Gary’s Story – Levaquin Toxicity

*The following is an individual’s story of surviving fluoroquinolone toxicity. It is not medical advice. Please see the disclaimer at the bottom of the story. Thank you, and please be cautious with all treatments. 

**Please note that Gary has added updates to his story over time, and continues to do so regularly. Please read through the whole story, and check back regularly. Thanks! 

Abstract:

In October of 2015, I was given Levaquin and some cough suppressants because I was very sick, with supposed pneumonia.

I only took 2 pills, 750mg per pill, out of 7, and it started a lethal assault on my body that resulted in long term disability that took at least 16 to 24 months to resolve for the critical symptoms, which include the following:

– Brain Fog
– Cognitive Defects
– Altered Mental Status (Per Emergency Room Doctor, post-Levaquin)
– Depersonalization
– Chronic, Crippling Fatigue
– Low Body Temperature
– Tendinopathy (Tendon Destruction in both my feet)
– Painful Achilles Tendon
– Burning Feet
– Autonomic Neuropathy (Reduced Sweating, cold skin)
– Rapid Weight loss (178 to 148 in 2 weeks)
– Panic Attacks
– Anxiety Attacks
– Bipolar / Mania
– Blood Sugar anomalies
– Rapid Mood Swings
– Depression
– Food Allergies
– Episodic Tachycardia
– Sore Muscles
– Muscle Atrophy / Wasting
– Vision Changes
– Increased in Eye Floaters
– Hair Loss
– Dry Skin
– Chronic Dry Eyes
– And more; A total of 35 chronic symptoms that developed within 30 days.

My pre-Levaquin health issues were nearly nonexistent, with a small patch of psoriasis behind my ears.

Every doctor I have seen, post-Levaquin, could not help me; I spent so much money on visits to every kind of doctor you can think of. I was insulted, pushed off, ignored, talked down to, by the same medical establishment that poisoned me.

I started reading the literature in late 2015 to find a cause, as a cause would lead to treatment. As of this writing, April of 2019, I have read over nearly 3,000 papers on various journals (Pubmed, PNAS, PLoS, Nature, etc), and I will give you a summary of what I attempted to make myself feel better. I do not recommend trying many of the things I did, as they could be dangerous.

I likely developed Levaquin-Induced Pre-Diabetes due to blood sugar range from being 75 to 150 during fasting over the course of 2 years, which I will go into later in this story.

I finally decided to rewrite the story to be more, clear, as the original story was formulated with a broken mind.

Full Story:

I became very sick in late September of 2015, with a URTI. I headed to Med Express, for the first time ever, to obtain antibiotics for an illness. The initial exam revealed the following:

High pulse rate (over 100)
Low O2 stats (96% on room air)
High Fever (101F)
Respiration Rate was elevated
Lung sounds were not clear and equal
Low Blood Pressure
Lethargic

The doctor ordered a Chest Xray, and confirmed some kind of discoloration on my right lung, near the top. Diagnosed it as ‘Pneumonia’ based on my symptoms, and then prescribed Levaquin, 7 pills, 750mg, for 7 days. The doctor told me that if my fever did not go away by Monday Morning, I should head to the ER because I could develop sepsis (which is unusual for someone at my age and health status). I asked the doctor about the Levaquin and said ‘Is there anything I should know about this?‘ to which he said ‘Don’t take it on an empty stomach‘. He made no mention of any interactions, side effects, etc (I had never heard of it before). Dropped off my prescription to Walgreens and headed home.

Next morning, picked it up and took 1x pill of Levaquin in the Parking Lot with some Gatorade, about 30 minutes later I noticed an electrical sensation in my arms, neck, hands, feet, and others – Shrugged it off and it went away. Later that night when I was trying to go back to sleep, I started to hallucinate… My heart rate surged to 140bpm, but they eventually subsided, at first.

Then on Sunday, October 4th at 2:30 pm, I took my 2nd and final pill; Within 90 minutes my hands, feet, and knees were hurting so badly I could not walk or hold anything in my hands. It felt like my feet had been run over by a school bus, set on fire with lava. My hands were hurting so bad, it felt like I suddenly developed arthritis. I took a 200mg NSAID to see if that would help – It did not. The pain.. oh my.. the pain was intense. I decided that a hot bath would help.

It did not.

I jumped on the computer and went to the FDA’s website and typed in ‘Levaquin’ into the search bar.. and I came across the very large print of its side effects. I was horrified!

I started researching possible treatments and what exactly what tendon ruptures were. The only treatment was time, according to PubMed. The pain was so bad that I could not sleep.. For the entire week, I slept a few hours, only because I used 3x packages of Epsom Salt in my Bathtub with very hot water, that caused my foot pain to reduced from 10/10 to a 3/10, enough for me to sleep, in the bathtub (until the water became cold). A few days later, I called Med Express and told them I am in a lot of pain and I am not sure what I should do – They told me ‘You need to finish the antibiotic‘. I said they are insane and I was fine before I took this medication and I hung up and stopped taking it, hoping the side effects would go away. They did not. After another week of agony and pain, I went BACK to med express and I was prescribed Painkillers, Sleeping Pills, and more NSAIDs. I took a painkiller nearly an hour later and my pain went from a 9 to a 0.5 in about 20 minutes. I felt alive again – I started to become hyper since I was in agony for a week. Later that night, when I got off of work, I took a sleeping pill and another painkiller – I went to bed at around 12:30 am and I slept for 20 hours until 8 pm the following day. When I awoke, I felt SO much better, the pain in my feet was about a 2 at this point, so I repeated the treatment for the next 10 days and I saw a massive improvement. Everything was starting to get back to normal and I thought the worst was over.

I was wrong.

Early on October 27th, around 1 am, I tried to drink a few glasses of wine so it would make me tired enough to sleep (I had 3 glasses a few days before because I ran out of sleeping pills with no issues). Finally went to bed after 3 glasses of wine; Next morning awoke to feelings of intoxication, foggy thinking, depersonalization, anxiety, short term memory problems, uncontrollable feelings of sadness, fear, cold hands and feet, unable to stay warm, chronic fatigue and dozens of more symptoms; I felt as if part of my mind was paralyzed. The mental stuff got worse over the next week and peaked around Nov 4th – Around Nov 5th just after midnight I went to my ED of my Hospital as 3 hours earlier I was vomiting up dinner because of anxiety and panic attacks. I was in sheer agony.

I approached the Charge Nurse and I didn’t even know what to say. If I said the wrong thing, they might think I was crazy, and throw me in the mental ward. I tried to give her a quick summary, but I was not really sure what to tell her. I was admitted. Initial vitals were a little unusual, probably because I was scared of puking, and it was raising my heart rate. The nurse comes into the room and asks me ‘what’s the problem?’ to which I said – This is going to take a few minutes. I flat out explained that my health had seriously gone to hell after taking 2 pills of Levaquin 3 weeks prior and that I have been having numerous CNS issues that I cannot explain. ED Doc comes in and asks me again, to which I was more detailed about everything. I was diagnosed with ‘Altered Mental Status’ and sent home.

I made an appointment with a Podiatrist, he did some checks of my feet and Achilles tendon and noticed some issues.. some being, numerous tendon ruptures, micro ones, in both of my feet. He came to the conclusion I have mild antibiotic-induced tendinopathy and not tendonosis due to only taking 2 pills of Levaquin – He stated long term usage of Levaquin would have caused tendonosis. On a side note, He did tell me that my foot orientation is not correct which wasn’t caused by Levaquin, but just ‘me’ not walking correctly (since I was a kid), using the right shoes, etc – So inserts were ordered. I was concerned about Neuropathy – He stated it’s likely I will continue to have some discomfort for a while as an indirect reaction to the damage to my tendons in my feet/toes – Again, he was quite helpful and very well versed in the side effects of Levaquin (I didn’t even have to tell him about tendon issues being a side effect, he knew from my chart why I was there)

(After all that was said and done, I went on a buying spree and bought numerous supplements)

The Suffering Continues

From Late October of 2015 until early to mid-2017 I was in horrible shape mentally and physically. I started to improve around 16 months out and I finally considered myself ‘healed’ about 24 months out.

