesthesia, exposure to heat and cold, chemicals, alcohol, stress, trauma, and even over-exercising. Too many supplements at the wrong time added to the problem. Ionizing radiation, MRI contrast, CT and PET scans, as well as other medical exposures, all aggravated my condition.

I later realized that infections, lack of sleep, poor nutrition, and certain immune challenges could also trigger setbacks. Environmental toxins such as mold, heavy metals, pesticides, polluted air, and even everyday foods played a role. Meat containing antibiotic residues, processed products, and chlorinated water — including swimming pools treated with chlorine or other chemicals — all contributed to my worsening symptoms. Flying, changes in pressure in the mountains, and even prolonged exposure to ultraviolet or infrared radiation also became serious triggers.

Fasting can be good for some people, but in severe mitochondrial dysfunction it is not recommended. My body simply didn’t have the energy reserves, and fasting only pushed me into greater weakness, unstable blood sugar, and deeper exhaustion. Only later, once I was more stable and stronger, could I even think about intermittent fasting in a cautious way.

Please don’t contact me for medical advice as I’m not a physician, and unable to legally provide medical guidance as well as risk liability for the Foundation. This message is meant to give support and hope — to show that it’s possible to survive hell and get back to something like a normal life, and in people with milder damage, even to full recovery. I share this not as advice, but as my experience. Recovery meant understanding what made me worse, learning to avoid my triggers, and holding on to hope. Even the smallest stressor could break me down, but faith, patience, and support from others helped me keep going. ✨

♦️Disclaimer: This is my personal story and what worked for me. It is not medical advice. Everyone is different — consult a medical professional before changing treatment, starting fasting, or using supplements or oxygen therapy.

♦️The Acumen lab unfortunately closed in 2021

*💊Medications in the fluoroquinolone class (incl: Cipro/ciprofloxacin, Levaquin (off market)/levofloxacin, Avelox/moxifloxacin etc) in all forms for humans and pets: https://t.co/OKH2DOWix0

Find support and resources on our sites:

🌐 Find Us: https://t.co/G9NJIEKEij
▶️ YouTube: https://t.co/lWJ0LMmfeq
🔵 Facebook: https://t.co/oVDvQDnync
🐦 X/Twitter: https://t.co/Gp9ZXyhyfZ

#Fluoroquinolones #MitochondrialHealth #AntibioticSideEffects #Floxed #Cipro #Levofloxacin #ciprofloxacin #FQAD #FQ #FQToxicity #Mitochondria #Neuropathy #antibiotics

[Jerzy Tyszkowski @TyszkowskiJerzy]

Why We’re Fighting Fluoroquinolone Harm https://t.co/DXOf42b238 via @YouTube

[Jerzy Tyszkowski @TyszkowskiJerzy]

Treating Antibiotic Adverse Effects - Dr. Pieper book interview Part 1 https://t.co/S4xvmRZ8Hl via @YouTube

[Fluoroquinolone Toxicity Study @FQ_100]

🔬🧬Stem Cells, Mitochondrial “Transplants,” and What Our Poland iPSC Work Suggests for FQAD (Part 3 Final)

When people hear “stem cells” or “mitochondrial transplantation,” it is easy to imagine a near-future medicine where damaged tissues simply receive fresh cellular “batteries” and everything switches back on.
The reality is more demanding:

➦the science is advancing quickly, but the biology is complex, the manufacturing is unforgiving, and patient-to-patient variability, especially in syndromes involving mitochondrial injury and extreme sensitivity, can make promising concepts behave unpredictably.

One of the most important reasons to stay realistic comes from our research work done in Poland in 2022, published in the journal Stem Cell Research & Therapy. This work examined whether fibroblasts from people with Fluoroquinolone-Associated Disability (FQAD) could be reprogrammed into induced pluripotent stem cells (iPSCs) and then expanded reliably. The central finding was uncomfortable but crucial: compared with healthy controls, reprogramming and stable line establishment were markedly harder in FQAD, with many patient samples failing to produce robust iPSC lines and showing signs consistent with impaired regenerative capacity under standard conditions. The paper’s message is not “give up,” but rather “do not assume autologous iPSC-based therapies will behave like they do in healthy donors; the manufacturing bottlenecks may reflect true biology.” That is exactly the kind of reality check that should shape next steps, including how we design cell-line models, what we consider “success” in culture, and how we interpret poor growth as data rather than “bad luck.” [1]

At the same time, regenerative medicine is not a single road. If iPSC routes can be blocked by the patient’s cellular state, the field increasingly looks at parallel strategies: mesenchymal stromal/stem cells (MSCs), cell-free products (secretome, extracellular vesicles), and, more experimentally, direct mitochondrial delivery. The reason mitochondria are at the center of this discussion is simple: mitochondria are not only energy producers; they are metabolic control hubs, immune-signaling hubs, and stress sensors. In conditions where mitochondria are damaged, the downstream effects can spread to detox pathways, redox balance, connective tissue remodeling, and neuro-immune stability, precisely the systems many FQAD patients report as fragile.

