Tag Archives: Oxidative stress

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

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

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

The first paragraph of the abstract to the article states:

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

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

Adverse Effects of Fluoroquinolones

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

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

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

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

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

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

Fluoroquinolone Damage Mechanisms

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Fluoroquinolone Toxicity Treatment

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

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

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

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

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

Conclusion

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

 

 

 

Floxie Hope Podcast Episode 14 – Dr. Terry Wahls

It was an absolute HONOR to interview Dr. Terry Wahls for episode 14 of The Floxie Hope Podcast. Dr. Wahls has inspired millions of people with her personal story of putting progressive multiple sclerosis (M.S) into remission through diet and lifestyle changes. She is the author of The Wahls Protocol: A Radical New Way to Treat all Chronic Autoimmune Conditions Using Paleo Principles. In addition to reversing the course of various autoimmune diseases, the Wahls Protocol has helped thousands of people to recover from mysterious chronic illnesses like Lyme Disease, fibromyalgia, chronic fatigue syndrome / M.E, and fluoroquinolone toxicity.

In this interview, Dr. Wahls and I discuss how mitochondria can be repaired through diet and lifestyle changes. We go over the basics of The Wahls Protocol diet, and we discuss how everyone who has been hurt by a mitochondrial poison can nourish their cells. Information about Dr. Wahls can be found on http://terrywahls.com/.

You can listen to the podcast through these links:

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

http://www.floxiehopepodcast.com/episode-014-dr-terry-wahls/

Please accept my sincere apologies for the horrible sound quality in the first 5 minutes of the podcast. It is better after the 5 minute mark, so please hang in there and listen past the fuzziness at the beginning.

Renee’s story illustrates how helpful The Wahls Protocol is for those suffering from fluoroquinolone toxicity – https://floxiehope.com/renees-story-cipro-reaction/.

Dr. Wahls’ TED talk has been viewed more than 2.2 million times and has inspired and touched every person who has viewed it. I encourage you to listen to the podcast, buy the book, and watch Dr. Wahls’ inspirational TED talk

 

flu tox get help you need banner click lisa

Fluoroquinolone Antibiotics Damage Mitochondria – FDA Does Little

Hormones Matter Logo2

The Pharmacovigilance folks at the FDA know that fluoroquinolones are damaging mitochondria.  Yet, they look the other way.  Adding a more severe warning about peripheral neuropathy to the warning label isn’t helpful.  People should know that they are increasing their risk of every chronic disease associated with mitochondrial damage and oxidative stress when they take a fluoroquinolone.  That would actually be helpful.

Here is the post, on Hormones Matter – http://www.hormonesmatter.com/fluoroquinolone-antibiotics-damage-mitochondria-fda-adds-warning/

 

flu tox get help you need banner click lisa

Fluoroquinolone Caused Mitochondrial Damage and Oxidative Stress – What are the Consequences for Floxies?

I’m working on a couple of posts/articles/essays right now about how all sorts of chronic diseases, from diabetes to alzheimer’s to autism, are caused by mitochondrial damage and oxidative stress.  I’m pointing out that pharmaceuticals cause mitochondrial damage and oxidative stress.  Of course, I’m focusing on my least-favorite pharmaceuticals, fluoroquinolones, and am trying to make a case that fluoroquinolones cause many chronic diseases.

That line of thinking is scary as hell for those of us who have had a bad reaction to a fluoroquinolone.

What does the connection between fluoroquinolone induced mitochondrial damage / oxidative stress and chronic diseases mean for us?  What is our prognosis?  Are we going to come down with diabetes or Alzheimer’s?  Are our kids going to be autistic?  Scary stuff – aaaarghhhh!!!  New plan – run and hide on a tropical island far from the internet.

Just so you all know, I’m not sure what it all means.  I am doing my best to put together the pieces of the puzzle.  I’m doing my best to draw conclusions from reputable sources.  I’m doing my best to understand what happened in my body when the Cipro bomb went off in me.  In trying to understand what happened, I’m stumbling upon articles that point to the possibility that the problem is bigger than we think.  It is possible that fluoroquinolones are causally related to fibromyalgia, chronic fatigue syndrome / M.E., all autoimmune diseases, depression, anxiety, bipolar disorder, diabetes, Alzheimer’s, autism, some kinds of cancer, and more.  Are all cases of those chronic diseases caused by fluoroquinolones?  Of course not – most of the diseases are older than fluoroquinolones.  But it’s possible that they have increased hand in hand with fluoroquinolone use because of the damage that fluoroquinolones do to mitochondria, and the oxidative stress that they induce.

It’s also possible that other drugs are the primary culprits.  And I suppose that it’s even possible that junk food that is full of free radical producting chemicals is the culprit behind all the oxidative stress that people who have chronic diseases experience.  Or maybe the problem is GMO corn or childhood vaccines or pesticides or something else.  There are pretty reputable sources that note that pharmaceuticals cause mitochondrial damage and oxidative stress though, so I’m betting that the culprits are Bayer, Johnson & Johnson, Merck, Pfizer, Abbvie and all the other pharmaceutical giants that are very good at making customers and very bad at actually promoting health.