I’ve tried numerous things to get better, some things which are dangerous:
– Antioxidant IVs. They helped, which I will go into detail.
– Megadosing Probiotics
– Megadosing S-Acetyl-L-Glutathione
– Supplements galore. I spent $2,000 on various supplements.
– Carbon 60

 

Treatment for Neuropathy (Autonomic/Peripheral)

Since my Levaquin exposure, I have noted abnormal sweating, lower feel for environmental temperature, and overall decreased CNS response, going on 4 years.

In January of 2019, the daytime temps were unusually cold and some snowfall left a massive mess in my neighborhood. I was out with my snowblower for hours assisting the neighbors. My feet and hands were very cold during that time frame (Air temps were 5F with a WC of -10F). A few days later, I noticed my feet were hurting again, similar to that of my 2015 Levaquin exposure.

The pain was about a 6/10 and peaked about an 8/10. Onset was rapid, which started within 72 hours. I became depressed because I assumed I had totally recovered. I was on no medication.

I figured I developed asymptomatic neuropathy that became symptomatic, so I needed to head back to the literature. Most pain medications for Neuropathy mask the symptoms and do not address the cause.

The first one I encountered was Pirenzepine. [It] is an antimuscarinic drug that was recently discovered to reverse neuropathy in studies (Calcutt et al., 2017). I was able to obtain some, and I started taking it for about 45 days. I noticed altered neurological feelings in my hands and feet, as well as increased pain (initially), then a rapid decrease in pain towards the end. I had to abort using it after 45 days because it gave me some /serious/ IBS issues (runny stools) and some cramps.

After I had stopped, the pain was nearly gone; but it was increasing again towards the mid-to-end of March – But I did not want to take it again because of the IBS issues. Back to the literature I went, to search for more purposed drugs for neuropathy.

Hello PDE5Is!

PDE5 Inhibitors, like Viagra, improve neuropathy in human studies, as well as animal studies. (Wang et al., 2017; 2016; 2015; 2011; Mostafa, 2008; Peixoto et al., 2015; Vlachopoulos et al., 2009; Hackett, 2006; Mehmet Fatih Korkmaz et al., 2016; etc)

This has been known to affect PN as far back as 2002 (Sairam and McNicholas, 2002). PN symptoms in Fluroquoinoline Patients is more or less the same in Diabetic Patients, as PN initially manifests itself as mitochondrial dysfunction.

PDE5I’s are showing other benefits, such as increased antioxidant status in humans, cardioprotection, and more.

According to Hackett (2006), 5 patients who were prescribed different PDE5Is showed dramatic results within 90 days, with some of the patients showing a nearly complete reversal of neuropathic pain.

The mechanisms behind PDE5I treatments are well documented; Tadalafil treatment improves motor and sensory conduction velocities in the sciatic nerve and peripheral thermal sensitivity, increased myelin thickness, enhances Nerve Growth Factor, regional blood flow in Sciatic Nerve Tissue, and more. (Wang, et al., 2016; 2017). Daily dosages of Tadalafil for a period of 90 days will likely reverse early-to-moderate stages of Neuropathy.

Going over the Pharmacodynamics of the PDE5is, Sildenafil (Viagra) has a biological half-life of 4 hours, which is likely /too/ short for effective treatment. Tadalafil has a biological half-life of 17 hours, with a great safety profile. However, Tadalafil, unlike Sildenafil, has no absorption issues when combined with food, etc. (Nichols, Muirhead and Harness, 2002), so Tadalafil is likely a better medication for treatment.

I was able to obtain Tadalafil, as well as Sildenafil and began treatment towards the beginning of the month. Tadalafil is quite expensive, I was effectively paying $20 a pill(!!) for 5mg. Increasing the dosage to 20mg had drastic effects, within 10 days of treatment.

– The core sections of my feet were warm again – Just like my Pre-Levaquin exposure
– My hands were warm again.
– My feet began sweating like normal, more than Pirenzepine treatment.
– My sleep quality has improved, I do not sleep as much (Similar to pre-Levaquin)
– My cerebral blood flow has increased – My ears have not been cold any longer.
– My feet have pre-Levaquin color (some reddish in toes)

Currently, the pain is isolated to a few spots on my feet, namely my toes, compared to the total foot. I’m hopeful that a treatment round of this for another 90 days will completely reverse it. To clarify, I’m seeing a vast reduction in neurological pain!

If it does not completely go away, then I may have to see about treatments that invoke vasculogenesis/angiogenesis.

Thymosin ß4 is the next one I will try, with injections into the feet, as it does appear to supply new blood vessel formation in various studies (Dubé and Smart, 2018; Zhao et al; 2018; Kim and Kwon, 2015; Philp et al., 2004; etc).

Additional Supplement information:

An outline of my supplementation experiments that either did not work, did work or did not notice anything.

– Carbon 60/Fullerene (WARNING! Experimental!)

One of the most powerful antioxidants I have ever taken in my life. Fullerene has a very unique structure that is composed of 60 Carbon Atoms that form a hollow sphere, nearly ~1 nanometer in diameter (Kroto et al.,1985) – This sphere behaves like a free radical sponge (Chistyakov et al., 2013), has no known toxicity (Gharbi et al., 2005; Spohn et al., 2009, Andrievsky et al., 2005; Tong et al., 2011), contains antioxidant activity several orders of magnitude higher than any known antioxidants like Glutathione (Krusic et al.,1991; Yang et al., 2014), prevents mitochondrial dysfunction and oxidative damage (Xiaoqing et al., 2008), restoring the level of Glutathione in cytoplasm and incorporation into mitochondria cell membrane to prevent lipid peroxidation (Prylutska et al., 2008).

According to a paper that describes how toxic, if any (Andrievsky et al., 2005) of C60 Fullerene and some other mechanisms which state the following:

“Nevertheless it is reasonable to mention that: (i) pure C60 possesses comparable and even higher anti-oxidant activity than natural anti-oxidant vitamin E (a-tocopherol) (33), (ii) micronized C60 demonstrates the powerful hepatoprotective activity, i.e., protects the liver from toxic damages (34).”

I did a blind test in August of 2016 with 1 bottle of C60-OO and then just regular olive oil and took some measurements (Body temp 3x a day, how long it took for me to become tired, etc) for 3 weeks. The first 10 days were not the Fullerene, but the regular olive oil. When I switched over to Fullerene, I noticed an immediate change within an hour of taking it. I had to have someone help me with the blind test so I didn’t experience the placebo effect.
Increased body temperature
– Stabilized my post-Levaquin body temperature issues (ie: no longer freezing cold when a room is 75F)
– Energy levels increased – Still below what I think ‘was’ normal, but a marked improvement
– I seemed to have better olfactory reception. Not annoying, but when you eat your favorite food and you can smell it as it used to be (stupid allergies)
– I seemed ‘happier’ – Possible GABA expression changes.
– Mental clarity has increased by at least 2 orders of magnitude. People were been telling me I’m much more like my old talkative self. (Seems to have been permanent)
– Less anxiety overall.
– Vivid, Awesome dreams.
– My blood is bright red and my o2 stats on a pulse ox are between 100 and 102 – I suppose oxygen saturation has increased. (Other c60 users are reporting it)
– Some of the above are more permanent (the mental clarity has remained), olfactory responses have remained improved.

August 6th to the 16th – Control (simple Olive Oil)

Date Body Temp Time Awake Notes
6th 95.5 13 Hours Caffeine at super high dosages have no effect
7th 95.9 12 Hours
8th 95.9 10 Hours Very tired
9th 96.1 10 Hours
10th 95.4 9 Hours Was not feeling well this day
11th 96.2 11 Hours
12th 95.9 12 Hours Intense Fatigue at 10 hours
13th 95.8 11 Hours Sudden onset of fatigue at 10 hours
14th 95.8 10 Hours Awoke after 13 hours of sleep – Became tired again 4 hours later.
15th 96.0 11 Hours
16th 95.5 10 Hours I wanted to nap all day long

August 17th to the 27th – Fullerene

Date Body Temp Time Awake Notes
17th 96.4 18 Hours Surge of energy, similar to Whey Protein, but much longer lasting.
18th 96.6 13 Hours Insonomia, and a constant feeling of napping.
19th 96.8 15 Hours Best Dreams I have ever had in my life.
20th 97.0 16 Hours Olfactory changes started this day – Pasta sauce etc smelled great.
21st 97.3 17 Hours I actually felt like cleaning this day.
22nd 97.2 15 Hours
23rd 98.5 18 Hours Was doing yard work all day, wanted to stay awake longer.
24th 98.4 16 Hours
25th 97.9 14 Hours
26th 98.0 16 Hours
27th 98.4 19 Hours Maximum – Woke up at 8 am, and went to bed at 2 am

I ended up not taking more because there are questions about its safety concerns and limited studies.