So how would mitochondria get from a donor source to a recipient cell in a way that could matter?

Nature already has a few “transport channels,” and researchers have been mapping them. One highly studied route is the formation of tunneling nanotubes (TNTs), thin actin-based bridges that can connect cells and allow organelle transfer. Work in different tissues has shown that TNT formation depends on specific proteins and stress signaling, and the system is not random. For example, TNFAIP2 (also called M-Sec) has been tied to TNT formation, and TNTs have been implicated as conduits for organelle movement in multiple models. [2] This matters because it reframes “mitochondrial transfer” from something mystical into something that can be engineered: if cells build highways under stress, the practical question becomes how to promote safe, controlled highway formation without triggering unwanted inflammation.

A second key concept is that mitochondrial movement is not just about having mitochondria available; it is about trafficking machinery. Several studies point to the mitochondrial Rho-GTPase Miro1 as a major regulator of mitochondrial transport. In the lung/airway context, Miro1 was shown to regulate intercellular mitochondrial movement from MSCs to epithelial cells, and increasing Miro1 expression in MSCs increased mitochondrial transfer and improved rescue effects in animal models. [3] In neural models, Miro1-enhanced MSCs transferred mitochondria more effectively and were associated with improved functional recovery after experimental injury. [4] In plain language: there are “biological transport knobs” that can change how effectively mitochondria are mobilized and delivered.

A third route is packaging: mitochondria (or mitochondrial components and mitochondrial-regulating molecules) can be moved inside extracellular vesicles/microvesicles or related membrane structures. This is often described as “horizontal transfer” of mitochondrial material and signals, and it is one reason cell-free therapies remain attractive: they may carry some regenerative signaling while avoiding the full complexity and risk profile of transplanting living, dividing cells. A recent review in Stem Cells discusses how extracellular vesicles/exosomes can participate in transfer of mitochondria and mitochondria-related regulatory molecules, framing them as potential “delivery vehicles” while still emphasizing open mechanistic questions. [5]

Then there is the idea that many patients find most intuitive: isolating mitochondria and administering them directly, hoping they will “go where they are needed.” Here, the field splits into hopeful data and serious skepticism. On the hopeful side, an International Journal of Molecular Sciences study reported that exogenous mitochondria showed preferential trafficking toward cells and tissues with mitochondrial damage in vitro and in vivo, supporting the idea that injury states can create “signals” that bias uptake. [6] On the skepticism side, a Journal of Clinical Investigation viewpoint laid out why extraordinary claims require extraordinary evidence, discussing basic barriers: survival of mitochondria in high extracellular calcium, immune clearance, endothelial barriers, actual entry into target cells, and whether enough mitochondria enter to meaningfully shift ATP production. [7] Both perspectives are valuable: the first motivates exploration; the second prevents the field from turning into marketing.

Because biology is only half the battle, the other half is production. If a therapy depends on MSCs, vesicles, or even standardized mitochondrial preparations, you need reproducible culture at meaningful scale. That is where advanced perfusion bioreactors and hollow-fiber systems enter the story: they are designed to sustain high-density cultures with controlled media exchange and stable conditions, often as a bridge between benchtop research and consistent manufacturing. Systems such as the AcuSyst-Xcellerator are marketed as flexible production-scale bioreactors for mammalian cell culture and related workflows, reflecting the broader industry shift toward controlled, scalable cell manufacturing rather than artisanal flask work. [8] Whether one calls this “the California accelerator” or simply the modern manufacturing layer, the point is the same: if regenerative medicine is to become real medicine, it must be reproducible, scalable, and quality-controlled.

➦For FQAD patients specifically, the most responsible message is “measured hope.” The hope is that mitochondrial delivery, via cells, nanotubes, vesicles, or engineered carriers, could one day help restore function in tissues where mitochondria are chronically impaired. The non-negotiable caution is that FQAD biology may make standard assumptions fail. If patient-derived cells reprogram poorly or expand unreliably, as shown in the iPSC work, then autologous “take your cells, fix them, give them back” models can run into real-world barriers before therapy even begins. [1] In addition, any intervention that moves mitochondria or mitochondrial material between cells risks immune activation, because mitochondria can behave like danger signals when they are damaged or released in the wrong context. And iPSC-derived therapies carry their own high-stakes risks, genomic instability, abnormal differentiation, tumorigenicity - requiring stringent QC and conservative clinical translation.