Anyhow, the theory that fluoroquinolones cause mitochondrial damage / oxidative stress and that mito damage / oxidative stress are behind all sorts of chronic diseases is the theory that I’m going with.  Whether I’m right or wrong is yet to be seen.  Even though my theory may scare the crap out of you, your support is still greatly appreciated.  🙂

If I’m wrong, the case against fluoroquinolones is still pretty damning.  With fluoroquinolones, one can convert an acute problem, an infection, into a chronic syndrome that includes destruction of connective tissue (tendons, ligaments, cartilage, fascia, etc.) throughout the body, damage to the nervous systems (central, peripheral and autonomic), and more.  Fluoroquinolone toxicity can develop slowly or quickly.  It can last for months or years.  Tragically, some people don’t recover.  But most people do – with time.

How fluoroquinolones cause the damage that they do is hugely complex and difficult to understand.  Part of the damage mechanism is mitochondrial damage and oxidative stress, hence the trip down chronic disease lane.  Other aspects of how fluoroquinolones work – DNA adducts, RNA transcription errors, disruption of tubulin assembly, etc. are equally daunting and potentially harmful.  Ugh.  Bad news.

But people do recover from fluoroquinolone toxicity.  I did.  I’m fully recovered.  So are the other people who have shared their stories on www.floxiehope.com.  I wonder if the chronic disease prognosis for those who recover is any different from the prognosis for those who don’t, or for those who take fluoroquinolones but don’t have an adverse reaction.  I don’t think that a study to answer that question has been done.  It would be interesting to find out the answer.

Right now, we don’t know the answers though, so we have to make assumptions about our health and our future.  If you’re going to make baseless assumptions about your personal health prognosis though, they may as well be hopeful ones.  Try to believe that you will heal and that once you heal you will be as capable, resilient and durable as you were before a fluoroquinolone knocked you down.  Or, better yet, believe that floxing gave you some sort of health super-powers.  Here is a crazy thought – what if our floxing reaction was actually protective against damaged cells and the conversion of those cells into chronic diseases?  What if our horrible reaction was because of mass apoptosis (programmed cell death), and in dying, those cells kept from reproducing and leading to a chronic disease at some later time?  Now that is a far-fetched hypothesis, but I kind of like it.  I just hope that my recovery doesn’t mean that my bad cells are sticking around now.  :p

Back to fluoroquinolones being related to the chronic diseases – what if I’m right?  What if fluoroquinolone caused mitochondrial damage and oxidative stress is behind all of the chronic diseases of modernity?  Well, it’s a sad state of affairs.  But people should know about it.  They should hear about it.  They have the right to know.

But you are going to be fine.  Try to believe it.

 

flu tox get help you need banner click lisa

 

Antioxidant Depletion by Fluoroquinolones

antioxidants

One of my favorite journal articles about the adverse effects of fluroquinolones is Oxidative Stress Induced by Fluoroquinolones on Treatment for Complicated Urinary Tract Infections in Indian Patients written by V. Talla and P.R. Veerareddy and published in the Journal of Young Pharmacists.  It’s a pretty damning article and it’s easy to read.  I highly recommend that you read it yourself.  Here is the link –

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3249743/?report=printable

Even though it’s written at a level that most people can understand, there are a few terms that I’m assuming aren’t known by the average person reading this blog.  So, I have taken the main points from the study, as I see them, and explained them to the best of my ability.  Basically, I did the Google and Wiki look-ups so you don’t have to.

Here are the main points of the article:

1. “There is a significant and gradual elevation of lipid peroxide levels in patients on ciprofloxacin and levofloxacin dosage regimen but not with gatifloxacin.” What is lipid peroxide and do we want our levels to be high or low?  Wikipedia tells us that, “Lipid peroxidation refers to the oxidative degradation of lipids. It is the process in which free radicals “steal” electrons from the lipids in cell membranes, resulting in cell damage.”  (1)  Basically, lipid peroxidation is not something you want going on in your body.  You don’t want your lipids to be degraded via oxidation.  You don’t want cell damage.  Drugs that significantly increase levels of lipid peroxide are hurting you – at least on that level.


2. “There was substantial depletion in both SOD and glutathione levels particularly with ciprofloxacin.”  Superoxide dismutases (SODs) “are enzymes that catalyze the dismutation of superoxide (O2−) into oxygen and hydrogen peroxide. Thus, they are an important antioxidant defense in nearly all cells exposed to oxygen.” (2)  Additionally, “Within a cell, the superoxide dismutases (SODs) constitute the first line of defence against ROS.” (3)  SOD is “Present both inside and outside cell membranes, SOD is one of the body’s primary internal anti-oxidant defenses, and plays a critical role in reducing the oxidative stress implicated in atherosclerosis and other life-threatening diseases. Studies have shown that SOD can play a critical role in reducing internal inflammation and lessening pain associated with conditions such as arthritis.” (4) SODs are necessary for neutralizing the oxidative damage done by reactive oxygen species (ROS) (more on ROS below).