 

– Nicotinamide Riboside.

Nicotinamide Riboside, a vitamin B3 and NAD precursor, boosts NAD levels and induces mitochondrial biogenesis, preventing mitochondrial abnormalities like mtDNA deletion formation, stimulates unfolding of protein response to offer protection on certain mitochondrial diseases (Khan et al., 2014), neuroprotection (Chi and Sauve, 2013), liver repair (Mukherjee et al., 2016), engages in mitochondrial quality control to eliminate mtDNA defects by lysosomes (Jang et al., 2012; Brady and Brady, 2015) Nicotinamide Riboside also has a long half-life in the body, about 6 hours (Trammell et al., 2016a) Nicotinamide Riboside is also present in Cow Milk (Trammell et al., 2016b), which may explain why Whey Protein + Milk was making my energy levels more normal. Nicotinamide Riboside is quite safe, even up to 1000 mg/kg (Conze et al., 2016). I started taking this in October. 3x pills a day, but have backed off to 1 pill a day. (300mg). Some of the noticeable effects:

– Improved energy levels
– Body temperature back to normal or just above normal. Probing shows 98.5 to 98.9. Cold weather does not bother me anymore and I actually feel pre-Levaquin (can’t sleep with a heavy blanket on, which is normal). I am physically more warm and not as cold intolerant as before.
– Reduced overall fatigue. I would rate my current fatigue levels as a 4/10, where 11 months ago I was a 9/10. My diet has not changed at all and I have not been taking anything else except for DHEA, which I was taking before NR. (no Fullerene since August)
– /Some/ insomnia – Which was normal, pre-Levaquin.
– Post physical activity crashing for days, is reduced.
– Reduced overall sleep (from 10 hours to 6/8)
– Reduced body heat is consistent with changes in mitochondrial mass (ie: smaller mitochondrial mass suggests less ATP). Nicotinamide Riboside appears to improve the quality of your mitochondrial via autophagy activation (Kang and Hwang, 2009).

– Organic Whey Protein

This was a hit or a miss. Organic, Cold Pressed Whey Protein had a 50/50 chance of making my energy levels close to normal, but the effect was short-lived, only lasted 5 hours a day. Whey protein stimulates mitochondrial activity, decreases oxidative stress (Shertzer et al.,2013), and increases cellular glutathione levels (Kent et al.,2003).

– IV Based Antioxidant Therapy

March 30th, 2016 I went to a local doctor (N.P.) that gave me a Myers Cocktail with a Glutathione Push. This made me feel worse for about a day, then my mental functionality got a lot better. I had to fork out $300 out of pocket for this. This was too expensive for multiple treatments (plus a 90-minute drive). My health insurance company did not want to pay me back for treatments since there’s no official diagnosis from a doctor.

– IV Antioxidant Therapy #2

In April 2016, I decided to try self-administered Intravenous IV therapy. I ordered Glutathione from a chemical supply company, as well as NAC, NACA – Experimental antioxidant that is just like NAC but much better (Ates et al,2008; Penugonda et al,2005). NACA was very, very expensive for the dosage I obtained. I also bought D-Ribose due to its antioxidant effects (Garnett et al.,1996)

So now I had plenty of supplies for 4x IVs with NAC, NACA, L-Glutathione 2mg (per IV) – with 10CC bags of saline. My first few IVs came under supervision from a colleague, and we set the drip rate to be slow and steady for the first bag – About 60 minutes. To clarify, the first bag contained about 50mg of NAC, 1mg of NACA, and a 5mg of D-Ribose for 60 minutes (I might be wrong about the dosages since I can’t find the paper where I wrote down the exact numbers)- Then when the bag was finished, we performed a push of Glutathione (2mg). The next few applications consisted of double the amount L-Glutathione (4mg) until I ran out. I ended up buying some… skin whitening vials.. which have the same Glutathione ($70 to $120 for 10 vials), just less of a dosage I wanted. The latest one I had ordered contained 6500mg of L-Glutathione, 600mg of Alpha Lipoic Acid, 5000mg of VitC, 600mg of Collagen Extract, and some smaller unrelated things. It’s 12 vials.

Within a month of doing the above, my heart palpations completely went away, as the remaining aches in my tendons/feet/hands when showering, and my eye floaters reduced with a double-digit percentage. My memory had gotten much better – however, energy levels didn’t see the same gains, a modest improvement. I can stay awake longer than 10 hours most of the time and get tired about 14 to 16 hours – It’s not back to normal but it’s a huge improvement overall. My resting heart rate went from 65bpm to about 43bpm. The abnormal sensations have gone away (the strange numbness). I can’t really say if this is placebo or not, but I don’t think so.

 

– NAC (N-Acetylcysteine)

NAC has very poor bioavailability, less than 5%, and data suggest that the drug itself does not accumulate in the body, but rather in its oxidized forms and in reduced and oxidized metabolites (Holdiness 1991; Watson and McKinney 1991). However, N-Acetylcysteine amide (NACA) is supposed to
address the shortcomings of NAC by making it cross the Blood-Brain-Barrier, increase bioavailability, etc (Sunitha et al., 2013). Also see Ketterer, Coles, and Meyer (1983) on glutathione/detoxification.

– Oral S-Acetyl-L-Glutathione

S-Acetyl-L-Glutathione is a highly absorbable lipophilic analog of glutathione – I performed 4x challenges on this, due to its low plasma half-life of 10 to 20 minutes (Hong et al., 2005, Table 1; Wendel and Cikryt, 1980; Lu, 1999). This low plasma half-life is not actually a bad thing since current literature makes references to direct uptake by cellular/organs. S-Acetyl-L-Glutathione seems to be able to cross the blood-brain barrier, but there are limited studies on this (Kidd, 1997; Adams et al., 1991). I performed the challenge because Glutathione deficiencies can cause Mitochrondia changes in vitro (Meister, 1995).

Anything I have tried/try antioxidant wise (any of the above treatments) to my body, gives me a surge of energy, to nearly pre-Levaquin levels. I have a hypothesis that my body has phase II detoxification genetic issues, which has been known in the literature to cause chronic, post-Fluoroquinolone health problems (Strauchman and Moringstar, 2012), or it’s possible that Levaquin disrupts the daily glycogen generation capacity, which is the total energy for a human body. (Lorini and Ciman, 1962; Michelakis, 2007; Mitchell, 1978) – but that value is slow to change in people and takes nearly 2 years to complete a cycle. (Michelakis, 2007). Mitochondrial dysfunction appears to be related to fatigue, according to Filler et al. (2014).

A challenge was 1 pill every hour, for 16 hours. I performed 4 of these within a month. The last challenge I performed, I did a dosage equivalent to 32 pills, which is one pill every 30 minutes for 16 hours. This should have kept my total GSH levels to over 1000 for almost an entire day. I felt a little better afterward, and no major changes. The mid-day fatigue episodes I was having were gone during this treatment. I could have probably stayed awake for over 24 hours. This was short-lived, though.

– Probiotics

Probiotics seem to have numerous health benefits. (7/2/16 is when I started taking them). I started to take them because antibiotics, can disrupt the homeostasis of your intestinal microbe for up to a year according to Zaura et al. (2015)

Lactobacillus is needed for proper Thyroid Function due to the fact your digestive bacteria needs to convert some inorganic forms of Selenium into more bioavailable forms to protect your thyroid from damage (Pessione,2012; Triggiani et al., 2009). There is strong evidence that your digestive system biome influences/controls levels of anxiety, depression, etc (Carabotti et al., 2015; Saulnier et al., 2013)

Applications of the Lactobacillus strain regulates emotional behavior and GABA receptor behavior via the vagus nerve system (GBA) (Bravo et al., 2011), chronic fatigue syndrome (Rao et al., 2009; Singh et al., 2012) alters brain biochemistry (Tillisch et al., 2012)

Alterations to gut microbiota have been shown to improve mood and reduce anxiety in patients with chronic fatigue (Logan and Katzman, 2005; Rao et al., 2009). Oral supplementation of probiotics resulted in reduced urinary cortisol and mental stress (Messaoudi et al., 2011) and reduced reactivity to sad mood (Steenbergen et al., 2015b) in healthy human volunteers.