💠This is why our research direction, grounded in careful mechanistic work, controlled models, and rigorous analytics, matters. If we want the future to be more than stories, we must build it from data: defining which signals are present in FQAD cells, what breaks during reprogramming and proliferation, how mitochondrial damage shapes trafficking and uptake, and which delivery routes can be made safe, targeted, and reproducible. It is not a “pink and beautiful” road, but a technical road. But it is a road that exists and it is getting wider.

🧿🧿🧿🧿🧿🧿🧿🧿🧿🧿🧿🧿🧿🧿🧿
✏️Disclaimer: This article is for general educational discussion and research-context planning only. It is not medical advice, does not establish a diagnosis or treatment recommendation, and should not be used to make clinical decisions without qualified medical oversight and appropriate regulatory-grade evidence.

💊Medications in the fluoroquinolone class (incl: Cipro/ciprofloxacin, Levaquin (off market)/levofloxacin, Avelox/moxifloxacin etc) in all forms for humans and pets: https://t.co/OKH2DOWix0

Find support and resources on our sites:

🌐Find Us: https://t.co/G9NJIEKEij
▶️YouTube: https://t.co/lWJ0LMmfeq
🔵 Facebook: https://t.co/oVDvQDnync
🐦 X/Twitter: https://t.co/Gp9ZXyhyfZ

[Jerzy Tyszkowski @TyszkowskiJerzy]

Dead Because he couldn't Sleep | The Story Of Ricard Siagian https://t.co/5B8cVzdabk via @YouTube

[Fluoroquinolone Toxicity Study @FQ_100]

Congrats Talia Smith on this win for the floxed community! @FVulneraries

[Fluoroquinolone Toxicity Study @FQ_100]

This is great news and a demonstration of what can happen when a community works together! (the 5k win appears at the video ending). To learn more of what this petition outcome means, click the link on the video 'see more' to read. The petition is complete, no more sigs needed!

https://t.co/s3apxzJNZr

[Fluoroquinolone Toxicity Study @FQ_100]

If you found this informative, show us some ❤️ , follow our page for updates, and share to help spread the word!

[Fluoroquinolone Toxicity Study @FQ_100]

Our peripheral nervous system ➤affected by fluoroquinolone antibiotics...
Think of the nervous system in two halves. The central side is your brain and spinal cord. The peripheral side is all the nerves linking your limbs and organs back to them, and that’s our focus here. As many of you know, in 2013, the FDA warned that fluoroquinolone antibiotics* can cause permanent peripheral neuropathy, and this post digs into what that means:

Peripheral Nervous System (PNS)

The PNS consists of all the nerves outside the brain and spinal cord (including most cranial nerves). It has two main components: the somatic nervous system and the autonomic nervous system.

🟣 Somatic Nervous System:
Voluntary Control — Controls voluntary movements by innervating skeletal muscles. For example, moving your arms or legs.
Sensory Input — Transmits sensory information from the body to the central nervous system (CNS), such as touch, pain, temperature, and proprioception (sense of body position).

🟣 Autonomic Nervous System (ANS):
The ANS controls involuntary body functions and is further divided into three branches: the sympathetic, parasympathetic, and enteric nervous systems (the enteric system is semi-autonomous but communicates with the CNS and the rest of the ANS). The ANS regulates involuntary physiological functions essential for survival and homeostasis. It has three main components:
1. Sympathetic Nervous System:
"Fight or Flight" Response: Prepares the body for stressful or emergency situations. This includes increasing heart rate, dilating pupils, dilating airways, and inhibiting digestion.
Energy Mobilization: Mobilizes energy stores to provide quick energy.

2. Parasympathetic Nervous System:
"Rest and Digest" Response: Promotes relaxation and recovery. It slows the heart rate, constricts pupils, stimulates digestion, and conserves energy.
Homeostasis: Maintains regular bodily functions and conserves energy.

3. Enteric Nervous System:
Gastrointestinal Control: Regulates the functions of the gastrointestinal tract, including peristalsis (movement of food), secretion of digestive enzymes, and blood flow to the gut.
Autonomous Functioning: Often referred to as the "second brain," it can operate independently of the CNS but also communicates with it.

🌀 Functions Controlled by PNS:

Voluntary movements (walking, typing, etc.)
Sensory perception (touch, temperature, pain)
Reflexes (knee-jerk reaction)

🌀 Functions Controlled by ANS:

Heart rate and blood pressure regulation
Modulation of airway tone, mucus secretion, and reflexes like bronchoconstriction; the basic breathing rate is generated by brainstem centers and executed by somatic nerves to the diaphragm.
Digestion
Gastrointestinal motility
Pupillary response and eye accommodation
Sweating and thermoregulation
Urination and sexual function

The PNS and ANS work together to ensure that the body can respond to both voluntary actions and involuntary needs, maintaining overall balance and homeostasis.

