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What is Fluoroquinolone Toxicity?

Published on May 21, 2015

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What happened to me? Why did it feel as if a bomb had exploded within my body and mind? Why did I go from doing CrossFit to being unable to walk a block? Why did I lose my memory and reading comprehension? Why was I so anxious and scared? Why were my tendons so weak and sore? Why did I suddenly lose my energy, endurance and flexibility?

I knew the short answer to those questions. I had suffered from an adverse reaction to ciprofloxacin, a fluoroquinolone antibiotic, and I had gone through fluoroquinolone toxicity syndrome—a multi-symptom, “mysterious” illness that involves damage to connective tissue (tendons, ligaments, cartilage, fascia, etc.) throughout the body, damage to the nervous systems (central, peripheral and autonomic), and more. Even though I knew why I was sick, I was still left wondering, what does fluoroquinolone toxicity mean? How do fluoroquinolones damage tendons, muscles, cartilage and nerves? What, exactly, is fluoroquinolone toxicity? What happened in my body?

No doctors that I consulted were able to give me any answers to those questions, so I went digging around myself. Here are some hypotheses for the mechanisms by which fluoroquinolones cause nervous system and musculoskeletal damage that manifests as multi-symptom, often chronic, illness.

Mitochondrial Toxicity

Is fluoroquinolone toxicity syndrome a result of mitochondrial damage? This hypothesis has the most evidence to support it. The FDA noted, in their April 27, 2013 Pharmacovigilance Review, “Disabling Peripheral Neuropathy Associated with Systemic Fluoroquinolone Exposure,” that:

“Ciprofloxacin has been found to affect mammalian topoisomerase II, especially in mitochondria. In vitro studies in drug-treated mammalian cells found that nalidixic acid and ciprofloxacin cause a loss of motichondrial DNA (mtDNA), resulting in a decrease of mitochondrial respiration and an arrest in cell growth. Further analysis found protein-linked double-stranded DNA breaks in the mtDNA from ciprofloxacin-treated cells, suggesting that ciprofloxacin was targeting topoisomerase II activity in the mitochondria.”

It is also noted in an article in Science Translational Medicine entitled “Bactericidal Antibiotics Induce Mitochondrial Dysfunction and Oxidative Damage in Mammalian Cells” that fluoroquinolones, and other bactericidal antibiotics, “damage mammalian tissues by triggering mitochondrial release of reactive oxygen species (ROS).” And that “increases in ROS led to DNA, protein, and lipid damage in vitro.”

Mitochondrial damage, and the vicious cycle of damaged mitochondria creating oxidative stress (another name for reactive oxygen species/ROS), which leads to more mitochondrial damage, which leads to more oxidative stress, and so on, and so on, can lead to multi-symptom, chronic illness. It is noted by Doctors Bruce H. Cohen, MD and Deborah R. Gold, MD, in Mitochondrial Cytopathy in Adults: What we Know So Far, that:

“A problem that has vexed the study of mitochondrial diseases ever since the first reported case (in 1962) is that their manifestations are remarkably diverse. Although the underlying characteristic of all of them is lack of adequate energy to meet cellular needs, they vary considerably from disease to disease and from case to case in their effects on different organ systems, age at onset, and rate of progression, even within families whose members have identical genetic mutations. No symptom is pathognomonic, and no single organ system is universally affected. Although a few syndromes are well-described, any combination of organ dysfunctions may occur.”

Doctors Cohen and Gold go on to say that:

“symptoms (of mitochondrial damage) such as fatigue, muscle pain, shortness of breath, and abdominal pain can easily be mistaken for collagen vascular disease, chronic fatigue syndrome, fibromyalgia, or psychosomatic illness.”

Mitochondrial dysfunction, and ROS overproduction (aka, oxidative stress), are associated with many chronic diseases including Parkinson’s, Alzheimer’s, ALS, autoimmune diseases, cancer, fibromyalgia, chronic fatigue syndrome, autism and more.

Fluoroquinolone toxicity symptoms resemble those of autoimmune diseases, neurodegenerative diseases, and mysterious diseases. On many levels, it makes sense that fluoroquinolone toxicity syndrome is a disease of mitochondrial damage and ensuing oxidative stress. Mitochondrial damage and oxidative stress are almost certainly part of the fluoroquinolone toxicity puzzle.

Recommended reading:

Science Translational Medicine, “Bactericidal Antibiotics Induce Mitochondrial Dysfunction and Oxidative Damage in Mammalian Cells”
Journal of Young Pharmacists, “Oxidative Stress Induced by Fluoroquinolones on Treatment for Complicated Urinary Tract Infections in Indian Patients”
Molecular Pharmacology, “Delayed Cytotocicity and Cleavage of Mitochondrial DNA in Ciprofloxacin Treated Mammalian Cells”

Neurotransmitter Malfunctions in Fluoroquinolone Toxicity

The central nervous system (CNS) symptoms of fluoroquinolone toxicity include depression, anxiety, psychosis, paranoia, severe insomnia, paraesthesia, tinnitus, hypersensitivity to light and sound, tremors and suicidal ideation and tendencies. Many of the CNS symptoms of fluoroquinolone toxicity can be attributed to the effects of fluoroquinolones on GABA receptors. Fluoroquinolones “are known to non-competitively inhibit the activity of the neurotransmitter, GABA, thus decreasing the activation threshold needed for that neuron to generate an impulse.” (source) Inhibition of GABA-A receptors, as well as activation of NMDA receptors, can lead to the many severe adverse effects of fluoroquinolones on the central nervous system.

Basically, fluoroquinolones do the same thing to GABA neurotransmitters as a protracted benzodiazepine withdrawal. It is noted in “Benzodiazepine tolerance, dependency, and withdrawal syndromes and interactions with fluoroquinolone antimicrobials” that:

“Chronic use of benzodiazepines causes compensatory adaptions which cause GABA receptors to become less sensitive to GABA. On discontinuation of benzodiazepines, withdrawal symptoms typically develop which may persist for weeks or months. Antagonism of the GABA-A receptor is believed to be responsible for the CNS toxicity of fluoroquinolones affecting 1–4% of patients treated. Fluoroquinolones have also been found to inhibit benzodiazepine receptor binding. The results of this small study seem to confirm that adverse reactions to fluoroquinolones occur more frequently in the benzodiazepine-dependent population than the 1–4% seen in the general public and may be severe.”

Those who have gone through benzodiazepine withdrawal can tell you that all aspects of one’s body are affected. It is possible that neurotransmitter dysfunction is at the root of all fluoroquinolone toxicity symptoms—though I strongly suspect that all of the potential theories that I mention in this post work in tandem.