Certain strains of probiotics, namely Lactobacillus and Bifidobacterium, produce GABA, in vivo. (Barrett et al., 2012; Boonstra et al., 2016). GABA and its receptors are widely distributed through the ENS (Auteri et al., 2015). Additionally, there is considerable communication between the gut and the brain through the vagal nerve (Cryan and O’Mahony, 2011; Cryan and Dinan, 2012). This nerve consists of sensory nerve fibers that relay information about the state of bodily organs to the central nervous system (Thayer and Sternberg, 2009).

I took them for a month over the summer I did not notice any changes to my mental functionality and/or energy levels. I stopped taking them.

I think the issue is that the dosage is too low for my health problems! If I increased the dosage, This should overload my digestive system with a very very large amount of ‘friendly’ bacteria.

The overall total number of bacterial cells in the intestinal flora is approximately 10^14, which is 100,000,000,000,000 or 100 trillion (Ott et al., 2004). Megadosing might have a profound effect on my recovery, since small dosages might not even be worthwhile and/or take a long time, perhaps months and years to actually do anything. With this test, I will end up flooding my body with 1% of the total number of gut flora, which is much larger than the standard dosages recommended.

On November 29th, just after 2 am, I did an initial loading test of 15 pills of 30 trillion (Dr. Tobias Probiotics: 30 Billion with Delay Release & Spore Forming Strains – Probiotic Supplement for Post-Antibiotic, Health & Immune Support Manufacturer: Dr. Tobias). Within 90 minutes, just before bed, I had a surge of happiness – similar to being high on painkillers but not in the same thing. The effect wasn’t short-lived and has progressed for over 24 hours. I feel slightly better, happier and content than before. I had a surge of energy that prevented me from sleeping. When I woke up, I felt pretty good, but not amazing. This lasted about a week.

– CDP Choline.

Choline influences nervous system functionality via acetylcholine. Choline is used for the biosynthesis of acetylcholine and the cell membrane phospholipid phosphatidylcholine, which increases the repair of <any> myelin sheath damage, and increases it’s density, in vitro. (Skripuletz et al., 2015; Weiss, 1995; Clement and Kent, 1999; Hunt et al., 2001). According to the paper by Skripuletz et al., (2015) CDP Choline increases the density of myelin, reversed motor coordination deficits, etc after 6 weeks of treatment, in vitro (Graph 1 & 2), also crosses the Blood-Brain-Barrier (Conant and Schauss, 2004; Garcia-Cobos et al., 2010) Choline is quite safe (Grieb, 2014; Adibhatla and Hatcher, 2002), Adverse effects are extremely rare, and consisted of stomach pain, diarrhea, and headaches. CDP-choline seems to have a lack of toxicity, but a fatal dosage in rodents is 8,000 mg/kg orally, which translates into 560,000 mg CDP-choline in a 70 kg person, which is almost not possible to ingest. (Skripuletz, et al., 2015)

Cipro, in Dogs, appears to affect Acetylcholine by inhibiting its release (Tagaya et al., 1995), Enrofloxacin exposure caused lipid peroxidation and neural dysfunction (lower AchE) in fish (Wang, et al., 2009)

– NAD+ research

Keeping NAD+ levels elevated, over 50%, for a week, decreases mtDNA mass by 50% in vitro via a 2009 paper “Nicotinamide enhances mitochondria quality through autophagy activation in human cells“. I never followed up with this because of other things I was trying.

– Resveratrol

Resveratrol facilitates oxidation of fatty acids, increases mitochondrial biogenesis, mitochondrial respiration, gluconeogenesis, mitochondrial function, protects against metabolic disease by activation of SIRT1 and PGC-1a, l prevents insulin resistance, improves vascular function, (Diaz-Gerevini et al., 2016; Lagouge et al 2006; Csiszar et al., 2009; Ungvari et al., 2011).. however, there’s some conflicting information about if it’s effective at all. Some users of this are even complaining of joint pain that doesn’t go away. I skipped over this because I didn’t have time to mess with it.

– Omega-3 [August 14th, 2016]

High-dose Fish Oil refluidizes Mitochondrial membranes by altering their plasticity. High dosage, meaning 2G a day. (Herbst et al., 2014). I did not try this more than 2 weeks, because I hated the fish-smelling burps.

– Nootropics [May 9th, 2016]

I tried these before, but I had a horrible reaction. According to numerous people, you need to take them /with/ Choline, as they deplete the Choline in your body. Curiously, when I took Oxiracetam (a small dosage), the negative effects I experienced are exactly like what happened on October 26th of 2015 (anxiety, vomiting, nervousness, brain fog, etc) Could there be a link between Levaquin and acetylcholine? Citicoline intake will increase acetylcholine production downstream, otherwise. Pramiracetam tasted horrible.

– MitoQ.

I took the entire bottle for 30 days and I didn’t notice anything major, but I was in agony from tendon pain. My energy levels were very bad from October 27th until my IV treatments, when they improved slightly. There are so many numerous papers on the literature about MitoQ and it’s health benefits. I might revisit it and take it for a long time. It’s expensive, though.

– Collagen Advanced Formula 1, 2 and 3 (6x pills a day, should have gotten the Powder).

When I started taking this, I noticed the throbbing pain in my tendons was reduced slightly. Could be placebo, though, as it takes your body 100 days to make new collagen (Khan et al., 2001; Bass, 2012)

– D-Ribose

1500 to 3000mg (2x) a day – Gave me /some/ energy. I get very bloated when I take more than one 1500mg pill in a 24 hour period. I took 4 pills one day and I almost shit myself because of the stomach pain, bloating and gas.

– DHEA

1x a day – Increases testosterone levels gradually. Seems to have increased my sex drive and body temperature. Was short-lived, though.

– BioPQQ.

Mitochondria Biogenesis / up-regulation. (20mg/day). I didn’t notice much of anything, but I took it as directed until I decided to shotgun 30 pills, and notice nothing at all.

– D-ribose-L-cysteine (RiboCene)

Seems to enhance/increase intracellular GSH aka Glutathione (Oz et al.,2007, Kader et al., 2014), reduces LDL (Kader et al.,2014), Reduces pro-inflammatory cytokines in the stomach and restores homeostasis in the gut (Kim et al.,2009). A 30 day supply is $70 USD (1x pill a day) – but the literature makes mention of serum levels of GSH increase rather quickly with that supplement, but then drop off since the cells absorb the GSH, directly. I took it for 2 weeks and didn’t notice anything. It’s very expensive, though.

– Methyl-B12

Made me very tired during the day. So tired I was falling asleep standing up. [Might be a dosage issue]. Methyl-B12, in some studies with super high dosages, appears to reverse peripheral neuropathy via nerve regeneration (Watanabe, et al 1994; Tanaka, 2015; Head, 2006; Okada et al., 2010), improves nerve conduction velocity (Morani et al., 2010). However, in a large scale trial, B12 supplementation did not appear to have much effect (Dangour et al., 2015). But, that study was only performed with patients mean age of >= 75 years. I might revisit this, though with super high dosages. Methyl-B12 deficiencies affect Adrenal functionality (Lodhi and Panchal, 2014; Majeed and Arafat, 2010), though.

Out of the 91 supplements/therapies I have tried, only 7 of them have shown any effect at all. 2 of them had very bad side effects (2 out of the 3 nootropics)

Why did Levaquin wreck my body?

There’s only been maybe a handful of papers that explore the mechanisms behind FQ toxicity.