Fluoroquinolones have been shown to cause mitochondrial effects in experimental systems (cell and animal data, with clinical signals in humans) and can affect the ANS. Given the high energy demands of neurons within the ANS, mitochondrial dysfunction can have several effects:

➧ Cardiovascular Issues: Mitochondrial dysfunction and dysautonomia*** can impair autonomic regulation of heart rate and blood pressure, potentially leading to orthostatic intolerance or orthostatic hypotension; some agents in this class also carry QT-prolongation risk, which can contribute to arrhythmias.

➧ Gastrointestinal Problems: The ANS controls motility, secretion, and blood flow. Mitochondrial and autonomic dysfunction can present as gastroparesis-like symptoms, constipation, diarrhea, or IBS-like patterns.

➧ Breath-control irregularities or exercise intolerance: linked to dysautonomia

➧ Thermoregulation: The ANS helps maintain body temperature. Mitochondrial dysfunction can impair this regulation, leading to heat or cold intolerance.

➧ Sweating Abnormalities: Autonomic dysfunction can alter sweat gland activity, leading to excessive sweating or reduced sweating, which impacts thermoregulation and skin health.

Burning pain, numbness, weakness, severe stand-up dizziness, or rapid heart-rate shifts after an antibiotic can possibly point to peripheral or autonomic neuropathy. Persistent cases are typically seen by dysautonomia specialists (autonomic neurologists) so check with your primary care. Resources are below.
______________________________________________________

* Drugs in the fluoroquinolone class (Cipro/ciprofloxacin, Levaquin (off market)/levofloxacin, Avelox/moxifloxacin etc) in all forms for humans and pets: https://t.co/OKH2DOWix0
** 2013 FDA Warnings: risk of permanent peripheral neuropathy https://t.co/D9PhrGaHQn
***Dysautonomia is an umbrella term for disorders in which the autonomic nervous system does not regulate automatic body functions properly, such as heart rate, blood pressure, temperature control, digestion, sweating, bladder and pupillary responses.

➥To learn more about nerve damage, please view Part 2 of our series with Dr. Stefan Pieper out of Germany, who has treated over 1500 "floxed" patients: https://t.co/37nXttfvNJ

🟡find clinicians:

• Dysautonomia International — doctor finder and support resources https://t.co/9EyYcBSH4K
• American Autonomic Society — physician directory: https://t.co/Ncdf9KPr17
• AANEM — find a specialist for EMG/NCS and neuromuscular evaluation: https://t.co/k8mqqib5re (patient info hub: https://t.co/unl3DP7xfY) (AANEM)
• The Dysautonomia Project — clinician map: https://t.co/jIN9IihZuE (organization site: https://t.co/Z6NWQY5NiD) (https://t.co/dG724GQuqj)
___________________________________________________

🟡Support groups and resources:

🌐 Find Us: https://t.co/G9NJIEKEij
▶️ YouTube: https://t.co/lWJ0LMmfeq
🔵 Facebook: https://t.co/oVDvQDnync
🐦 X/Twitter: https://t.co/Gp9ZXyhyfZ

⚠️Disclaimer: Fluoroquinolone Toxicity Study does not provide medical advice, and all articles and written content are intended for informational purposes only. We do our best to provide accurate information. Such information is not a substitute for professional medical advice, diagnosis or treatment. For multiple reasons, supplements, treatments, and pharmaceutical effects and outcomes can possibly vary significantly among those affected by fluoroquinolone drugs.⚠️

References:
Autonomic Nervous System
https://t.co/WSsTRkxJg4
Peripheral Nervous System (PNS)
https://t.co/Cq47GFT3SG
Peripheral Neuropathy Associated with Fluoroquinolones
https://t.co/k5eAhOBUwb...
Ciprofloxacin impairs mitochondrial DNA replication initiation through inhibition of Topoisomerase 2
https://t.co/qShIAtQuFy...
Chemical Proteomics Reveals Human Off-Targets of Fluoroquinolone Induced Mitochondrial Toxicity
https://t.co/ZOSVcvrKGw

#FluoroquinoloneToxicity #FQToxicity #FQAwareness #Fluoroquinolones #Ciprofloxacin #Levofloxacin #Moxifloxacin #MitochondrialDysfunction #AntibioticsAwareness #floxed #Cipro #FQAD

[Fluoroquinolone Toxicity Study @FQ_100]

Such a sad loss for our community - ever grateful and happy birthday Jay. 💝

[Fluoroquinolone Toxicity Study @FQ_100]

https://t.co/t6e0Gu8P4O

[Fluoroquinolone Toxicity Study @FQ_100]

So many of us suffering systemic, adverse effects can sadly relate to brain issues. We hope such work will drive further study for the community.

[Jerzy Tyszkowski @TyszkowskiJerzy]

@FQ_100 Over the past years, researchers have repeatedly reported serious mitochondrial toxicity linked to fluoroquinolones, but this evidence has not translated into meaningful awareness within the medical community or public-health institutions