Recommended reading:

Toxicology Mechanisms and Methods, “Ciprofloxacin-induced neurotoxicity: evaluation of possible underlying mechanisms.”
British Journal of Clinical Pharmacology, “Neurotoxic effects associated with antibiotic use: management considerations”
Pharmacology Weekly, “What is the mechanism by which the fluoroquinolone antibiotics (e.g., ciprofloxacin, gemifloxacin, levofloxacin, moxifloxacin) can increase a patient’s risk for developing a seizure or worsen epilepsy?”

Magnesium Deficiency

Fluoroquinolones deplete intracellular magnesium. Magnesium is necessary for more than 300 enzymatic reactions, it is vital for the synthesis of vitamins, and magnesium depletion can lead to many symptoms of fluoroquinolone toxicity and other chronic diseases. Many people suffering from fluoroquinolone toxicity are helped by supplementing magnesium (in various forms). Studies have indicated that the binding of quinolones to DNA is mediated by magnesium.

The hypothesis that fluoroquinolones deplete intracellular magnesium is well described in the article, “Fluoroquinolone antibiotics and type 2 diabetes mellitus:”

“Fluoroquinolones are broad-spectrum antibiotics derived from nalidixic acid that inhibit bacterial topoisomerases. Although very effective therapeutically, fluoroquinolones have been linked with serious side effects such as tendinopathy, peripheral neuropathy, retinopathy, renal failure, hypertension, and seizures. These effects can be rationalized as resulting from a drug-induced magnesium deficiency, and according to the hypothesis it is not coincidental that they resemble the complications resulting from type 2 and gestational diabetes. There has, moreover, been a history of dysglycemia associated with certain fluoroquinolone antibiotics. Gatifloxacin was withdrawn from clinical use after reports of drug-induced hyperglycemia and other fluoroquinolones have been reported to interfere with glucose homeostasis.”
“The precise mechanism by which fluoroquinolones might induce intracellular magnesium deficiency is unclear. It may involve the metal-chelating properties of the 3-carboxyquinolone substructure that is common to all fluoroquinolone antibiotics and the fact that the 6-fluoro substituent on the pharmacophore gives rise to sufficient lipophilicity that the drugs can dissolve in and penetrate cell membranes. It has been suggested that intracellular fluoroquinolones may exist almost exclusively as the magnesium complex. Diffusion or active transport of such a complex into the extracellular environment would lead to depletion of intracellular magnesium – a process that may be stoichiometric or catalytic and would be only very slowly reversible, if at all. Thus, the effects of fluoroquinolones on intracellular magnesium levels might be considered to be almost cumulative (and it is noteworthy that the side-effects of fluoroquinolone therapy may manifest or persist many months after treatment). Alternatively, it is perhaps possible that fluoroquinolones could affect magnesium metabolism by disruption of renal reabsorption of this electrolyte.”

Recommended reading:

Medical Hypotheses, “Fluoroquinolone antibiotics and type 2 diabetes mellitus”
Natural News, “Magnesium Helps Heal Cipro Damage”
Proceedings of the National Academy of Sciences of the United States, Biochemistry, “Quinolone Binding to DNA Mediated by Magnesium Ions”

Microbiome Destruction

Fluoroquinolones are powerful antibiotics that wreak havoc on the bacteria in the gut. In addition to indiscriminately killing bacteria in the gut of the person who takes a fluoroquinolone, fluoroquinolones have also been shown to induce large amounts of oxidative stress within the gut.

The importance of the microbiome for all areas of health is just now being explored. An unhealthy microbiome is associated with Parkinson’s, Alzheimer’s, depression, rheumatoid arthritis, diabetes, Crohn’s, and many other diseases. There are many who think that the root of all disease is in the gut.

Destruction of vital bacteria, and the induction of oxidative stress within the gut, could be responsible for the havoc wreaked on the health and well-being of those who take fluoroquinolones.

Recommended reading:

Antimicrobial Agents and Chemotherapy, “The Fluoroquinolone Levofloxacin Triggers the Transcriptional Activation of Iron Transport Genes That Contribute to Cell Death in Streptococcus pneumonia”
National Institutes of Health, “Human Microbiome Project”
Scientific American, “Think Twice: How the Gut’s ‘Second Brain’ Influences Mood and Well-Being”

Epigenetic Changes

Fluoroquinolones are topoisomerase interrupters. The mechanism for Cipro/ciprofloxacin, and all other fluoroquinolone antibiotics is:

“The bactericidal action of ciprofloxacin results from inhibition of the enzymes topoisomerase II (DNA gyrase) and topoisomerase IV (both Type II topoisomerases), which are required for bacterial DNA replication, transcription, repair, and recombination.”

Topoisomerases are enzymes that are necessary for DNA and RNA transcription. Topoisomerase interrupting drugs have been found to profoundly affect gene expression. It may be possible that fluoroquinolones trigger the expression of dormant genes. So, for example, those who have a predisposition toward an autoimmune disease may bring on the autoimmune disease with the fluoroquinolone. Anecdotally, it seems as if any existing weakness a person has is exacerbated by fluoroquinolones.

It is hypothesized in “Epigenetic side-effects of common pharmaceuticals: A potential new field in medicine and pharmacology,” that all adverse reactions to fluoroquinolones are due to epigenetic mechanisms:

“The quinolones are a family of broad-spectrum antibiotics. They inhibit the bacterial DNA gyrase or the topoisomerase IV enzyme, thereby inhibiting DNA replication and transcription. Eukaryotic cells do not contain DNA gyrase or topoisomerase IV, so it has been assumed that quinolones and fluoroquinolones have no effect on human cells, but they have been shown to inhibit eukaryotic DNA polymerase alpha and beta, and terminal deoxynucleotidyl transferase, affect cell cycle progression and function of lymphocytes in vitro, and cause other genotoxic effects. These agents have been associated with a diverse array of side-effects including hypoglycemia, hyperglycemia, dysglycemia, QTc prolongation, torsades des pointes, seizures, phototoxicity, tendon rupture, and pseudomembranous colitis. Cases of persistent neuropathy resulting in paresthesias, hypoaesthesias, dysesthesias, and weakness are quite common. Even more common are ruptures of the shoulder, hand, Achilles, or other tendons that require surgical repair or result in prolonged disability. Interestingly, extensive changes in gene expression were found in articular cartilage of rats receiving the quinolone antibacterial agent ofloxacin, suggesting a potential epigenetic mechanism for the arthropathy caused by these agents. It has also been documented that the incidence of hepatic and dysrhythmic cardiovascular events following use of fluoroquinolones is increased compared to controls, suggesting the possibility of persistent gene expression changes in the liver and heart.”

Fluoroquinolones have been found to deplete mitochondrial DNA, and mitochondria have been found to affect gene expression.

It is possible that fluoroquinolones are profoundly changing gene expression, and that the adverse effects of fluoroquinolones are a result of altered gene expression. Fluoroquinolones are, after all, topoisomerase interrupters.