According to Telfer (2014), Fluoroquinolones seem to induce intracellular magnesium deficiency, as the 3-carboxyquinolone substructure of FQs is metal-cleating, and 6-fluoro substituent on the pharmacophore gives rise to sufficient lipophilicity that the drugs can dissolve in and penetrate cell membranes. It has also been suggested that intracellular fluoroquinolones can exist as a magnesium complex! Cellular Diffusion and/or Active Transport of such a complex would deplete Magnesium from the cells. (Lecomte et al., 1994; Bensikaddour, 2008) The effects of fluoroquinolones on intracellular magnesium levels might be considered to be almost cumulative, and slow to reverse overall. (Jahnen-Dechent and M. Ketteler, 2012)

Levaquin, like other FQs, appears to cause significant dysglycemia (Friedrich and Dougherty 2004, Singh and Jacob 2008, Kelesidis and Canseco 2009) Dysglycemia is a broad term that refers to an abnormality in blood sugar stability, which is what I had, post-Levaquin. I also developed a ‘beer gut’ and some elevated fasting blood glucose levels, post-Levaquin. I tested my fasting glucose levels on about a dozen occasions over 20 months, and they were between 75 and 135 for no reason at all. It’s likely that Levaquin altered my Mg2 status, causing insulin resistance, and my abdominal area started to put on fat (hence the beer gut), which is reducing Beta Cell functionality. There are NUMEROUS studies that show prolonged fasting can reverse Type 2 Diabetes because the Pancreas will rewire itself under calorie restriction, therefore normalising Beta Cell Production (Lim, et al., 2011; Petersen et al., 2005; White et al., 2016, Cheng et al., 2017; Barnosky et al., 2014). I may have contributed to those because during the early to middle stages of my Levaquin Toxicity, I was drinking a large number of sodas/coffee, because of the caffeine content, to try and stay awake to do my job.

Mg2 is needed for numerous cellular functions, including Glutathione production, Glucose Homeostasis, and hundreds more. A disruption in this would likely cause systemic issues that persist for years. A treatment option would be [more] aggressive magnesium supplementation that has so far been attempted, in order to keep a bit higher concentrations of both ions in the blood plasma, which makes it possible to reduce the concentration gradients across the cell membranes and facilitate entering both to the cell. (This is also covered by Michalak et al., 2017). There’s a possibility that Mg2 depletion causes a chain reaction (delayed toxicity?), but there needs to be further study of this.

Next, Michalak et al., (?2017) is probably the most comprehensive study of Fluoroquinolone Toxicity ever published (so far). It does mention Mg2/Fe2/etc being removed from the cells, but it also dives into other areas.

I will focus on something that really stands out in the paper – At least for me – The authors argue that because FQs have a very high melting point, over 200C, the crystals are likely to become ‘stuck’ within your body and cannot be removed by normal biological processes. FQ molecule data was published nearly 2 decades ago (Andriole et al., 2000). However, even they argue that because this phenomenon is unusual, there is some other process(es) that causes this since it’s not affecting every single person who takes Cipro, Levaquin, etc.

Strauchman and Morningstar (2012) described a patient that had Fluoroquinolone Toxicity Syndrome. Genetic testing revealed polymorphisms in cytochrome P-450 pathway, as well as genetic variations in the catechol-o-methyl transferase enzyme, the N-acetyl transferase enzyme, and the glutathione-s-transferase enzyme necessary for glutathione conjugation and phase II detoxification. After a course of antioxidant IV therapy, a majority of the patients’ symptoms had improved except for a few which were likely something else.

I had an earlier hypothesis that my symptoms were more or less caused by detoxification issues, and this evidence strongly links my symptoms to prolonged accumulation of FQs(!!)

The paper (pp. 3-5) also makes it clear that it’s highly likely, though indirectly, that CYP450 polymorphisms are the culprit for FQ accumulation in human cells. CYP450 inhibition by FQs were found in chicken by Shlosberg et al. (1997) and Granfors et al. (2004) Regmi et al. pointed to the inhibiting effect of FQs in dogs on P-450 1A but not on P-450 3A (Regmi et al., 2005; 2007) Ozone therapy appears to remove FQ’s from liquid water (Feng et al., 2016).

If I really do have polymorphisms – A solution to removing the accumulated FQs would be antioxidant IV therapy such as NAC (which also reversal many modes of mitochondrial dysfunction), Glutathione(?).

Of course, this is all in-vivo but the evidence that FQs accumulate in the body – The accumulation is likely because of detoxification polymorphisms – And FQ removal seems possible – Is /all/ backed up by evidence.

More evidence that antioxidant IV therapy removes FQ accumulation is an article by Cohen (2008) where he reports a patient was disabled for 3 years from Fluoroquinolone treatment, but once the user started antioxidant IV therapy, the patient improved dramatically. (http://www.medicationsense. com/articles/jan_dec_08/ toxicity070508.php)

Conclusion:

It’s likely that Levaquin treatment started a chain reaction in my body that left me nearly crippled for a year and a half.

I consider myself 98% recovered, and I hope my research can help someone.