Glutathione is also depleted by fluoroquinolones.  Per Dr. Mark Hyman, Glutathione is “the most important molecule you need to stay healthy and prevent disease.”  (5)  Dr. Hyman notes that glutathione depletion “leaves you susceptible to unrestrained cell disintegration from oxidative stress, free radicals, infections and cancer.  And your liver gets overloaded and damaged, making it unable to do its job of detoxification.”  Glutathione is an extremely important antioxidant.

SOD and glutathione work together to neutralize oxidative damage done by ROS.  Here is a brief description of how SOD and glutathione work together:

SOD is responsible for catalyzing the conversion of superoxide to elemental oxygen and hydrogen peroxide. This transformation is called dismutation, hence the enzyme’s name. Although hydrogen peroxide is also a pro-oxidant compound, it is subsequently converted by the enzymes catalase and glutathione peroxidase to simple water and oxygen. (4)

Without the proper amount of SOD or glutathione in your body, ROS will wreak havoc on your system, causing oxidative stress and damage to every bodily system.   

fluoroquinolone-lawsuit-banner-trulaw

3. “On the 5th day of treatment, plasma antioxidant status decreased by 77.6%, 50.5%, 7.56% for ciprofloxacin, levofloxacin and gatifloxacin respectively.”  Antioxidants are molecules “that inhibit the oxidation of other molecules. Oxidation is a chemical reaction that transfers electrons or hydrogen from a substance to an oxidizing agent. Oxidation reactions can produce free radicals. In turn, these radicals can start chain reactions. When the chain reaction occurs in a cell, it can cause damage or death to the cell.” (6)  Oxidation is bad, antioxidants are good, cell death is bad – we want plasma antioxidant levels to be high, not low.  Decreasing plasma antioxidant status is bad for your health on a cellular level.

4. “In conclusion ciprofloxacin and levofloxacin induce more reactive oxygen species that lead to cell damage than gatifloxacin.”  The researchers also note that, “Several in vitro and in vivo study using animals revealed that fluoroquinolones induced oxidative stress by producing reactive oxygen species (ROS).”  ROS are described as follows:

Without oxygen, we could not exist. However, in the process of generating energy by “burning” nutrients with oxygen, certain “rogue” oxygen molecules are created as inevitable byproducts. Known as free radicals and reactive oxygen species, these unstable, highly reactive molecules play a role in cell signaling and other beneficial processes when they exist in benign concentrations.  But when their numbers climb, as may occur as a result of aging and other conditions, they may wreak havoc with other molecules with which they come into contact, such as DNA, proteins, and lipids. As such, these “pro-oxidant” molecules become especially toxic.

In fact, a prevailing theory of disease and aging states that the gradual accumulation of pro-oxidant molecules, and the harm they incur, is responsible for many of the adverse changes that eventually cause various diseases. These include cancer (possibly triggered by free radical-induced damage to cellular DNA) and inflammatory and degenerative diseases such as Alzheimer’s, arthritis, atherosclerosis, and diabetes. While scientists have not yet reached consensus on the topic, accumulated evidence overwhelmingly identifies increased oxidative stress with age as a source of damage to cellular structure and function.  (4)

Additionally, the wikipedia article on ROS does a nice job of explaining the damage that ROS can do – http://en.wikipedia.org/wiki/Reactive_oxygen_species

5. The authors of the study also note that, “The efforts of the endogenous antioxidant enzymes like SOD to remove the continuously generated free radicals initially increase due to an induction but later enzyme depletion occurs by 73.3% and 32.2% for ciprofloxacin and levofloxacin respectively, resulting in oxidative cell damage. Hence when the generation of reactive free radicals overwhelms the antioxidant defence, lipid peroxidation of the cell membrane occurs. This causes disturbances in cell integrity leading to cell damage/death. In the present study the repeated administration of CFX (ciprofloxacin) (recommended dosage regimen of CFX for UTI) resulted in increase free radical adduct generation by CYP450 mediated metabolism that cumulate and may result in increased ROS and substantial reduction in antioxidant defense.”

I think it’s a pretty damning article.  It’s easy to read and understand.  It doesn’t answer all questions about the damage done by fluoroquinolones, but it does a nice job at describing some of the issues that go on in the body when fluoroquinolones are ingested.  I suggest that you bring a copy to your next doctor’s appointment.

Sources:

  1. http://en.wikipedia.org/wiki/Lipid_peroxidation
  2. http://en.wikipedia.org/wiki/Superoxide_dismutase
  3. Alscher RGErturk NHeath LS., “Role of superoxide dismutases (SODs) in controlling oxidative stress in plants” Journal of Experimental Botany 2002 May; 53(372):1331-41. http://www.ncbi.nlm.nih.gov/pubmed/11997379
  4. Dale Keifer, “Superoxide Dismutase Boosting the Body’s Primary Antioxidant Defense” Life Extension Magazine.  June, 2006 http://www.lef.org/magazine/mag2006/jun2006_report_sod_01.htm
  5. Mark Hyman, MD, “Glutathione:  The Mother of All Antioxidants” 04/10/2010 http://www.huffingtonpost.com/dr-mark-hyman/glutathione-the-mother-of_b_530494.html
  6. http://en.wikipedia.org/wiki/Antioxidant

 

flu tox get help you need banner click lisa