Recommended reading:

Medical Hypotheses, “Epigenetic side-effects of common pharmaceuticals: A potential new ﬁeld in medicine and pharmacology”
Mutation Research, “Ciprofloxacin: Mammalian DNA Topoisomerase Type II Poison In Vivo”
Nature, “Topoisomerases facilitate transcription of long genes linked to autism”

Thyroid Harm

The harm that fluoroquinolones do to the thyroid is described well in “Fluoroquinolone Antibiotics and Thyroid Problems: Is there a Connection?” on Hormones Matter. A more in-depth look at fluoroquinolone induced thyroid problems can be found on FluoroquinoloneThyroid.com.

Please don’t interpret the brevity of this section as a reason to discount it as a possible explanation for fluoroquinolone toxicity syndrome. Thyroid dysfunction can wreak havoc on a person’s health and the deleterious effects of fluoroquinolones on the thyroid are a potential explanation for the multi-symptom, chronic illness of fluoroquinolone toxicity. The articles by JMR on both Hormones Matter and fluoroquinolonethyroid.com explore the relationship thoroughly.

All of the source links in “Fluoroquinolone Antibiotics and Thyroid Problems: Is there a Connection?” on Hormones Matter are recommended.

Post-hepatic Syndrome / Liver Damage

Do fluoroquinolones form poisonous acyl glucuronides that lead to post-hepatic syndrome?

I think that it’s a definite possibility, but I also think that I’m not qualified or able to form a coherent and correct explanation of this hypothesis. Please ask a biochemist to explain the following articles to you:

Drug Metabolism and Disposition, “Acyl Glucuronidation of Fluoroquinolone Antibiotics by the UDP-Glucuronosyltransferase 1A Subfaminly in the Human Liver Microsomes”.
Current Drug Metabolism, “Editorial [Hot Topic:Acyl Glucuronides: Mechanistic Role in Drug Toxicity? (Guest Editor: Urs A. Boelsterli)]”
BMC Public Health, “Adverse effects of the antimalaria drug, mefloquine: due to primary liver damage with secondary thyroid involvement?” (Note that mefloquine and fluoroquinolones are cousin drugs – they’re both quinine analogues.)

This is a long, and fairly complex, post. Yet I am leaving out many possible explanations for the causes of fluoroquinolone toxicity. Not even touched on are the possibilities that fluoroquinolone toxicity is a lysosomal disorder, autoimmune disease, fluoride overdose, “leaky gut,” histamine response, mast cell activation, serum sickness, and many other possibilities. I suspect that fluoroquinolone toxicity is a combination of all of the things mentioned above, and in this paragraph, and that there are multiple interactions between all of the biological systems. Fluoroquinolone toxicity is a systemic illness and all bodily systems work together.

Though fluoroquinolones can throw a wrench in our biochemistry, the multiple systems that work together to make us sick can also work together to make us well. We have amazing healing mechanisms that are less-understood than the mechanisms that make us sick (and those are pitifully poorly understood). Our bodies are a complex and wondrous web. All of our bodily systems work together perfectly most of the time, and they strive to return to health in every moment of life.

Though there are hundreds of articles about the deleterious effects of fluoroquinolones, the question – What is fluoroquinolone toxicity? – remains unanswered. Any one of the possibilities mentioned above is complex. Put them all together and, well, comprehension becomes close to impossible. Luckily, comprehension isn’t required for healing. But it would be very, very, very nice if some efforts toward understanding adverse reactions to fluoroquinolones were being made.

Post script: The first post I ever wrote on my site about fluoroquinolone toxicity (www.floxiehope.com) was a post like this one, also entitled, “What is Fluoroquinolone Toxicity?” You can read it HERE. The 2015 post above is much more thoughtful, well-researched and, in almost every way, it is better. But the 2013 post on Floxie Hope is interesting in its own right. It went over what it feels like to go through fluoroquinolone toxicity, and it was written from the perspective of a recent victim of fluoroquinolones, not the perspective of someone who has spent hundreds of hours researching fluoroquinolones. The patient perspective, and noting what fluoroquinolone toxicity feels like is valuable, though I think that the connections made in this 2015 post are more accurate.

Information about Fluoroquinolone Toxicity

Information about the author, and adverse reactions to fluoroquinolone antibiotics (Cipro/ciprofloxacin, Levaquin/levofloxacin, Avelox/moxifloxacin and Floxin/ofloxacin) can be found on Lisa Bloomquist’s site, www.floxiehope.com.

Participate in Research

Hormones Matter^TM is conducting research on the side effects and adverse events associated with the fluoroquinolone antibiotics, Cipro, Levaquin, Avelox and others: The Fluoroquinolone Antibiotics Side Effects Study. The study is anonymous, takes 20-30 minutes to complete and is open to anyone who has used a fluoroquinolone antibiotic. Please complete the study and help us understand the scope of fluoroquinolone reactions.

Hormones Matter^TM conducts other crowdsourced surveys on medication reactions. To take one of our other surveys, click here.

To sign up for our newsletter and receive weekly updates on the latest research news, click here.

What Else Can I Do To Help?

Hormones Matter^TM is completely unfunded at this juncture and we rely entirely on crowdsourcing and volunteers to conduct the research and produce quality health education materials for the public. If you’d like help us improve healthcare with better data, get involved. Become an advocate, spread the word about our site, our research and our mission. Suggest a study. Share a study. Join our team. Write for us. Partner with us. Help us grow.

To support Hormones Matter and our research projects – Crowdfund Us.

Same Disease, Different Symptoms: It’s all in the Mitochondria

by Lisa Bloomquist

Published on March 27, 2014

11632 views

Adverse reactions to fluoroquinolone antibiotics (Cipro/Ciprofloxacin, Levaquin/Levofloxacin, Avelox/Moxifloxacin and Floxin/Ofloxacin) can manifest in patients as a multi-symptom chronic illness that most resembles fibromyalgia, chronic fatigue syndrome / myalgic encephalopathy (ME) and/or an autoimmune diseases. As is the case with those chronic multi-symptom illnesses, the symptoms of fluoroquinolone toxicity vary greatly from one individual to another. Though almost everyone who suffers from fluoroquinolone toxicity has some sort of musculoskeletal issues (fluoroquinolones have a black box warning about the risk of tendon rupture), neuropathy and autonomic nervous system dysfunction, those broad categories of symptoms are where the similarities between individuals affected end. Some people suffering from fluoroquinolone toxicity have severe insomnia, others don’t. Some develop dietary intolerances, others don’t. Some become anemic, others don’t. Some develop Raynaud’s, others don’t. Some have urticaria, others don’t. I could go on and on.

Why are there such vast differences between how fluoroquinolone toxicity manifests itself from one person to another?

Look Beyond the Disease Model of Medicine

The traditional approach to medicine, using our existing paradigms, would answer that question by saying that fluoroquinolone toxicity is only responsible for the musculoskeletal issues, neuropathy and autonomic nervous system dysfunction that are the common links between those who are suffering from it; and that insomnia, dietary intolerances, Raynaud’s, anemia, etc. are from something else.

I don’t buy that answer though. The people suffering from fluoroquinolone toxicity were healthy before they crossed their tolerance threshold for fluoroquinolones, and it was only after they were exposed to fluoroquinolones that any of their symptoms emerged. The reports of thousands of people suffering from fluoroquinolone toxicity lead me to believe that fluoroquinolones cause a multi-symptom illness that can manifest itself in a variety of different ways.

Oxidatative Stress and the Mitochondrial Damage: Explaining Chronic Multi-Symptom Illness

Another possible answer to the question of why symptoms differ so much from one person to another, one that I think is closer to the truth, is that fluoroquinolones cause mitochondrial damage and that mitochondrial disorders can manifest themselves in a variety of different ways. It is noted by Doctors Bruce H. Cohen, MD and Deborah R. Gold, MD, in Mitochondrial Cytopathy in Adults: What we Know So Far, that:

“A problem that has vexed the study of mitochondrial diseases ever since the first reported case (in 1962) is that their manifestations are remarkably diverse. Although the underlying characteristic of all of them is lack of adequate energy to meet cellular needs, they vary considerably from disease to disease and from case to case in their effects on different organ systems, age at onset, and rate of progression, even within families whose members have identical genetic mutations. No symptom is pathognomonic, and no single organ system is universally affected. Although a few syndromes are well-described, any combination of organ dysfunctions may occur.”

Doctors Cohen and Gold go on to say that:

“symptoms (of mitochondrial damage) such as fatigue, muscle pain, shortness of breath, and abdominal pain can easily be mistaken for collagen vascular disease, chronic fatigue syndrome, fibromyalgia, or psychosomatic illness.”

Multiple studies have shown that fluoroquinolones deplete mitochondrial DNA and lead to an increase in oxidative stress and depletion of antioxidants within cells (source 1 and source 2). Oxidative stress and mitochondrial dysfunction (OSMD) are almost certainly why fluoroquinolone toxicity manifests itself in the form of chronic multi-symptom illness (CMI).

Even though it has been shown that oxidative stress and mitochondrial dysfunction can cause chronic multi-symptom illness, the question still remains, WHY are there such vast differences between how mitochondrial damage manifests itself from one individual to another?

A possible answer to this question lies in the fact that reactive oxygen species (ROS) generated by damaged mitochondria are signaling mechanisms that control gene expression / epigenetics.

Please excuse the momentary pause while I point out how mind blowing and important that sentence is. MITOCHONDRIAL PRODUCED REACTIVE OXYGEN SPECIES CONTROL GENE EXPRESSION. It is a huge discovery that is just now being accepted and verified by scientists. It is noted in the article Oxidative Stress and Oxidative Damage in Carcinogenesis that, “Through regulation of gene transcription factors, and disruption of signal transduction pathways, ROS are intimately involved in the maintenance of concerted networks of gene expression.” Also, per Dr. Marcin Kaminski, “The notion that mitochondria can play a role in a cell as a generator of strictly regulated oxidative signals is more recent, and some 10 years ago was regarded almost as heresy. Now the opinion has changed since a number of new observations have been made.”

Dr. Kaminski also pointed out in a personal conversation that topoisomerase enzymes, which are blocked by fluoroquinolones are also crucial for regulating gene expression. According to the FDA warning label for Cipro/ciprofloxacin:

“The bactericidal action of ciprofloxacin results from inhibition of the enzymes topoisomerase II (DNA gyrase) and topoisomerase IV (both Type II topoisomerases), which are required for bacterial DNA replication, transcription, repair, and recombination”

Perhaps the differences in how individuals react to fluoroquinolones are due to the differences in which genes are triggered as a result of both mitochondrial damage (and resultant oxidative stress) and the influence of topoisomerase interrupters on gene expression.

Individual Susceptibilities Influence Mitochondrial Damage

To use myself as an example, my 23andme genetic test results showed that I had a genetic predisposition toward rheumatoid arthritis (RA), an autoimmune disease. When I first was struck with fluoroquinolone toxicity, I was not aware that Cipro was the culprit behind the sudden deterioration in my health, and I thought that I had an autoimmune disease – with RA being the one that I suspected because my joints were swollen, inflamed and painful. It turns out that I didn’t have RA, rather, I was suffering from fluoroquinolone toxicity. But the symptoms manifested themselves in a way that made it look and feel very much like I had RA Another example is of a gentleman who commented on a blog about fluoroquinolone toxicity, www.floxiehope.com, who noted that his hereditary haemochromatosis (excess iron in the body) was brought on (or at least worsened) by his adverse reaction to a fluoroquinolone. I, on the other hand, was helped greatly by supplementing iron and suspect that I was anemic after having an adverse reaction to Cipro.

Even though there are genetic differences from person to person, and the expression of those differences may explain why the symptoms of fluoroquinolone toxicity syndrome differ from one individual to another, the entire chronic disease state – with all of the symptomatic differences between individuals, is brought on by fluoroquinolones and thus, despite the individual differences, the symptoms cumulatively should be considered to be part of fluoroquinolone toxicity syndrome. Even though I had a genetic predisposition for R.A., it likely would have remained dormant (I don’t know of anyone in my family who has ever had R.A.) had it not been triggered, (along with musculoskeletal issues, neuropathy and autonomic nervous system dysfunction) if I had not taken Cipro and had not suffered through damage to my mitochondria. I cannot be sure of that – it’s not possible for anyone to know at this point, but it is an interesting assertion to ponder.

My assertion, that fluoroquinolones cause changes in gene expression, and that the genes that are expressed determine what symptoms of fluoroquinolone toxicity present themselves, of course needs to be tested and verified before it is accepted as truth. I hope that more scientists look into the adverse effects of fluoroquinolones and all other mitochondrial damaging pharmaceuticals. After all, our mitochondria and the ROS that they produce affect our GENES, and our genes are pretty important.

Information about Fluoroquinolone Toxicity

Information about the author, and adverse reactions to fluoroquinolone antibiotics (Cipro/ciprofloxacin, Levaquin/levofloxacin, Avelox/moxifloxacin and Floxin/ofloxacin) can be found on Lisa Bloomquist’s site, www.floxiehope.com.

Participate in Research

Hormones MatterTM is conducting research on the side effects and adverse events associated with the fluoroquinolone antibiotics, Cipro, Levaquin, Avelox and others: The Fluoroquinolone Antibiotics Side Effects Study. The study is anonymous, takes 20-30 minutes to complete and is open to anyone who has used a fluoroquinolone antibiotic. Please complete the study and help us understand the scope of fluoroquinolone reactions.

Hormones MatterTM conducts other crowdsourced surveys on medication reactions. To take one of our other surveys, click here.

To sign up for our newsletter and receive weekly updates on the latest research news, click here.

What Else Can I Do To Help?

Hormones MatterTM is completely unfunded at this juncture and we rely entirely on crowdsourcing and volunteers to conduct the research and produce quality health education materials for the public. If you’d like help us improve healthcare with better data, get involved. Become an advocate, spread the word about our site, our research and our mission. Suggest a study. Share a study. Join our team. Write for us. Partner with us. Help us grow.

Please support Hormones Matter and our research projects. Contribute to our crowdfunding campaign – Crowdfund Us.

Of Oxygen, Spark Plugs, and Mitochondria

by Derrick Lonsdale MD, FACN, CNS

Published on March 25, 2014

7974 views

Everyone knows that we need oxygen to live. Few know or care what the body does with it. Although everyone knows that it is extracted from the air by the lungs and carried by the blood to body tissues, it is left to scientists to understand what happens to it in the 50 to 100 trillion cells that make up an adult human body. The reaction that makes it possible for oxygen to maintain life is called oxidation. This reaction takes place in the mitochondria and produces energy that is used by each cell to carry out its program of function. Perhaps we can understand this better by using an analogy.

Car Engines and Human Engines: Each Need Fuel

A car uses gasoline as a fuel. It is ignited by a spark plug that causes a controlled explosion in a cylinder. This drives a piston that passes the energy through a series of mechanical levers known collectively as the transmission. It is the conversion of chemical energy in gasoline to what Newton called kinetic energy that enables the car to move. The machine that does this is an engine. Perhaps it stretches the imagination to state that the body works on exactly the same principles. It is the details that make the difference. Oxidation is the equivalent of explosion in the cylinder. In other words, it is combustion. Now we have to compare it to the relatively simple mechanism of explosion.

First, combustion is merely the union of oxygen with a fuel. If we do not carry the reaction out in some controlled way, the energy is dissipated as heat into the surrounding air. In a car, the cylinder encloses the combustion and forces the energy into the transmission. In the body it is controlled in a much more complex way. Yes, heat is produced and is used to make us “warm blooded creatures” but there is no noise, fire or smoke as in the car engine. The energy is guided through an ingenious series of chemical reactions in what we might term “the engines of the cell”.

Mitochondria: The Engines in Our Cells

Each cell has a whole series of “engines” called mitochondria and it is in these organelles where oxidation occurs. A mitochondrion is so small that its structure can only be seen with the aid of an electron microscope and yet it is in each of the millions of cellular mitochondria where energy is produced for the use of each cell to perform its designed function. The usual fuel for this is glucose and it is not surprising that people have concluded that the consumption of sugar provides “quick energy”.

Good Sugar and Bad Sugar: Mitochondria Know the Difference

When sugar is ingested in its proper form, meaning as it is found in nature, it is stored in the liver and muscles as glycogen, a complex substance built up by sticking glucose molecules together, making something that looks like a miniature tree. As fuel is required, the glycogen is broken down and released as glucose into the blood. This requires an enzyme and there is an inborn error of metabolism where this enzyme is missing. The affected infant is found to have an enlarged liver stuffed with glycogen, together with low blood sugar, a situation that is not compatible with life and the patient dies in infancy.

Blood glucose is absorbed from the blood into cells under the influence of insulin and then goes into an ingenious “pipeline” that processes it. The beginning of this process requires a number of B group vitamins. There is a well known nutritional disease known as beriberi where the carbohydrate load is too great for this action to occur efficiently. It is now known that vitamin B1 is insufficient to meet the caloric demand and is the key to understanding the disease and how it is treated, a discovery that took many years to unravel.

Let us look again at the simpler method by which gasoline is ignited in a car. An electrically energized spark plug is used to ignite the fuel as it is passed into the cylinder by carefully controlled mechanisms. Some people will remember that cars once had a gadget called a choke, used for starting the cold engine. This allowed gasoline to flow into the cylinder with a relative deficiency of air, the so-called “rich” mixture. When the engine was warm the choke was automatically removed and the mixture weakened by allowing more air and less gas into the cylinder. If the choke mechanism stuck, there would be an excess of black smoke issuing from the exhaust pipe and the engine would not run properly. The smoke represents the hydrocarbons in gas that have not been ignited and a simple equation shows us why:

Fuel + Oxygen + Catalyst = Energy

The Figure shows the ratio of calories to B vitamins in a healthy diet. The line AB represents the calorie intake (protein, fat and carbohydrate) and the line ED the vitamin intake that enables its efficient processing. If the line AB is extended to C (line AC) without the increase in vitamin intake, the triangle BCE represents “empty calories” equivalent to a “choked engine”. The remedy is obvious: we can extend line DE to F, thus restoring the ratio as in line FC, reduce the calories back to line AB, or meet each other half way (not shown).

Beriberi: Bad Sugar and Empty Calories

Beriberi is caused by consuming empty calories (triangle BCE), where the line AC represents carbohydrate calories and ED the corresponding ingestion of vitamin B 1. (thiamin). The disease, throughout history, has been primarily in Eastern countries where the diet has been white rice based, particularly in times of greater affluence. This is because the grain in rice is starch and the cusp contains the necessary vitamins. When the Chinese peasants became more affluent they would take their rice to a rice mill where white rice was produced by removing the cusps. This was because it looked better when served to their friends, thus demonstrating their new found affluence. Outbreaks of beriberi were always associated with an increase in consumption of white rice.

What is the lesson to be learned from this in our modern age where diseases like beriberi have been thought to be of only historical interest? Think of the enormous load of simple carbohydrate consumed by millions in the U.S. Everything supplied by the food industry is sweetened or it would not sell. White bread (the equivalent of white rice), cookies, pastry in general, ice cream, soft drinks, desserts, tomato ketchup——— the list goes on and on! Even the vitamin enrichment indicated on the label is insufficient. Obesity, often associated with inflammatory disease, is affecting millions. Our health bills are threatening us with national bankruptcy and we wonder why we are being “hit” with so many diseases and health catastrophies. Pockets are being lined with money made from a variety of reducing diets and pills.

Diet is Everything: Feed your Mitochondria

That is why I have a standard answer to every query that I get about diet. Eat only nature made food and the less that it is handled by mankind the better. The balance of calories and vitamins is automatically produced. If the food had not been available when life started on Earth animal evolution could not have occurred and we would never have survived. Granted, unfortunately with population explosion, fresh food of this nature is expensive and we have all given up back yard gardening The First Lady has shown the example. Will we take a “leaf from her book” and acknowledge that a lot of our health is in our own hands.

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Your Mighty Mitochondria

by Lisa Bloomquist

Published on March 20, 2014

10236 views

There are over ten million billion mitochondria in the human body (Lane p. 1). Each cell (with a few exceptions) contains an average of 300-400 mitochondria that are responsible for generating cellular energy through a process called ATP (Adenosine Triphosphate). Both oxidative stress and antioxidants are created within/by mitochondria. The oxidative stress (caused by reactive oxygen species – ROS) and antioxidant molecules regulate the aging process (Lane p. 4) and are also cellular signals that “regulate diverse physiological parameters ranging from the response to growth factor stimulation to the generation of the inflammatory response, and dysregulated ROS signaling may contribute to a host of human diseases.” (1)

Mitochondria are metabolic signaling centers that “influence an organism’s physiology by regulating communication between cells and tissues.” (2). Mitochondria regulate apoptosis – programmed cell death, as well as autophagy – the breakdown of cellular components during times of starvation. Mitochondria also play key roles in cellular processes including “calcium, copper and iron homeostatis; heme and iron-sulfer cluster assembly; synthesis of pyrimidines and steroids; thermogenesis and fever response; and calcium signaling” (3)

Are you confused? Do the above paragraphs sound like scientific gibberish to you leaving you wondering, “Yes, but what does that MEAN??”

The Importance of Mitochondria

Basically, it, along with the pages of information that I left out, means that mitochondria are really important to cellular functioning and health. They regulate energy production, aging, epigenetic signaling between and within cells and many other important functions. Proper functioning of mitochondria is vital, and when mitochondria are not operating properly, a wide range of disease states can ensue (2). It makes sense that if the energy centers of cells are not operating properly; the system (the body) starts to shut down in a variety of ways. “Mitochondrial dysfunction is associated with an increasingly large proportion of human inherited disorders and is implicated in common diseases, such as neurodegenerative disorders, cardiomyopathies, metabolic syndrome, cancer, and obesity.” (2) Additionally, there is significant evidence that many of the mysterious diseases of modernity, such as fibromyalgia, chronic fatigue syndrome / myalgic encephalomyelitis, Gulf War Syndrome, autism and many other chronic, multi-symptom illnesses, have their roots in mitochondrial dysfunction and resultant oxidative stress. (4)

The History of Mitochondria

The existence of mitochondria was discovered in the late 1800s. Their purpose was unknown until the 1950s when “it was first established that mitochondria are the seat of power in cells, generating almost all our energy.” (Lane p. 6) In 1967 Lynn Margulis proved the “existence of DNA and RNA in mitochondria.” (Lane p. 15) From 1967 through 1999, according to Immo Scheffler, “’Molecular biologists may have ignored mitochondria because they did not immediately recognize the far-reaching implications and applications of the discovery of the mitochondrial genes. It took time to accumulate a database of sufficient scope and content to address many challenging questions related to anthropology,biogenesis, disease, evolution, and more.’” (Lane p. 7) Almost everything that is known about the role of mitochondria in cellular signaling and gene expression (5), apoptosis, autophagy, metal metabolism, regulation of enzymes, and many other important functions, has been discovered since the turn of the century. Despite the fact that all eukaryotic organisms have (or at least once had) mitochondria, the realization that mitochondrial health is vital to over-all human health is a recent realization. The link between mitochondrial dysfunction and disease, especially chronic multi-symptom disease, is well documented in peer-reviewed journals, yet it is not an officially recognized cause of those diseases and they are considered by many to be mysterious.

Vulnerable yet Strong: Mitochondria and Tolerance Thresholds

The role of mitochondrial dysfunction in disease remains unacknowledged because of some fascinating features of mitochondria. Mitochondria are an interesting mix of vulnerable and resilient. Mitochondrial DNA (mtDNA) and mitochondrial genes are more vulnerable than nuclear DNA and nuclear genes to damage caused by chemical toxicants (like pharmaceuticals and environmental pollutants) because mitochondrial genes “sit on a single circular chromosome (unlike the linear chromosomes of the nucleus) and are ‘naked’ – they’re not wrapped up in histone proteins.” (Lane p. 15) Histone proteins protect nuclear DNA and because mtDNA isn’t wrapped in histone proteins, it is vulnerable. This vulnerability means that mtDNA is easily damaged. This slide describes additional factors that affect mitochondrial vulnerability to environmental pollutants:

Factors that affect mitochondrial vulnerability to environmental toxicants — Mitochondria as a Target of Environmental Toxicants. Permission to print graphic provided by Joel N. Meyer.

Despite its vulnerability, mtDNA is, at the same time, quite hearty and resilient. MtDNA can take a punch, and a threshold of damage must be crossed over before a disease state will ensue. In Mechanisms of Pathogenesis in Drug Hepatotoxicity Putting the Stress on Mitochondria it is noted that, “damage to mitochondria often reflects successive chemical insults, such that no immediate cause for functional changes or pathological alterations can be established. There is indeed experimental evidence that prolonged injury to mitochondria, such as that which typifies oxidative injury to mitochondrial DNA or to components of the electron transport chain (ETC), has to cross a certain threshold (or a number of thresholds) before cell damage or cell death becomes manifest.” The researchers go on to note that, “This non-linear response can be explained upon consideration that the molecules that subserve mitochondrial function (e.g., mitochondrial DNA, mRNA, and ETC proteins) are present in excess of amounts required for normal cell function. This reserve (or buffering) capacity acts as a protective mechanism; however, at a certain stage of damage, the supply of biomolecules needed to support wild-type mitochondrial function becomes compromised.” (6)

Pharmaceutical Safety and Mitochondria: No Testing Required

To put it simply, because of the tolerance threshold that mitochondria have to damage, the damage done to mitochondria will not show up as a disease until the threshold is crossed. This makes the testing of the deleterious effects of pharmaceuticals and environmental toxins on mitochondria difficult. The damage done by the chemical toxin doesn’t show up until multiple exposures to mitochondrial damaging toxins have been experienced (and it likely doesn’t need to be the same toxin – different mitochondrial damaging toxins can erode the mitochondria’s tolerance threshold). Also, mitochondria display an “initial adaptive response was followed by a toxic response” (6) to damaging toxins.

The mitochondrial tolerance threshold for damage would need to be taken into consideration when testing drugs or environmental pollutants for their adverse effects on mitochondria, IF drugs and pollutants were tested for their effects on mitochondria at all. Unfortunately, “mitochondrial toxicity testing is still not required by the US FDA for drug approval.” (7) The authors of Mitochondria as a Target of Environmental Toxicants note that, “growing literature indicates that mitochondria are also targeted by environmental pollutants” but the EPA does not require testing of environmental pollutants for their affects on mitochondria either.

Studies have shown that bactericidal antibiotics (including fluorouquinolones) (8), statins (9), chemotherapy drugs (3), acetaminophen (6), metformin (a diabetes drug) (10), and others, damage mitochondria. The environmental pollutants that have been shown to damage mitochondria include rotenone, cyanide, lipopolysaccharide, PAH quinones, arsenic, and others (3).

Though it’s not excusable, it’s understandable that the FDA and EPA have not historically required testing of pharmaceuticals or environmental pollutants for their effects on mitochondria. Until very recently, much of what is currently known about mitochondria was not yet discovered. The link between multi-symptom chronic illnesses (including autism) and mitochondrial dysfunction and damage (4) was not yet known when the vast majority of the drugs that are on the market were going through their initial testing and review. What is known now about the important role of mitochondria in epigenetic signaling was not known until recently – and almost all laymen and probably plenty of scientists still don’t realize how much the molecules generated in our mitochondria affect our genes. All of the drugs and environmental pollutants that are on the market have been put on the market without their effects on mitochondria being studied, or even noted by the regulatory agencies that are entrusted with protecting our health and safety. The ignorance of everyone involved would be less consequential if people weren’t so sick. In addition to being connected to the mysterious diseases of modernity, mitochondrial damage is also implicated in the following disorders: “schizophrenia, bipolar disease, dementia, Alzheimer’s disease, epilepsy, migraine headaches, strokes, neuropathic pain, Parkinson’s disease, ataxia, transient ischemic attack, cardiomyopathy, coronary artery disease, chronic fatigue syndrome, fibromyalgia, retinitis pigmentosa, diabetes, hepatitis C, and primary biliary cirrhosis” (7) as well as cancer (11).

The Paradigm Shift

We’re in an interesting and strange situation where medicine hasn’t caught up to science and science hasn’t caught up to medicine. By this I mean that mitochondria damaging chemicals were created long before we knew the importance of our mitochondria, but now that scientists are realizing the importance of our mitochondria, the damaging pharmaceutical culprits are so entrenched in medicine that they can’t be extricated. For example, nalidixic acid, the precursor to fluoroquinolones (mitochondria damaging antibiotics) (8), was first created in the 1960s, long before what we currently know about mitochondria and the effects of mitochondrial damage was discovered. Now that the effects of depleting mtDNA on human health has been discovered, the myriad of strange health symptoms observed in patients who have taken fluoroquinolones can be explained. Mitochondrial damage can cause multi-symptom chronic illness (4). We know this now. However, fluoroquinolones are so widely used (20+ million annual prescriptions in America alone), and so widely regarded as safe, that it would be difficult, if not impossible, to restrict their use now – even though they have been found to cause mitochondrial damage and oxidative stress (8). It’s time for disease paradigms to shift to note the importance of mitochondria in human health. After all, chronic diseases, many of which are related to mitochondrial function, are the leading cause of death in the U.S.

Mitochondria are important. It’s time we started paying attention to them. It’s time for disease models to shift. It’s time for iatrogenic mitochondrial dysfunction to be recognized as a cause of chronic diseases. The chronic diseases are happening, whether we recognize the role of mitochondrial damage, and the role of pharmaceutical and environmental pollutants in damaging mitochondria, or not. Ignorance isn’t bliss – people are sick. With recognition of the importance of mitochondrial health, maybe we can prevent others from getting sick in the future.

Information about Fluoroquinolone Toxicity

Information about the author, and adverse reactions to fluoroquinolone antibiotics (Cipro/ciprofloxacin, Levaquin/levofloxacin, Avelox/moxifloxacin and Floxin/ofloxacin) can be found on Lisa Bloomquist’s site, www.floxiehope.com.

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References

Lane, Nick (2005). “Power, Sex, Suicide: Mitochondria and the Meaning of Life” Oxford University Press Inc., New York.

Journal of Cell Biology, “Signal Transduction by Reactive Oxygen Species”
Cell, “Mitochondria: In Sickness and in Health”
Toxicological Sciences, “Mitochondria as a Target of Environmental Toxicants”
Nature Preceedings, “Oxidative Stress and Mitochondrial Injury in Chronic Multisymptom Conditions: From Gulf War Illness to Autism Spectrum Disorder”
Biochimica et Biophysica Acta (BBA) – Gene Regulatory Mechanisms, “Mitochondrial DNA Damage and its Consequences for Mitochondrial Gene Expression”
Molecular Interventions, “Mechanisms of Pathogenesis in Drug Hepatotoxicity Putting the Stress on Mitochondria”
Molecular Nutrition & Food Research, “Medication-Induced Mitochondrial Damage and Disease”
Science Translational Medicine, “Bactericidal Antibiotics Induce Mitochondrial Dysfunction and Oxidative Damage in Mammalian Cells”
NIH Public Access, “Statin Adverse Effects: A Review of the Literature and Evidence for a Mitochondrial Mechanisms”
Biochemical Journal, “Metformin inhibits mitochondrial permeability transition and cell death: a pharmacological in vitro
Contemporary Oncology, “Oxidative Damage and Carcinogenesis”

Exercise to Alleviate Fatigue

by Chandler Marrs, PhD

Published on November 5, 2013

6306 views

We all know that exercise is good for us, but few know how truly important it really is. I work with a woman who was injured by Gardasil. Prior to her vaccination, she was healthy and active, but after the vaccination, immediately, and in the years that followed, she has endured a complex array of symptoms that included intense and unremitting fatigue, regular bouts of dizziness and syncope, hypersomnia, muscle pain, neuropathies, intense salt and water cravings, and excessive weight loss.

As we have worked to identify various possible culprits, and we have identified a few, one thing that struck me as absolutely fascinating is how she managed her ordeal, how she managed her dizziness, syncope and hypersomnia before knowing what was wrong. She managed with exercise (and salt, water, and now some medications). She told me, that although it was excruciatingly difficult at first, exercising reduced her dizziness. More specifically, aerobic exercise provided her with 4-6 hours of non-dizzy, non-blackout functioning, while weight-lifting could provide her with as much as 24 hours of functioning. This was intriguing, to say the least. What biochemical factors were altered by exercise that allowed her periods of functioning and how did the type of exercise moderate the duration of functioning?

Before I tell you what I think may be the answer, let me backtrack a bit and tell you about something else I have been pondering as of late, the nature of fatigue. Fatigue is one of those symptoms that is ubiquitous across so many syndromes that it is often overlooked as a clinically important indicator of anything. This is a shame because fatigue can tell us so much. Even with the syndrome that bears its name – chronic fatigue syndrome – the debates about the reality of fatigue as a meaningful physiological attribute of disease are rampant. What is fatigue? Where does it come from? Does chronic fatigue even exist?

What is Fatigue?

At its most basic level, fatigue is a lack of energy. And while there may be a myriad of environmental or outside sources of fatigue, like stress, workload, exercise, lack of sleep, poor nutrition, and even an array of disease states whose core symptoms include fatigue, the internal components of fatigue all point to a change in biochemistry that reduces cellular energy production and usage. Something in our external or internal environments flips an energy switch. What is that switch?

Mitochondria and Fatigue

Yes, I said mitochondria. Harken back to your high school biology, remember those energy powerhouses inside the cell, responsible for generating ATP – adenosine triphosphate – the cell’s chemical energy – without which, the cell dies. Even if you don’t remember, trust me on this, we need working mitochondria to survive. Mitochondrial disease can be devastating because it affects the most basic functioning of the cell, its energy usage. From a cellular perspective, damaged or deficient mitochondria impair all the major metabolic pathways necessary for building, breaking down or recycling the cell’s molecular machinery, even down to preventing DNA and RNA synthesis. And as logic would have it, organs that require the greatest energy are affected most by mitochondrial disease or injury; think heart, lungs, brain, liver, GI tract and muscles.

Mitochondrial injury or dysfunction can occur by a number of mechanisms, by an inherited mutation, a spontaneous mutation or by environmental factors. Mitochondria are particularly sensitive to all the toxic insults of modern living, bad food, sedentary lifestyle, stress, environmental chemicals, medications and vaccines. Over time, and after repeated exposures, these insults reduce mitochondrial functioning through a process called oxidative stress. All those ‘anti-oxidant’ concoctions on the market are to reduce oxidative stress.

Long story short, and by way of a gross over-simplification, low or dysfunctioning mitochondria create a myriad of complicated symptoms. Depending upon the organ(s) where the dysfunction occurs, that’s where disease develops. No matter where the mitochondrial insults take place, the loss of energy will lead not only the dysfunction of that organ system, but also, to an overall sense of fatigue. Thus, fatigue, at its most basic level, means some sort of mitochondrial loss of function. When fatigue is severe, unremitting and presents with what seems like a cluster of unrelated symptoms, it is very clinically relevant. Indeed, fatigue may be the key clinical indicator.

Exercise and Mitochondrial Biogenesis

What does all this have to do with exercise and our post Gardasil patient with symptoms that included fatigue, dizziness, hypersomnia, muscle pain, among others? Well, it turns out, a lot. Let’s begin with exercise.

Exercise increases mitochondria, in number and in size. The act of exercising tells our cells to produce more mitochondria. It’s called mitochondrial biogenesis. On the most obvious level, this makes perfect sense. When we exercise our demands for energy increase and to meet those needs our cells respond by birthing more of the machinery that produces this energy.

Not knowing any of this, or that post vaccine injuries could be attributable to mitochondrial insults (see our article about thiamine deficiency post Gardasil and oxidative stress), somehow, intuitively, our Gardasil injured woman felt she needed to exercise to survive and, unlike so many of us, she listened to her body. By exercising, she increased the number of mitochondria, effectively compensating for their deficits in functioning. Think about it, if you can’t have optimum energy production in the machinery you have, but you still need a certain amount of energy output to survive, increase the number of machines producing that energy. The exercise didn’t fix what was broken, but it may have helped her body to function and survive. She increased her cellular energy by exercising. And the increase in energy reduced her dizziness and blackouts.*

The fact that exercise may alleviate fatigue and do so by changing the most fundamental aspect of cellular functioning, points to the possibility of a wonderfully simple and elegant, non-medication based, therapeutic option for folks suffering with fatigue – related symptoms. Some physician/researchers suggest that exercise, under the guidance of trained experts, also improves symptoms associated with some mitochondrial related conditions.

I have not yet figured out why the different types of exercise yielded different levels of functioning, perhaps an exercise physiologist can weigh in and clarify that for us, but it is clear from this case and from the research materials on the subject of exercise and mitochondrial disease and injury that exercise is a critical component of maintaining or managing cellular energy requirements. Sometimes it is the most simple solutions that alleviate the most complicated of problems.

*Post Script

I should mention that exercise is in no way a ‘cure’ for the serious injuries and illnesses that she and others sustain. There is quite a bit of controversy regarding whether exercise is safe or effective for individuals with chronic fatigue and other conditions. Individuals with health issues should not begin an exercise program without consulting their healthcare provider. It should also be noted that the case presented here represents a particular history of symptoms and in no way reflects a prescription or recommendation for salt or water loading or even exercise.

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Answering Infertility with Genetic Modification: Evolution or Playing God?

by Lisbeth Prifogle, MFA

Published on July 2, 2012

5620 views

I am the middle of 5 children. We are all from the same parents who are still married. Since the time I was 5 years old, there has never been a time when there wasn’t a toddler in our house. I’m 30 years old now. I think I’m officially immune to baby fever. The gene to love shopping at malls and having babies somehow skipped me and I’m happy for that. However, the older I get I see it happen. First, one of my girlfriends gets infected and then, it quickly passes to each and every one. I don’t know if it’s through touch or some sort of mental telepathy, but it happens quick and there’s no stopping it. I call it the, I want a baby and I want it now syndrome. The only known cure is reproduction.

More and more I watch couples around me struggle with infertility. I had one friend go to multiple fertility centers across the US trying to get pregnant with endometriosis. She was finally successful and jokes that her baby, “spent his inheritance getting here.” My sister, happy mother of 2, has had a horrible year with two miscarriages. After multiple tests, they discovered that she has a blood clotting disorder and hopefully she will be able to carry full term next time.
Keep Reading

mitochondria - Page 5

Mitochondrial Toxicity

Neurotransmitter Malfunctions in Fluoroquinolone Toxicity

Magnesium Deficiency

Microbiome Destruction

Epigenetic Changes

Thyroid Harm

Post-hepatic Syndrome / Liver Damage

Information about Fluoroquinolone Toxicity

Participate in Research

What Else Can I Do To Help?

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Look Beyond the Disease Model of Medicine

Oxidatative Stress and the Mitochondrial Damage: Explaining Chronic Multi-Symptom Illness

Individual Susceptibilities Influence Mitochondrial Damage

Information about Fluoroquinolone Toxicity

Participate in Research

What Else Can I Do To Help?

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Car Engines and Human Engines: Each Need Fuel

Mitochondria: The Engines in Our Cells

Good Sugar and Bad Sugar: Mitochondria Know the Difference

Beriberi: Bad Sugar and Empty Calories

Diet is Everything: Feed your Mitochondria

We Need Your Help

Related posts:

You might be interested in

The Importance of Mitochondria

The History of Mitochondria

Vulnerable yet Strong: Mitochondria and Tolerance Thresholds

Pharmaceutical Safety and Mitochondria: No Testing Required

The Paradigm Shift

Information about Fluoroquinolone Toxicity

Participate in Research

What Else Can I Do To Help?

References

Related posts:

You might be interested in

What is Fatigue?

Mitochondria and Fatigue

Exercise and Mitochondrial Biogenesis

*Post Script

Participate in Research

Related posts:

You might be interested in

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