– Sairam K, McNicholas T. Sildenafil in diabetic peripheral neuropathy. Br J Diabetes Vasc Dis 2002
– Korkmaz MF, Parlakpinar H, Ceylan MF, et al. The Effect of Sildenafil on Recuperation from Sciatic Nerve Injury in Rats. Balkan Med J. 2016;33(2):204–211. doi:10.5152/balkanmedj.2016.14701
– Wang L, Chopp M, Szalad A, Lu X, Jia L, Lu M, Zhang RL, Zhang ZG. Tadalafil Promotes the Recovery of Peripheral Neuropathy in Type II Diabetic Mice. PLoS One. 2016
– Wang L, Chopp M, Szalad A, Liu Z, Bolz M, Alvarez FM, Lu M, Zhang L, Cui Y, Zhang RL, Zhang ZG. Phosphodiesterase-5 is a therapeutic target for peripheral neuropathy in diabetic mice. Neuroscience. 2011
– L. Wang, M. Chopp, A. Szalad, Z. Liu, M. Bolz, F.M. Ãlvarez, M. Lu, L. Zhang, Y. Cui, R.L. Zhang, and Z.G. Zhang, Phosphodiesterase-5 is a therapeutic target for peripheral neuropathy in diabetic mice, Neuroscience, 193, (399), (2011).
– Lei Wang, Michael Chopp, and ZhengGang Zhang, PDE5 inhibitors promote recovery of peripheral neuropathy in diabetic mice, Neural Regeneration Research, 12, 2, (218), (2017).
– Christina Alves Peixoto, Ana Karolina Santana Nunes, and Ana Garcia-Osta, Phosphodiesterase-5 Inhibitors: Action on the Signaling Pathways of Neuroinflammation, Neurodegeneration, and Cognition, Mediators of Inflammation, 10.1155/2015/940207, 2015, (1-17), (2015).
– Lei Wang, Michael Chopp, Alexandra Szalad, LongFei Jia, XueRong Lu, Mei Lu, Li Zhang, Yi Zhang, RuiLan Zhang, Zheng Gang Zhang and Julie A. Chowen, Sildenafil Ameliorates Long Term Peripheral Neuropathy in Type II Diabetic Mice, PLOS ONE, 10, 2, (e0118134), (2015).
– Taymour Mostafa, Oral Phosphodiesterase Type 5 Inhibitors: Nonerectogenic Beneficial Uses, The Journal of Sexual Medicine, 5, 11, (2502-2518), (2008).
– C. Vlachopoulos, D. Terentes-Printzios, N. Ioakeimidis, K. Rokkas, and C. Stefanadis, “ PDE5 Inhibitors in Non-Urological Conditions”, Current Pharmaceutical Design (2009) 15: 3521. https://doi.org/10.2174/138161209789206980
– Duranti G, Ceci R, Sgrò P, Sabatini S, Di Luigi L. Influence of the PDE5 inhibitor tadalafil on redox status and antioxidant defense system in C2C12 skeletal muscle cells. Cell Stress Chaperones. 2017;22(3):389–396. doi:10.1007/s12192-017-0778-9
– Pauls MM, Moynihan B, Barrick TR, Kruuse C, Madigan JB, Hainsworth AH, Isaacs JD. The effect of phosphodiesterase-5 inhibitors on cerebral blood flow in humans: A systematic review. J Cereb Blood Flow Metab. 2018 Feb;38(2):189-203.
– Dubé KN, Smart N. Thymosin ß4 and the vasculature: multiple roles in development, repair, and protection against disease. Expert Opin Biol Ther. 2018 Jul;18(sup1):131-139. doi: 10.1080/14712598.2018.1459558. Review. PubMed PMID: 30063849.
– Zhao Y, Song J, Bi X, Gao J, Shen Z, Zhu J, Fu G. Thymosin ß4 promotes endothelial progenitor cell angiogenesis via a vascular endothelial growth factor-dependent mechanism. Mol Med Rep. 2018 Aug;18(2):2314-2320. doi: 10.3892/mmr.2018.9199. Epub 2018 Jun 20. PubMed PMID: 29956769.
– Kim, S., & Kwon, J. (2015). Effect of thymosin beta 4 in the presence of up-regulation of the insulin-like growth factor-1 signaling pathway on high-glucose-exposed vascular endothelial cells. Molecular and Cellular Endocrinology, 401, 238–247. doi:10.1016/j.mce.2014.12.008
– Philp, D., Goldstein, A.L., Kleinman, H.K., 2004. Thymosin beta4 promotes angiogenesis, wound healing, and hair follicle development. Mech. Ageing Dev. 125, 113–115.
– Calcutt NA, Smith DR, Frizzi K, et al. Selective antagonism of muscarinic receptors is neuroprotective in peripheral neuropathy. J Clin Invest. 2017;127(2):608–622. doi:10.1172/JCI88321
– Ilgin S, Can OD, Atli O, Ucel UI, Sener E, Guven I. Ciprofloxacin-induced
neurotoxicity: evaluation of possible underlying mechanisms. Toxicol Mech
Methods. 2015;25(5):374-81. doi: 10.3109/15376516.2015.1026008. PubMed PMID:
25902267.
– Talla V, Veerareddy P. Oxidative Stress Induced by Fluoroquinolones on Treatment for Complicated Urinary Tract Infections in Indian Patients. Journal of Young Pharmacists : JYP. 2011;3(4):304-309. doi:10.4103/0975-1483.90242.
– Ott SJ, Musfeldt M, Ullmann U, Hampe J, Schreiber S. Quantification of Intestinal Bacterial Populations by Real-Time PCR with a Universal Primer Set and Minor Groove Binder Probes: a Global Approach to the Enteric Flora. Journal of Clinical Microbiology. 2004;42(6):2566-2572. doi:10.1128/JCM.42.6.2566-2572.2004.
– Barrett E, Ross RP, O’Toole PW, Fitzgerald GF, Stanton C. ?-Aminobutyric acid production by culturable bacteria from the human intestine. J Appl Microbiol.
2012 Aug;113(2):411-7. doi: 10.1111/j.1365-2672.2012.05344.x. Erratum in: J Appl
Microbiol. 2014 May;116(5):1384-6. PubMed PMID: 22612585.
– Boonstra E, de Kleijn R, Colzato LS, Alkemade A, Forstmann BU, Nieuwenhuis S. Neurotransmitters as food supplements: the effects of GABA on brain and behavior. Frontiers in Psychology. 2015;6:1520. doi:10.3389/fpsyg.2015.01520.
– A.V. Rao, A.C. Bested, T.M. Beaulne, et al. A randomized, double-blind, placebo-controlled pilot study of a probiotic in emotional symptoms of chronic fatigue syndromeGut Pathogens, 1 (2009), p. 6
Singh, P. K., et al. “Role of Lactobacillus acidophilus loaded floating beads in chronic fatigue syndrome: behavioral and biochemical evidences.” Neurogastroenterology & Motility 24.4 (2012): 366-e170.
– Dangour, Alan D., et al. “Effects of vitamin B-12 supplementation on neurologic and cognitive function in older people: a randomized controlled trial.” The American journal of clinical nutrition 102.3 (2015): 639-647.
Interrelationship of Vitamin B12, Androgens, and Cortisol in Chronic Stress and associated Vascular Dysfunction
http://www.jscimedcentral.com/Pharmacology/pharmacology-2-1028.pdf Methylcobalamin has an Effect on Hypothalamic-Hypophyseal-Adrenal Axis
-http://www.researchgate.net/profile/Osama_Arafat/publication/234135338_METHYLCOBALAMIN_HAS_AN_EFFECT_ON_HYPOTHALAMICHYPOPHYSEALADRENAL_AXIS/links/00b7d535ff904b4c57000000.pdf
– Nutrients and Botanicals for Treatment of Stress: Adrenal Fatigue, Neurotransmitter Imbalance, Anxiety, and Restless Sleep http://032912b.membershipsoftware.org/libdocuments/Nutrients_HM_Stress_Review.pdf
– Tagaya E, Tamaoki J, Takemura H, Chiyotani A, Konno K. [Effect of
ciprofloxacin on contractile responses of canine airway smooth muscle].
Kansenshogaku Zasshi. 1995 Apr;69(4):404-7. Japanese. PubMed PMID: 7751748.
– Okada, Kiyoshi, et al. “Methylcobalamin increases Erk1/2 and Akt activities through the methylation cycle
and promotes nerve regeneration in a rat sciatic nerve injury model.” Experimental neurology 222.2 (2010): 191-203.
– Tanaka H. [Old or new medicine? Vitamin B12 and peripheral nerve neuropathy].
Brain Nerve. 2013 Sep;65(9):1077-82. Review. Japanese. PubMed PMID: 24018744.
– Head, Kathleen A. “Peripheral neuropathy: pathogenic mechanisms and alternative therapies.” Alternative medicine review 11.4 (2006): 294.
– Wang N, Nkejabega N, Hien NN, Huynh TT, Silvestre F, Phuong NT, Danyi S,
Widart J, Douny C, Scippo ML, Kestemont P, Huong DT. Adverse effects of
enrofloxacin when associated with environmental stress in Tra catfish
(Pangasianodon hypophthalmus). Chemosphere. 2009 Dec;77(11):1577-84. doi: 10.1016/j.chemosphere.2009.09.038. PubMed PMID: 19836822.
Grieb P. Neuroprotective properties of citicoline: facts, doubts and unresolved issues. CNS Drugs. 2014;28:185–193.
– Grieb P. Beneficial effects of exogenous CDP-cholinê (citicoline) in EAE. Brain. 2015 doi: 10.1093/brain/awv140.
– Watanabe T, Kaji R, Oka N, Bara W, Kimura J. Ultra-high dose methylcobalamin promotes nerve regeneration in experimental acrylamide neuropathy. J Neurol Sci. 1994 Apr;122(2):140-3. PubMed PMID: 8021696.
– Adibhatla RM, Hatcher JF. Citicoline mechanisms and clinical efficacy in cerebral ischemia. J Neurosci Res. 2002;70:133–139.
– Kremer, D., Göttle, P., Hartung, H. P., & Küry, P. (2016). Pushing Forward: Remyelination as the New Frontier in CNS Diseases. Trends in neurosciences, 39(4), 246-263.
– Hamacher-Brady A, Brady NR. Mitophagy programs: mechanisms and physiological implications of mitochondrial targeting by autophagy. Cellular and Molecular Life Sciences. 2016;73:775-795. doi:10.1007/s00018-015-2087-8.
– Jang S, Kang HT, Hwang ES. Nicotinamide-induced Mitophagy: EVENT MEDIATED BY HIGH NAD+/NADH RATIO AND SIRT1 PROTEIN ACTIVATION. The Journal of Biological Chemistry. 2012;287(23):19304-19314. doi:10.1074/jbc.M112.363747.
– Shibasaki M, Crandall CG. Mechanisms and controllers of eccrine sweating in humans. Frontiers in bioscience (Scholar edition). 2010;2:685-696.
– Grill MF, Maganti RK. Neurotoxic effects associated with antibiotic use: management considerations. British Journal of Clinical Pharmacology. 2011;72(3):381-393. doi:10.1111/j.1365-2125.2011.03991.x.
– Csiszar A, Labinskyy N, Pinto JT, Ballabh P, Zhang H, Losonczy G, Pearson K, de Cabo R, Pacher P, Zhang C, Ungvari Z. Resveratrol induces mitochondrial biogenesis in endothelial cells. Am J Physiol Heart Circ Physiol. 2009 Jul;297(1):H13-20. doi: 10.1152/ajpheart.00368.2009. PubMed PMID: 19429820; PubMed Central PMCID: PMC2711732.
– Zoltan Ungvari; William E. Sonntag; Rafael de Cabo; Joseph A. Baur; Anna Csiszar. Mitochondrial Protection by Resveratrol
Exerc Sport Sci Rev. 2011;39(3):128-132.
– Lagouge et al., 2006 M. Lagouge, C. Argmann, Z. Gerhart-Hines, H. Meziane, C. Lerin, F. Daussin, N. Messadeq, J. Milne, P. Lambert, P. Elliott, et al. Resveratrol improves mitochondrial function and protects against metabolic disease by activating SIRT1 and PGC-1alpha
Diaz-Gerevini GT, Repossi G, Dain A, Tarres MC, Das UN, Eynard AR. Beneficial action of resveratrol: How and why? Nutrition. 2016 Feb;32(2):174-8. doi:
10.1016/j.nut.2015.08.017. Review. PubMed PMID: 26706021.
– Khan KM, Cook JL, Taunton JE, et al. Overuse tendinosis, not tendinitis—Part 1: A new paradigm for a difficult clinical problem. [Accessed 13 February 2012];Physician Sportsmed. 2000 28(5)
Bass E. Tendinopathy: Why the Difference Between Tendinitis and Tendinosis Matters. International Journal of Therapeutic Massage & Bodywork. 2012;5(1):14-17.
– Kang, H. T., and Hwang, E. S. (2009),
Nicotinamide enhances mitochondria quality through autophagy activation in human cells.
Aging Cell, 8: 426–438. doi:10.1111/j.1474-9726.2009.00487.x
– Trammell SA, Schmidt MS, Weidemann BJ, Redpath P, Jaksch F, Dellinger RW, Li Z, Abel ED, Migaud ME, Brenner C. Nicotinamide riboside is uniquely and orally bioavailable in mice and humans. Nat Commun. 2016 Oct 10;7:12948. doi:
10.1038/ncomms12948. PubMed PMID: 27721479; PubMed Central PMCID: PMC5062546.
– Khan NA, Auranen M, Paetau I, Pirinen E, Euro L, Forsström S, Pasila L,
Velagapudi V, Carroll CJ, Auwerx J, Suomalainen A. Effective treatment of
mitochondrial myopathy by nicotinamide riboside, a vitamin B3. EMBO Mol Med. 2014
Apr 6;6(6):721-31. doi: 10.1002/emmm.201403943. PubMed PMID: 24711540; PubMed
Central PMCID: PMC4203351.
– Chi Y, Sauve AA. Nicotinamide riboside, a trace nutrient in foods, is a
vitamin B3 with effects on energy metabolism and neuroprotection. Curr Opin Clin
Nutr Metab Care. 2013 Nov;16(6):657-61. doi: 10.1097/MCO.0b013e32836510c0.
Review. PubMed PMID: 24071780.
– Mukherjee S, Chellappa K, Moffitt A, Ndungu J, Dellinger RW, Davis JG, Agarwal B, Baur JA. Nicotinamide adenine dinucleotide biosynthesis promotes liver regeneration. Hepatology. 2016 Nov 3. doi: 10.1002/hep.28912. [Epub ahead of
print] PubMed PMID: 27809334.
– Trammell SA, Yu L, Redpath P, Migaud ME, Brenner C. Nicotinamide Riboside Is a Major NAD+ Precursor Vitamin in Cow Milk. J Nutr. 2016 May;146(5):957-63. doi:
10.3945/jn.116.230078. PubMed PMID: 27052539.
– Conze DB, Crespo-Barreto J, Kruger CL. Safety assessment of nicotinamide
riboside, a form of vitamin B3. Hum Exp Toxicol. 2016 Jan 20. pii:
0960327115626254. [Epub ahead of print] PubMed PMID: 26791540.
Adams JD Jr, Klaidman LK, Odunze IN, et al.
Alzheimer’s and Parkinson’s Disease. Brain
levels of glutathione, glutathione disulfide, and
vitamin E. Mol Clin Neuropathol 1991;
14:213-226
Meister A. Mitochondrial changes associated with glutathione deficiency.
Biochim Biophys Acta. 1995 May 24;1271(1):35-42. Review. PubMed PMID: 7599223.
– Hong SY, Gil HW, Yang JO, Lee EY, Kim HK, Kim SH, Chung YH, Hwang SK, Lee ZW. Pharmacokinetics of glutathione and its metabolites in normal subjects. J Korean
Med Sci. 2005 Oct;20(5):721-6. PubMed PMID: 16224142; PubMed Central PMCID:
PMC2779265.
Strauchman M, Morningstar MW. Fluoroquinolone toxicity symptoms in a patient presenting
with low back pain. Clinics and Practice. 2012;2(4):e87. doi:10.4081/cp.2012.e87.
– Skripuletz T, Manzel A, Gropengießer K, Schäfer N, Gudi V, Singh V, Salinas Tejedor L, Jörg S, Hammer A, Voss E, Vulinovic F, Degen D, Wolf R, Lee DH, Pul R, Moharregh-Khiabani D, Baumgärtner W, Gold R, Linker RA, Stangel M. Pivotal role of choline metabolites in remyelination. Brain. 2015 Feb;138(Pt 2):398-413. doi: 10.1093/brain/awu358. PubMed PMID: 25524711.
– Conant R, Schauss AG. Therapeutic applications of citicoline for stroke and cognitive dysfunction
in the elderly: a review of the literature. Altern Med Rev 2004;9:17-31
Weiss GB. Metabolism and actions of CDP-choline as an endogenous compound and administered exogenously as citicoline. Life Sci 1995;56:637-660
– Hunt AN, Clark GT, Attard GS, Postle AD. Highly saturated endonuclear phosphatidylcholine is synthesized in situ and colocated with CDP-choline pathway enzymes. J Biol Chem 2001;276:8492-9
Garcia-Cobos R, Frank-Garcia A, Gutierrez-Fernandez M, Diez-Tejedor E. Citicoline, use in cognitive decline: vascular and degenerative. J Neurol Sci 2010;299:188-92.
– Herbst EA, Paglialunga S, Gerling C, Whitfield J, Mukai K, Chabowski A,
Heigenhauser GJ, Spriet LL, Holloway GP. Omega-3 supplementation alters
mitochondrial membrane composition and respiration kinetics in human skeletal
muscle. J Physiol. 2014 Mar 15;592(6):1341-52. doi: 10.1113/jphysiol.2013.267336.
PubMed PMID: 24396061; PubMed Central PMCID: PMC3961091.
– J.A. Bravo, P. Forsythe, M.V. Chew, E. Escaravage, H.M. Savignac, T.G. Dinan, J. Bienenstock, J.F. Cryan
Ingestion of Lactobacillus strain regulates emotional behavior and central GABA receptor expression in a mouse via the vagus nerve
Proc. Natl. Acad. Sci. USA, 108 (2011), pp. 16050–16055
Frantz MC, Wipf P. Mitochondria as a target in treatment. Environ Mol Mutagen. 2010 Jun;51(5):462-75. doi: 10.1002/em.20554.
– Michelakis, Evangelos. “A Mitochondria-K+ Channel Axis Is Suppressed in Cancer and Its Normalization Promotes Apoptosis and Inhibits Cancer Growth”. University of Alberta. University of Alberta, 2007.
Kalghatgi S, Spina CS, Costello JC, et al. Bactericidal Antibiotics Induce Mitochondrial Dysfunction and Oxidative Damage in Mammalian Cells. Science translational medicine. 2013;5(192):192ra85. doi:10.1126/scitranslmed.3006055.
– Ates B1, Abraham L, Ercal N. 2008 “Antioxidant and free radical scavenging properties of N-acetylcysteine amide (NACA) and comparison with N-acetylcysteine (NAC).”
– Penugonda S1, Mare S, Goldstein G, Banks WA, Ercal N. “Effects of N-acetylcysteine amide (NACA), a novel thiol antioxidant against glutamate-induced cytotoxicity in neuronal cell line PC12.”
– Garnett W, Garnett M. Paper presented at the Conference on: Oxygen Metabolites in Nonheme Metabollichemistry, June 23, 1996. University of Minnesota; Charge relay from molybdate oxyradicals to palladium-lipoic complex to DNA
– Raj A, Praveen KV, Varghese S, Mukkadan JK, Joseph PK. Biochemical effects of feeding soft drink and ethanol. Indian J Exp Biol. 2009 May;47(5):333-7. PubMed PMID: 19579797.
Kristensen M, Jensen M, Kudsk J, Henriksen M, Mølgaard C. Short-term effects on bone turnover of replacing milk with cola beverages: a 10-day interventional study in young men. Osteoporos Int. 2005 Dec;16(12):1803-8. Epub 2005 May 11. PubMed PMID: 15886860.
Strauchman M, Morningstar MW. Fluoroquinolone toxicity symptoms in a patient presenting with low back pain. Clinics and Practice. 2012;2(4):e87. doi:10.4081/cp.2012.e87.
– Huang J, Zhou C, He J, Hu Z, Guan WC, Liu SH. Protective effect of reduced glutathione C60 derivative against hydrogen peroxide-induced apoptosis in HEK 293T cells. J Huazhong Univ Sci Technolog Med Sci. 2016 Jun;36(3):356-63. doi: 10.1007/s11596-016-1591-x. Epub 2016 Jul 5. PubMed PMID: 27376803.
Mamontova TV, Vesnina LE, Mikityuk MV, Bobrova NA, Kutsenko LA, Gordinskaya IL, Kaidashev IP. [FULLERENE C60 INHIBITED FREE RADICAL AND DESTRUCTIVE PROCESSES IN CONNECTIVE TISSUE DURING ADJUVANT ARTHRITIS IN RATS]. Fiziol Zh. 2015;61(2):80-6. Ukrainian. PubMed PMID: 26387164.
– Ye S, Zhou T, Cheng K, Chen M, Wang Y, Jiang Y, Yang P. Carboxylic Acid Fullerene (C60) Derivatives Attenuated Neuroinflammatory Responses by Modulating Mitochondrial Dynamics. Nanoscale Res Lett. 2015 Dec;10(1):953. doi: 10.1186/s11671-015-0953-9. Epub 2015 May 30. PubMed PMID: 26058514; PubMed Central PMCID: PMC4481245.
Ngan CL, Basri M, Tripathy M, Abedi Karjiban R, Abdul-Malek E. Skin intervention of fullerene-integrated nanoemulsion in structural and collagen regeneration against skin aging. Eur J Pharm Sci. 2015 Apr 5;70:22-8. doi: 10.1016/j.ejps.2015.01.006. Epub 2015 Jan 22. PubMed PMID: 25619806.
– Artem A. Tykhomyrova, Victor S. Nedzvetskya, Vladimir K. Klochkovb, Grigory V. Andrievskyb Nanostructures of hydrated C60 fullerene (C60HyFn) protect rat brain against alcohol impact and attenuate behavioral impairments of alcoholized animals
– Yang X, Li C-J, Wan Y, Smith P, Shang G, Cui Q. Antioxidative fullerol promotes osteogenesis of human adipose-derived stem cells. International Journal of Nanomedicine. 2014;9:4023-4031. doi:10.2147/IJN.S66785.
Krusic PJ, Wasserman E, Keizer PN, Morton JR, Preston KF Radical reactions of c60. Science. 1991
-V. A. Chistyakov, Yu. O. Smirnova, E. V. Prazdnova, and A. V. Soldatov, “Possible Mechanisms of Fullerene C60 Antioxidant Action,” BioMed Research International, vol. 2013, Article ID 821498, 4 pages, 2013. doi:10.1155/2013/821498
– Najla Gharbi ,† Monique Pressac ,‡ Michelle Hadchouel ,§ Henri Szwarc ,† Stephen R. Wilson ,‖ and Fathi Moussa *† [60]Fullerene is a Powerful Antioxidant in Vivo with No Acute or Subacute Toxicity. 2005
OZ HS, CHEN TS, NAGASAWA H. Comparative efficacies of 2 cysteine prodrugs and a glutathione delivery agent in a colitis model. Translational research : the journal of laboratory and clinical medicine. 2007;150(2):122-129. doi:10.1016/j.trsl.2006.12.010.
– Shershakova N, Baraboshkina E, Andreev S, Purgina D, Struchkova I, Kamyshnikov O, Nikonova A, Khaitov M. Anti-inflammatory effect of fullerene C60 in a mice model of atopic dermatitis. J Nanobiotechnology. 2016 Jan 25;14:8. doi: 10.1186/s12951-016-0159-z. PubMed PMID: 26810232; PubMed Central PMCID: PMC4727272.

** The story above is truthful, accurate and told to the best of the ability of the writer. It is not intended as medical advice. No person who submits his or her story, nor the people associated with Floxie Hope, diagnoses or treats any illness. The story above should not be substituted for professionally provided medical advice. Please consult your doctor before trying anything that has been mentioned in this story, or in any other story on this site. Please also note that people have varying responses to the treatments mentioned in each story. What helps one person may not help, and may even hurt, another person. It is important that you understand that supplements, IVs, essential oils, and all other treatments, effect people differently depending on the millions of variables that make each of us unique. Please use appropriate caution and prudence, and get professional medical advice.

200 thoughts on “Gary’s Story – Levaquin Toxicity

  1. Krabiwi May 4, 2019 at 10:57 am Reply

    Just saw that I wrote my first comment here on 24 May 2018, two month after I had a strong crippling onset reaction and was still in a critical phase, fully crippled and unable to walk more than 10 metres because of weak knees and strong muscular loss, trying to find a solution.

    I am now 14 month out and back to around 80-90% depending on symtpom wave, I walk 2 km easily. Tendons feel still weakened, but dont hurt anymore. Recovering slowly but steadily each month. Intermittend fasting 18/6, low carb, good nutrition and supplement of everything to maximize antioxidant capacity does the job for me.

    Gary, can you write more about your nutrition? Cutted out empty carbs like sugars and wheat flour? Fasting?

    Thanks

    • Elaine May 17, 2019 at 7:32 am Reply

      Krabiwi. Can you go more into detail about the supplements you take to help your antioxidants? Glad you are doing much better!! Bravo!!!

      • Krabiwi May 19, 2019 at 6:44 pm Reply

        Daily:
        Q10 100mg with oil
        Vit C 500mg
        Vit + Mineral complex which covers everything 100%
        Clucosamin, Chondroitin, MSM complex
        Omega 3 fish oil 1g
        Protein Whey 20g
        Vit D 5000 i.e. + Vit K 100 µg
        Magnesium citrate 600-800 mg in filtered water

        But I can tell supplements are only a small part of therapy, in fact low carb diet and cutting out empty carbs like sugar und wheat flour / bread is essential to recover as fast as possible as carbs are glucosis and increase oxidative stress in mitochondria.

        • Krabiwi May 19, 2019 at 6:47 pm

          In the first 6 month, the serious phase, I also took S-Acetyl-Glutathion 100mg daily.

  2. Gary Stanley June 1, 2019 at 7:33 pm Reply

    I have not done any special dieting. I dropped a lot of the things I was attempting because I felt they were worthless (and snakeoil)

  3. L Simon September 12, 2019 at 5:59 am Reply

    Hi! Has anyone in the Maryland, DC, Virginia area had any luck with anyone in the medical community – anyone in health care that understands what is going on? My son Is over 2.5 years out and still has the same issues of malabsorption, bad gut, bladder and bowel issues, tendoitis, endocrine issues….

  4. Felicia September 26, 2019 at 12:45 pm Reply

    Gary,
    Thank you for such a thoroughly researched collection of facts as they relate to your harrowing quarrel with Levaquin.

    Q1: I’m particularly intrigued by your dysglycemia notes. How did you resolve this? With magnesium? I’m trying EVERYTHING.

    Also, Q2: are you still mega dosing probiotics?

    Thank you.

    • Gary Stanley October 7, 2019 at 7:16 pm Reply

      Felicia

      I stopped megadosing probiotics ages ago. As for your other question. I was taking small but frequent amounts of Magnesium (3x a day) for months.

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out /  Change )

Google photo

You are commenting using your Google account. Log Out /  Change )

Twitter picture

You are commenting using your Twitter account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )

Connecting to %s

This site uses Akismet to reduce spam. Learn how your comment data is processed.

%d bloggers like this: