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The Fluoroquinolone Time Bomb – Answers in the Mitochondria

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Two of the more perplexing features of Fluoroquinolone Toxicity (an adverse reaction to a fluoroquinolone antibiotic – Cipro/Ciprofloxacin, Levaquin/Levofloxacin, Avelox/Moxifloxacin or Floxin/Ofloxacin) are delayed reactions and tolerance thresholds. Both of these features of Fluoroquinolone Toxicity can be explained by noting that fluoroquinolones have been shown to damage mitochondria and cause oxidative stress, and that delayed onset of a disease state, as well as tolerance thresholds, are features of illnesses brought on by pharmaceutical induced mitochondrial damage and oxidative stress.

Delayed Reactions and Tolerance Thresholds with Fluoroquinolone Reactions

By “delayed reactions” I mean that adverse reactions to fluoroquinolones can occur weeks, months or even years after administration of the fluoroquinolone has stopped.  For the lawsuit filed by Public Citizen on behalf of patients who tore or ruptured tendons after taking a fluoroquinolone, (a suit that prompted the addition of the black box warning on all orally and IV administered fluoroquinolones) notes that “Fluoroquinolones, including CIPRO®, are associated with an increased risk of tendinitis and tendon rupture in all ages. This risk is further increased in older patients usually over 60 years of age, in patients taking corticosteroid drugs, and in patients with kidney, heart or lung transplants”. Tendon tears and ruptures that occurred within one year of the patient taking the fluoroquinolone were accepted as being related to the patient’s fluoroquinolone use. Patient reports have noted that new adverse symptoms of fluoroquinolone toxicity have occurred years after administration of the fluoroquinolone has ceased.

Many patients also experience a tolerance threshold for fluoroquinolone use.  A patient can tolerate fluoroquinolones well, experiencing few or no side-effects, until his or her threshold is reached.  After the patient’s tolerance threshold is reached, multisymptom systemic illness ensues. This patient’s story, found on the Fluoroquinolone Wall of Pain, illustrates the issue of tolerance thresholds:

On April 15, 2013 I was prescribed Avelox. I had been on this drug many times for chronic sinus infections. This time was different. Within 10 minutes of the first dose I went into anaphylaxis. I stopped breathing, had numerous convulsions and two grand Mal seizures. Since that day I have suffered with seizures, convulsions, tremors, debilitating fatigue, muscle weakness, vision loss, severe neuropathic pain, vomiting, nausea, lack of appetite, tendon, and vein problems.

This patient tolerated Avelox (moxifloxacin – a fluoroquinolone) well until her tolerance threshold was reached. Once her tolerance threshold was reached, she experienced multi-symptom systemic illness.

I personally experienced both a delayed reaction to Cipro/Ciprofloxacin (also a fluoroquinolone) and a tolerance threshold for it. I took 7 500-milligram pills of Cipro in 2009 without notable incident. I was even able to hike the entire 500-mile Colorado Trail in 2010 (no peripheral neuropathy or weakness were present at that time). When I took 7 more 500-milligram pills in 2011 I experienced a severe adverse reaction that began two full weeks after I was done taking the pills. I experienced multiple musculoskeletal (I couldn’t walk more than a block) and nervous system symptoms (I lost my memory and reading comprehension), and I would describe the reaction as feeling like a bomb had gone off in my body.

Fluoroquinolone Time Bomb: It’s All About the Mitochondria

My experience of a delayed onset of systemic health issues after having previously tolerated Cipro/Ciprofloxacin well, is typical of diseases that are brought on by a pharmaceutical causing mitochondrial dysfunction. (Multiple journal articles have noted that fluoroquinolones cause mitochondrial damage and oxidative stress.)

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.

Each time mitochondria is injured, the patient gets closer to his or her personal tolerance threshold for mitochondrial damage. Once the threshold is crossed, cell damage and apoptosis occur – which manifest themselves in various states of illness.

It is further explained in “Mechanisms of Pathogenesis” that:

…approximately 60% of mitochondrial DNA must be deleted from the mouse genome before complex IV activity is compromised and serum levels of lactate are elevated. 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.

The lay person’s summary of the above excerpts is that we have excess mitochondrial DNA and that excess mitochondrial DNA keeps each of us from developing a systemic multi-symptom illness whenever mitochondrial DNA is adversely affected (many pharmaceuticals and environmental toxins adversely affect mitochondrial DNA). However, when mitochondrial DNA is depleted sufficiently, cellular dysfunction, oxidative stress and cell death, ensue.

Multiple studies have noted that fluoroquinolones deplete mitochondrial DNA (here, here and here).  When enough mitochondrial DNA are depleted, adverse reactions that are systemic and include multiple symptoms simultaneously, occur.

Multi-Symptom Reaction: Look to Mitochondrial Damage

It is often difficult for the patient who is experiencing a systemic multi-symptom illness to connect his or her illness to the mitochondria damaging drug or toxin that hurt him or her because of the time delay between the cause (mitochondria damaging chemical) and the effect (bomb going off in body and mind). Though the delayed onset of fluoroquinolone toxicity and mitochondrial dysfunction symptoms are noted in many articles (here, here), the reason for the delayed onset of symptoms is not known.  In “Mechanisms of Pathogenesis” it is hypothesized that “an initial adaptive response was followed by a toxic response” when cells are exposed to a mitochondria damaging chemical. Perhaps the delay in adverse reaction onset is due to a toxic response taking time to develop.

Many pharmaceuticals damage mitochondria. Bactericidal antibiotics (including fluoroquinolones), Statins, acetaminophen, some chemotherapy drugs, vaccines, and many others, cause mitochondrial dysfunction, oxidative stress and cell death. Mitochondrial dysfunction and oxidative stress are connected to a variety of ailments, from chronic fatigue syndrome to Alzheimer’s disease and obesity. However, the FDA and other drug regulatory agencies have systematically ignored damage to mitochondria caused by pharmaceuticals and “mitochondrial toxicity testing is not required by the US FDA for drug approval.”

The recognition of delayed adverse reactions and tolerance thresholds for mitochondrial damaging drugs and vaccines will go far in helping both doctors and patients to recognize mitochondrial damage related adverse drug reactions (and adverse vaccine reactions). Once the reactions are recognized, perhaps some pressure can be put on the FDA and/or the pharmaceutical companies to test how drugs affect mitochondria before they are released onto the market. After all, mitochondrial damage and oxidative stress are causally related to almost every chronic illness.  It would be nice if doctors, those in the pharmaceutical industry, the FDA regulators, and others, recognized the harm that drugs do to mitochondria, and the symptoms of iatrogenic mitochondrial dysfunction.

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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If you have suffered from a fluoroquinolone or any other medication reaction, please consider sharing it on Hormones Matter.

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Image was created using Canva AI.

This story was published originally on Hormones Matter in March 2014.

 

 

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Post Gardasil Heart Failure, Ragged Red Fibers and Thiamine

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I recently became aware of a case of a boy who had died from a myocarditis and subsequent heart failure after he had received the Gardasil vaccination. He was reportedly completely healthy before the vaccination and the death had been directly attributed to it. The autopsy report was very striking. Examination of heart muscle had revealed a “long narrow band of dark reddish discoloration, somewhat darker than the rest of the myocardium”. Although this was not described more fully, it strongly suggested that the description was that known in medical jargon as “ragged red fibers”.

Ragged red fibers are commonly seen with mitochondrial dysfunction in muscle tissue. The ragged red fibers indicate an accumulation of abnormally functioning mitochondria in the muscle tissue. Though ragged red fibers have been studied extensively in individuals with inherited mitochondrial disease, it is not clear whether this type of damage can be acquired or induced in individuals with or even without mtDNA mutations. Studies in rats, however, have shown that thiamine deficiency does result in the finding of ragged red fibers in muscle tissue, suggesting that this damage can be induced. In view of the many posts on this website discussing the association of thiamine deficiency with Gardasil vaccination, I became very interested and began to search the literature for what was known about the relationship of thiamine with ragged red fibers.

Mitochondria

Before I offer an explanation, let me remind the reader about mitochondria. We have between 70 and 100 trillion cells that make up the human body. Each cell has a prescribed function and each of the body organs consist of highly specialized cells. What we tend to forget is that our food provides the fuel from which energy is generated. To use a simple analogy, a car without an engine would not be capable of functioning. Mitochondria are the “engines” that exist in each one of those cells. They provide the energy for which function is dependent. We inherit from our parents thousands of genes that control how we look, behave and perform as personalities. These are known as cellular genes, but mitochondria have entirely separate genes inherited only from the mother. They control the mechanisms of the “engines” (mitochondria) in generating energy. Disease can be caused by genetic mutations in cellular genes but in the past decade it has been recognized that mitochondrial genes can be responsible for disease and more than 50 different mutations have been described. The majority of these mutations are single base changes in the DNA strand. They do not necessarily produce disease by themselves. Other factors related to nutrition, lifestyle, and as I suspect, medications and vaccines, may have to come into play.

To express this fully, a deficiency of thiamine (or other vitamins) can be so mild that the symptoms, if any, are regarded as inconsequential or ascribed to other causes. This obviously becomes more important if there is an associated unknown genetic risk that affects the metabolism of the vitamin. Because thiamine is so vital to energy synthesis, the imposition of a stress factor such as a mild infection or an inoculation can precipitate more severe symptoms. Meeting stress requires adaptive energy. To provide an analogy, a car with an inefficient engine may be adequate on the level but be inadequate to meet the stress of climbing a hill.

Mitochondrial Disorders are Multi-Systemic

I should note that mitochondrial disorders are often multi-systemic due to impaired oxidation that results in defective mitochondrial energy production. That means there can be symptoms from damage to multiple organ systems simultaneously. Mitochondrial disorders are also phenotypically different amongst family members with the same mutation and amongst individuals with acquired mitochondrial dysfunction. In other words, how mitochondrial disorders or damage can present symptomatically varies radically from person to person. This variation is what makes diagnosing mitochondrial dysfunction difficult for many practitioners. The symptoms don’t always fit into nice, neat, discrete diagnostic categories that so many of us are accustomed too. This variability in mitochondrial dysfunction makes it difficult to attribute the action of a vaccine or medication as the cause of a subsequent illness, or in some cases, death. How is it possible for a medication or vaccine to induce so many seemingly disparate symptoms? To answer that question, we need to understand a few mechanisms.

Thiamine Deficiency Post Gardasil

Over the last several years, we have identified several cases of laboratory confirmed thiamine deficiency post Gardasil. Additionally, when lab testing was unavailable (few labs offer the appropriate assays for thiamine testing), clinical response to thiamine treatment has been confirmatory. In more recent research, we have identified thiamine transporter gene mutations (SLC19A2) in a group of young women who experienced severe reactions to the Gardasil vaccine (reported within this article). Combined, this suggests that thiamine deficiency is involved in some of the adverse reactions observed and that the potential danger from the use of a vaccine requires more information from the patient and his/her family. How can something as simple as thiamine cause so many adverse reactions and even death? And can a medication or vaccine induce thiamine deficiency?

Thiamine is Critical for Mitochondrial Functioning

Thiamine is a critical co-factor in multiple pathways involved in mitochondrial energy production (ATP). It is necessary for carbohydrate processing via the pyruvate pathway and it is necessary for fatty acid processing because of its involvement with the HACL1 enzyme.  In other words, the mitochondria depend upon thiamine to function. Diminish thiamine and all sorts of compensatory reactions are initiated which, if not stopped, can cause death. Thiamine deficiency in adults, particularly those with chronic alcoholism, is considered a medical emergency. It has not, however, been readily recognized in reference to other causes of malnutrition where there is an imbalance between the ingested calories and the necessary vitamins – high calorie malnutrition. This particularly applies to thiamine.

The Gardasil Thiamine Relationship

There are multiple mechanisms by which a vaccine or medication can induce thiamine deficiency or push an existing or subclinical deficiency into a danger zone. Beginning with the later first, the modern western diet is replete with highly processed foods that are dense in calories but lack non-caloric nutrients. It is entirely likely that many individuals, even those that appear healthy, are borderline thiamine deficient or intermittently thiamine deficient when stressors or illnesses arise. Vaccines are toxicological stressors to the immune system and broadly speaking, any stressor, but particularly one that demands an immune reaction like a vaccine, is capable of inducing a thiamine deficient state. In individuals with latent errors in thiamine absorption (GI disorders), distribution or metabolism (like those with thiamine transporter mutations), or anything that evokes even a slight degradation in thiamine nutrient availability, thiamine deficiency will be exacerbated exponentially.

The Gardasil vaccine was developed using a yeast type base*. The yeast produces an enzyme called thiaminase that inactivates thiamine. Again, against the backdrop of poor diet or diet high in foods that also produce thiaminase (coffee, tea, certain fish), but especially, against the backdrop of a genetic or acquired mitochondrial issue recognized or latent, the reaction to the vaccine (or medication, as many medications can block thiamine directly or indirectly), can be devastating.

Finally, vaccines, because of the adjuvant carriers like aluminum, damage to mitochondrial functioning more broadly, with both structural and functional changes are noted. Damaged mitochondria are not only less capable of producing appropriate amounts of cellular energy but are also incapable of performing the myriad of other functions with which the mitochondria are tasked.

Ragged Red Fibers and Cardiomyopathy

Let us continue with this case and the ragged red fibers observed in the myocardium, the heart muscle, of the deceased boy. For those who study mitochondrial disorders, one of the more common histological hallmarks of the disease process in mitochondrial disorders are ragged red fibers.  These are muscle fibers with abnormal focal accumulations of mitochondria. According to the coroner’s report:

“a long narrow band of dark reddish discoloration which is somewhat darker than the rest of the myocardium, extends over a length of 6 cm and has a width of 0.4 cm extending from the anterior base of the heart almost to the apex. ..this lesion is limited to the anterior free wall”

was observed. The coroner concluded that the boy developed asymptomatic myocarditis in weeks preceding his death. The myocarditis evoked a heart attack which was the determined cause of death. A subsequent review by a medical expert hired by the attorneys presenting the case against the vaccine manufacturer, went a little deeper, attributing the dark fibers to a vaccine-induced inflammatory reaction resulting from the first dose of Gardasil. He argued that the first dose of the vaccine initiated a heart attack that was somehow not noticed by the child, as he continued to play football. Upon receiving the second dose, however, the damage initiated by the first dose was exacerbated, slowing heart function until it failed entirely. In either case, the heart muscle was irreparably damaged such that the child died in his sleep with the Gardasil as the causal agent.

Given my background in thiamine research, and thiamine’s role in heart function (as well as in brain function), I immediately wondered if the observed “band of darkish reddish discolorations” could be the ragged red fibers so common in mitochondrial dysfunction and if there presence indicated thiamine deficiency. Furthermore, I suspected that the fact that he died in his sleep strongly suggested that the automatic respiratory mechanism governed by the brain stem was implicated. This too, is a strong support for thiamine deficiency. I should note, I did not have access to the full report; only that which was published online.

Thiamine Deficiency and Ragged Red Fibers: Experimental Evidence

As I have argued previously and elaborated above, the HPV vaccines can induce and/or exacerbate thiamine deficiency. The question is whether thiamine deficiency can induce ragged red fibers in muscle.

To that end, I discovered a manuscript in the Archives of Neurology: Neuropathic and mitochondrial changes induced in rat muscle, showing that experimentally in rodents this was possible. Thiamine deficiency could induce ragged red fibers in muscle tissue. In this particular study, two groups of rats were compared. One group was fed a normal diet and the other group was fed a diet deficient in thiamine. The rats with thiamine deficient diets developed ragged red fibers in the muscles. Other abnormalities were described not found in the muscles of the control rats.  The authors concluded that thiamine deficiency was responsible for  the observed ragged red fibers and may be involved in what are now called the “ragged-red diseases”.

Case Studies: Ragged Red Fibers, Thiamine and Mitochondrial Disease

Japanese investigators studied two siblings with muscle disease due to mitochondrial dysfunction, a mutation in the mitochondrial DNA, and familial thiamine deficiency. Ragged red fibers were found in muscle biopsies. The older brother had presented at the age of 20 years when he developed muscle disease and beriberi heart disease. Thiamine deficiency was present in the siblings and parents and ragged red fibers were noted in muscle biopsies from the siblings. The development of symptoms at the age of 20 years certainly indicates that it was not a purely genetically determined disease.

Another article in a Japanese journal reported a nine year-old boy with muscle and brain disease in whom thiamine administration gave temporary improvement. A muscle biopsy had revealed numerous ragged-red fibers.

Mitochondrial diseases have a special predilection to involve the brain in view of its high metabolic demand. Patients with a form of disease known as myoclonic epilepsy have ragged red fibers in muscle tissue thus identifying the underlying mitochondrial cause.

Mitochondrial Dysfunction in Myocardial Infarction and Sudden Death

In a recent review of mitochondrial cardiomyopathies we see some striking similarities between this case and what has been recently recognized. Accordingly:

The presentation of mitochondrial cardiomyopathy includes hypertrophic, dilated, and left ventricular (LV) noncompaction, and the severity can range from no symptoms to devastating multisystemic disease. Severe cardiac manifestations include heart failure and ventricular tachyarrhythmia—which can worsen acutely during a metabolic crisis —and sudden cardiac death. Mitochondrial crisis is often precipitated by physiologic stressors such as febrile illness or surgery [a vaccine] and can be accompanied by acute heart failure.

Bioenergetic derangements are increasingly recognized as major culprits in the development of cardiac hypertrophy and in the progression to heart failure, in both acquired and inherited disease. The mitochondria are a crucial platform for energy transduction, signaling, and cell-death pathways that are broadly relevant to heart failure, even in the absence of an underlying mitochondrial myopathy. Oxidative stress and mitochondrial dysfunction are key factors in the development of most heart failure.

Connecting the Dots

The question remains, how could this boy’s death from a vaccination have been predicted and thus avoided? It is clear that there was temporal relationship between the vaccine, the damage to his heart, and his subsequent death. Mechanistically, the evidence is collaborative with this association. From an evidentiary standpoint, the vaccine appears capable of inducing mitochondrial dysfunction via its ability to diminish thiamine, and likely, via other, yet to be identified, mechanisms. Of key importance, however, is that thiamine depletion on its own, can induce ragged red fibers in muscle tissue, probably including the heart muscle. When the vaccine is given to an individual with genetic or other risk factors (like comorbid health issues, poor diet, and/or the high metabolic demands of sports training), the results can be devastating. Given that this combination of variables includes most teenagers, it is difficult not to see the dangers of this vaccine. In conclusion, if the long band of dark reddish muscle tissue described in the heart muscle of the boy had been shown to be ragged red fibers, it would have supported mitochondrial dysfunction as the cause of death.

*It should be noted that the Cervarix HPV vaccine was not developed using a yeast base, and thus, it is not clear by what mechanism(s) it might diminish thiamine concentrations.

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More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

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Image: Very high magnification micrograph showing ragged red fibres (also ragged red fibers), commonly abbreviated RRF, in a mitochondrial myopathy. Gomori trichrome stain.

Nephron, CC BY-SA 3.0, via Wikimedia Commons

This article was published originally on Hormones Matter on January 5, 2016. 

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HPV Vaccine Reactions: A Response to Walking on the Edge of a Sword

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Derrick Lonsdale, MD

This post is an attempt to answer the questions raised by the extraordinary post vaccination medical history of this 16 year old girl. Of all the HPV vaccine histories that have been recorded on “Hormones Matter” this is, in my view, one of the worst. We seem to be carrying out a vicious experiment on human beings and if this is not recognized as an indictment on the HPV vaccine, I do not know what will move the powers that be. With a very detailed history like this it is easy to see the relationship of the symptoms with the HPV vaccine. There is absolutely no doubt in my mind that this represents massive mitochondrial dysfunction affecting the brain and nervous system, particular the autonomic nervous system. I will try to discuss each symptom as it appears in the history.

Clues in the Pre – HPV Vaccine History

First of all it must be recognized that this young lady had pervasive developmental disorder, asthma, pyelitis, a topic dermatitis, otitis media, Candida, hemolytic streptococcus, pneumonia, “wart”, periodic fever, agrochemical sensitivity and recurrent stomatitis before she received the HPV vaccine. We are not told whether these symptoms were related to previous vaccinations. This appears to be consistent with a persistent concept among parents that infancy vaccines sometimes do more harm than good in a minority of children. The history here suggests a genetic or nutritional risk factor in addition to the stress of the vaccination.

Post – HPV Vaccine Reaction

Her attitude towards this dreadful post HPV vaccine legacy was excellent since she attended school in spite of fever. She is described as athletic with a good nature prior to vaccination and there was a major post vaccination personality change. The slow pulse suggested parasympathetic dominance that made at least a partial post-vaccination switch to sympathetic dominance. I base this on the description of an average post vaccination increase in pulse rate. I believe that the timeline reported in the medical history is important. She had the usual three injections. After the first one she developed asthma and since this was an early affliction I assume that the injection was a stress factor that triggered it. Asthma is caused by an imbalance in the autonomic nervous system. After the second injection she developed urticaria. This was again a signal through the autonomic system that delivered a message to histamine releasing cells in the skin.

The worst situation arose after the third HPV vaccine injection. Symptoms described were arrhythmia, an increase in circulating eosinophils, fever, hypersomnia, aggressiveness, childish behavior, hyperpnea, muscle weakness, headache, parotitis, temporo-mandibular joint syndrome, dysphagia, stomatitis, abdominal pain, vomiting, diarrhea, photophobia, double vision, and “blood stagnation” in the hippocampus. The gradual worsening with each injection might be compared with the repeated blows of a hammer where a nail is driven in a little bit more with each blow.  With this detailed description, a cause and effect relationship with each injection seems to be obvious and it would be stupid to regard this as a coincidence.

Oxidative Stress and the Brain

Let me try to explain these symptoms because I can assure you that they are all related to the brain. In particular, I am referring to the limbic system of the brain, that part of the brain that computes our adaptive mechanisms through the autonomic nervous and endocrine systems. The reference to the hippocampus makes it clear that the limbic system is involved because this is an important organ within that system. We can sum up the situation by saying that this young lady is now maladapted to her physical and mental environment.

When this part of the brain suffers from reduced energy efficiency from defective oxidative metabolism in mitochondria, it becomes erratic in the way it reacts to input signals delivered through the sensory system. This continuous process of brain and body signaling is how we adapt to our environment throughout life. We have to go back to the writings of Hans Selye whose professional career was spent in studying the effect of physical stress in animal systems. He reported his work as “The General Adaptation Syndrome” and referred to the diseases of mankind as the diseases of adaptation. I would have preferred to call it the diseases of maladaptation. What Selye emphasized throughout his writings was that it was consumption of energy that was required for adapting and its failure resulted in the syndrome that he described.

Now we know that the mitochondria are responsible for producing energy required for this, the General Adaptation Syndrome makes perfect sense. When Selye was doing his work, the biochemistry of energy metabolism was in its infancy. Now we have much more information about oxidative metabolism and energy production. Until recently, any mitochondrial dysfunction was considered to be invariably genetic in origin. We are now aware that it can be acquired as a result of environmental stress that results in insufficient energy to meet the mental or physical demand.

Diminished Oxidative Metabolism and the Limbic System: HPV Vaccine and Personality

The change in personality from a gentle to an aggressive individual is absolutely characteristic of diminished oxidative metabolism in the limbic system. In particular, the autonomic nervous system becomes extremely erratic in its behavior. It winds up by misdirecting the normal signals that go to the organs of the body and the associated symptoms are chaotic, referred to as dysautonomia. For example, the reaction to a mild reprimand might be an explosive temper tantrum and dietary indiscretion might well be an important factor in the waves of juvenile violence that seem to be otherwise inexplicable.  For the past 35 years I have been seeing the personality of children change because of abnormal biochemistry in the limbic system. They have wicked temper tantrums, kick the door or the wall, are rude to parents and teachers and are generally out of control. By rescuing them from their appalling diet and giving them supplements, nearly all of them would gradually come back to being a normal child.

We are suffering from an epidemic of biochemical rather than psychological disease. Of course there is a genetic principle behind it; there always is!  The smarter the child the greater the dietary risk. This should be fairly obvious to anybody because, like our cars, the better the car the better the fuel has to be.  Because the brain, central nervous system and the heart are the most oxygen consuming tissues in the whole body, it is hardly surprising that they are the first to succumb. They are the organs most affected by vitamin B1 deficiency that causes beriberi. This vitamin, like a spark plug in a car, is a necessity to the oxidation of glucose, the primary fuel used by our cells, particularly in brain. Of course, it is not the only non caloric nutrient required, but its association with energy metabolism is clearly dominant.

We have seen from previous posts on this web site that some victims of post vaccination postural orthostatic tachycardia syndrome (POTS) were thiamine deficient and the dysfunction in the autonomic nervous system could legitimately be called beriberi.  I have suggested several times that a marginal state of brain biochemistry may exist before the vaccination is given and that it acts as a stress factor. This might be from an unknown genetic risk or from a diet that does not meet the mental and physical activity required by the individual or a variable combination of both. It would explain why this HPV vaccine appears to pick off the brightest and the best.

In my opinion this young lady can only be helped by the administration of intravenous vitamins since that is the only way in which the necessary concentrations can be built up.  It can be compared with changing the spark plugs in the engine of a car to improve its performance. Thiamine tetrahydrofurfuryl disulfide is available in Japan under the trade name of Alinamin, I have no doubt that this would be an important addition to the intravenous concentration of water soluble vitamins.

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Thiamine Deficiency and Aberrant Fat Metabolism: Clues to Adverse Reactions

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Derrick Lonsdale, MD

Over the last several months, the writers and researchers at Hormones Matter have posted a number of articles about mitochondrial dysfunction and thiamine deficiency.  Thiamin, or thiamine as the internet search engines prefer, is critical to mitochondrial function. We’ve learned that thiamine deficiency can emerge gradually due to dietary inadequacies or more suddenly as a result of a medication, environmental or surgical insult. Regardless of the cause, deficits in thiamine evoke devastating health issues that can be treated easily if identified. More often than not, however, thiamine deficiency is not assessed and symptoms are left to escalate, mitochondrial damage increases, and patient suffering continues. Because thiamine deficiency is rarely considered in the modern scientific era, mild symptoms are ascribed to other causes such as “an allergy” or “it’s all in the patient’s head”. If, however, the cause is not revealed, the same old dietary habits will continue and can be guaranteed to produce much more severe and difficult to treat chronic disease.

Although there are a myriad reasons why mitochondria are damaged, medication or vaccine reactions paired with latent nutritional deficiencies seem to be common. Predicting who and how the mitochondrial dysfunction might appear, however, is more complicated. Quite often, athletes and individuals considered healthy are hit harder by a stress factor such as a vaccine than those whom we might not regard as particularly healthy. There are several potential reasons for this, some of which have been outlined previously. In this post, I would like to add one more reason why highly active, high performing individuals might be hit harder and more quickly than their less active counterparts with vaccine or medication reactions that induce thiamine deficiency.

Mitochondria are the Engines of the Cell

To use an analogy, the usefulness of a car obviously depends upon its engine. Mitochondria are the “engines” of each cell within our bodies, all 70 to 100 trillion cells that make up an adult body. They are known as organelles and are so small that their structure can only be seen with an electron microscope. But we can take this analogy further by comparing each cell to a different car model. A high powered car uses more gasoline than a low powered one and there are many models of each type of car. So some cells in the body require more energy than others, depending on the special function of the cell.  The most energy consuming cells are in the brain, the nervous system and the heart, followed by the gastrointestinal system and muscles. That is why those organs and tissues are most affected in the disease known as beriberi, the thiamine deficiency disease that we have discussed previously in other posts. The function of other organs is affected by the deficiency because of the changes in the control mechanisms originating in the brain through the autonomic (automatic) nervous system.

It has been pointed out that this disease in its early stages affects the autonomic nervous system by causing POTS. Beriberi and POTS, both being examples of dysautonomia (abnormal activity of the autonomic nervous system), can only be distinguished by finding evidence of thiamine or other nutrient deficiency as a cause. Thiamine is but one factor whose deficiency causes loss of cellular energy, resulting in defective brain metabolism and dysautonomia.  Although the relationship with vaccination is conjectural, some individuals with post Gardasil POTS were found to be thiamine deficient and had some relief of symptoms by taking supplementary fat soluble thiamine, an important derivative that occurs in garlic and has been synthesized. Not all of these thiamine deficient individuals have benefited to the same degree, suggesting that other deficiencies might also be involved. This post is to provide some information about more recent knowledge concerning the action of thiamine and the incredible, far-reaching effects of its deficiency, particularly in the brain. Experimental work in animals has shown that thiamine deficiency will damage mitochondria, a devastating effect for an acquired rather than a genetic cause. Far too much research has been devoted to genetic cause without sufficient attention to the way genes are influenced by diet and lifestyle.

The Importance of Enzymes to Mitochondrial Function

Before I provide this new information, let me remind the reader that enzymes, like cogwheels in a man-made machine, enable bodily function to occur. The importance of thiamine is that it is a cofactor to many of the enzymes that preside over energy metabolism. Without its cofactor an enzyme becomes inefficient. Perhaps it might be compared with missing teeth in a cog wheel. With missing teeth the cog wheel may still function but not nearly as well as it would with all of its component parts.

In previous posts we have discussed how thiamine deficiency can be caused by an excess of sugar in the diet. I have likened this to a “choked engine” in a car where an excess of gasoline, relative to insufficient oxygen concentration in the mixture, makes ignition of the gasoline extremely inefficient. Bad diet, one that is rich in sugary, carbohydrate laden foods may be one of the more common contributors to latent thiamine deficiencies. Excessive intake of processed fats and the concomitant changes to mitochondrial function and energy metabolism may be another important contributor.

Thiamine and Fat Metabolism

All the enzymes affected by thiamine deficiency have a vital part to play in obtaining cellular energy from food by the process of oxidation. Most of them have been known for many years but in the nineties a new enzyme was discovered. It has a very fancy name that has been simplified by calling it HACL1.  Only in recent years has it been found that HACL1 is dependent on thiamine as its cofactor. Although not reported, it may mean that it is also dependent on magnesium. This is exceedingly important because it introduces the fact that thiamine is involved in fat as well as carbohydrate metabolism, something brand new, even to biochemists.

Here I must digress again to describe another type of organelle called a peroxisome that occurs in our cells.  Like mitochondria, they are infinitesimally small. Their job is to break down fatty acids and they have a double purpose. One purpose is to synthesize very important substances that construct and maintain cells and their function: they are particularly important in the brain. The other purpose is what might be called fuel preparation. As the fatty acids, consisting of long carbon chains, are broken down, the resulting smaller fragments can be used by mitochondria as fuel to produce energy.  Failure to break down these fatty acids can result in the accumulation of natural components that may be toxic in the brain and nervous system or simply result in lack of one type of fuel. That is why feeding medium chain triglycerides by administration of coconut oil has been reported useful to treat early Alzheimer disease. They can be oxidized in mitochondria.

The Important Use of Fatty Acids in Mitochondrial Health

Here, I want to use another analogy. Imagine a lake that admits water to a river through a sluice gate that has to be opened and closed by a farmer who regulates the supply of water. If the gate is open the river will supply water to the surrounding fields. If however the gate is closed, the river will begin to dry up and the crops in the fields will suffer. Perhaps the farmer half closed the gate during a rainy period and has forgotten to open it when a dry period follows. High temperatures in the dry period results in insufficient water to meet the growth needs of the crops.

In this analogy, the lake represents food, the sluice gate is the HACL1 enzyme and the farmer who controls the gate represents thiamine. The water in the river represents the flow of fatty acids to the tissues for the double purpose of cellular construction and fuel for oxidation. The half open gate represents a minor thiamine deficiency, more or less sufficient for everyday life but not enough when there is greater demand. A high temperature that increases the water needs for crops represents Gardasil and many other medications as a stress factor, placing a greater demand on essential metabolic action.  The analogy also implicates the nature of the crops, some of which require more water than others. The crops, of course, represent body tissues and organs.

If we consider high performing individuals, whether academically or athletically, like high performance cars or crops that demand more nutrients, we can see how a previously unrecognized minor deficiency might trigger clinical disease by the stressful demands of a vaccine or medication. Some pharmaceuticals can attack thiamine directly, like Gardasil and the fluoroquinolones, while others attack different pathways within the mitochondria.

No matter the pathway, high performing individuals, with high energy needs not covered by diet, may be hit harder when a medication attacks mitochondrial energy.

The Outcome of Defective Fatty Acid Metabolism

Returning back to the HACL1 enzyme, we now know that HACL1 is the first thiamine dependent enzyme to be discovered in peroxisomes. It is research news of the highest importance, affecting us all. Its action is to oxidize a diet related fatty acid called phytanic acid and fatty acids with long carbon chains that cannot be used for fuel until they are broken down. Phytanic acid is obtained through consumption of dairy products, ruminant animal fats and some fish. People who consume meat have higher plasma phytanic acid concentrations than vegans. If the action of HACL1 is impaired because of thiamine deficiency the concentration of phytanic acid will be increased. The river in the analogy actually represents a series of enzymatic reactions that may be thought of as down-stream effects, whereas thiamine deficiency, being up-stream, affects all down-stream phenomena. One of the reasons thiamine deficiency is such an important contributor to illness is because its effects are broad.

These enzymatic reactions, known technically as alpha oxidation, involve four separate stages. It has been known for some time that if another enzyme at stage two is missing because of a gene defect, the result will be damage to the neurological system known as Refsum’s disease. Symptoms include cerebellar ataxia (also reported after Gardasil vaccination), scaly skin eruptions, difficulty in hearing, cataracts and night blindness. Other genetic mutations in alpha oxidation, resulting in various biochemical effects, result in a whole variety of different diseases. This places thiamine deficiency as a potential cause for all the down-stream effects resulting from defective alpha oxidation, for it has been shown in mice that this vitally important chemistry is totally dependent on presence of thiamine. Since its complete absence would be lethal, we have to assume that it is mild to moderate deficiency, equivalent to a partial closure of the sluice gate in the analogy.

Sources of Phytanic Acid: How Diet Affects Thiamine

In ruminant animals, our source of beef, the gut fermentation of consumed plant materials liberates phytol, a constituent of chlorophyll, which is then converted to phytanic acid and stored in fat. The major source of phytol in our diet is, however, milk and dairy products.  It raises several important questions. If thiamine deficiency is capable of causing an increase in phytanic acid in blood and urine, it might be a means of depicting such a deficiency in a patient with confusing symptoms. It might also explain why some individuals who have been shown to have thiamine deficiency by means of an abnormal transketolase test have symptoms that are not traditionally accepted as those of such a deficiency, perhaps because of loss of efficiency in HACL1.

If an excess of sugar in the diet gives rise to a secondary (relative) thiamine deficiency, we are provided with an excellent view of the extraordinary danger of empty simple carbohydrate and fat calories, perhaps explaining much widespread illness in Western civilization. Interestingly, it would also suggest that something as benign as milk could give rise to abnormal brain action in the presence of thiamine deficiency, because of phytanic acid accumulation. Our problems with dairy products may go well beyond lactose intolerance and immune dysregulation.

In sum, the discovery of HCAL1 enzyme and its dependence upon thiamine suggests one more mechanism by which thiamine deficiency affects mitochondrial functioning. As emerging evidence indicates a myriad of environmental and pharmaceutical insults impair mitochondrial functioning, thiamine deficiency ought to be considered of prime importance. Deficits in thiamine evoke devastating health issues that can be treated easily if identified.  If, however, thiamine deficiency is not identified and the same old dietary habits continue, the latent thiamine deficiency can be guaranteed to produce a much more severe and difficult to treat chronic disease. Moreover, individuals with thiamine deficiency who do not respond sufficiently to thiamine replacement might also have aberrant fatty acid metabolism. This too should be investigated and dietary changes adopted.

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Testing for Cerebral Mitochondrial Dysfunction Post Medication or Vaccine Induced Damage

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Chander Marrs

Over the last several weeks I have been the beneficiary of a fair amount of synchronicity; seemingly random introductions to interesting people and research connections from disparate sources. Not the least of which was a recent introduction to the concept of lactate doublets. What the heck are lactate doublets?  I had no idea and I am certain most of you reading this do not know either. Well, it turns out lactate doublets may be a missing piece in the diagnostic puzzles that present post medication and vaccine adverse reactions. Let me explain, but first a bit of background.

Mitochondrial Dysfunction

If you’ve followed Hormones Matter for any length of time, you know that we cover complicated diseases and medication and vaccine reactions. Inevitably, these reactions include neurological and neuromuscular symptoms that, almost to tee, fail to show up on standard diagnostic testing. This is particularly troubling when the symptoms include seizures, migraines, tremors, ataxias, neuropathies, dysautonomias and other obvious signs of nervous system damage.

We’ve attributed many of these cases to mitochondrial damage and subsequent dysfunction but testing for damage has proved problematic in most cases. While genetic disorders of mitochondrial dysfunction are reasonably well documented, the more dynamic, environmental and even epigenetic functional changes suspected in toxin, medication or vaccine induced mitochondrial disease are neither well documented nor easily recognized. With no easy testing, folks whose mitochondria are functionally or operational deficient, suffer needlessly and chronically. So when I read the report about lactate doublets as evidence of mitochondrial dysfunction in autism, I was intrigued. And, since I had just attended a talk on the mechanics of measuring basal metabolic rate as indicator of mitochondrial respiration e.g. mitochondrial functioning, I was doubly intrigued.  Could we use these measures as pre-screening tools for mitochondrial damage in health and disease? After all, what could be more fundamental to overall health and cellular energetics than aerobic and anaerobic metabolism? Identify problems with energy metabolism and there’s a good chance something is hinky in mitochondria land.

The Wonders of Lactate

For those of you who are athletes, lactic acid and lactate are familiar topics. For those who are not athletes, consider the last time you exercised rigorously and that point at which the demand for oxygen and fuel for your muscles out-paced your body’s ability to adapt and provide that fuel. What happened? Your muscles began to fatigue, you slowed down, you may have begun to hyperventilate and eventually you hit the wall, exhausted.

If you’re an athlete, a large part of your training involves moving that exhaustion threshold, that wall, further and further away. You train to increase muscle strength – anaerobic capacity, cardiopulmonary functioning- aerobic capacity and the tolerance for pain. Lactate production and utilization is the key to training and athletic success. In the common vernacular, lactate is incorrectly referred to as lactic acid. They are two different molecules. Lactic acid is precursor to lactate and lactate is both a substrate and a product of anaerobic metabolism. Lactate is currency for energy metabolism between cells, tissues and organs. The point at which lactate production outstrips its utilization as fuel or energy is one of the first steps of fatigue in healthy, athletic individuals. In not so healthy individuals and many disease processes, excess lactate can be a marker for mitochondrial dysfunction. In not so healthy individuals where the mitochondria are functioning sub-optimally, that feeling of hitting the exercise wall, is continuous with normal activity.

Lactate and Mitochondria

Over the last several months we’ve discussed mitochondrial ATP production on a number of occasions, mostly in relation to the aerobic process of the energy production that converts glucose (sugars) to adenosine triphosphate (ATP), the cellular energy that fuels our existence. This process requires large amounts of oxygen and numerous chemical co-factors, thiamine being one of the more major among them. Diminish oxygen levels or one of the necessary co-factors and energy/ATP production is reduced.

Not to worry yet, we have a backup or secondary ATP production cycle involving lactate. Here glucose is converted to compound called pyruvate which then is either shuttled into the mitochondria to produce ATP or it remains in either the extracellular or  intracellular cytosolic (cell fluid) space and is converted to lactic acid and then to lactate. The pyruvate>lactate path is anaerobic. That is, it does not require oxygen. The heart, kidneys and liver prefer lactate for fuel and rely heavily on anaerobic metabolism. In our exercise model, anaerobic metabolism and increasing lactate production parallel increasing exercise intensity, though it is less efficient. In comparison to aerobic metabolism that produces 38 mol of ATP, the anaerobic pyruvate>lactate path produces only 2 mol ATP.

The connection between lactate and mitochondrial functioning was only recently discovered and remains hotly debated. For a long time, it was believed that lactate remained outside the mitochondrion. Now, evidence suggests that mitochondria can convert lactate to ATP and that lactate is shuttled in and out of mitochondria to be used when needed. Based upon this possibility, measuring lactate either alone or in combination with respirometry measures may provide an indirect marker of mitochondrial functioning. Here’s where it gets interesting.

Body and Brain Lactate

Lactate is a fuel used readily in the body. Lactate levels change relative to metabolic needs (exertion and stressors) and efficiencies (oxygen usage, co-factor availability). Exercise physiologist have been measuring lactate and other indicators of metabolic functioning and path (aerobic versus anaerobic) for decades using a variety of respirometry tools, from breathing apparatus to blood tests and tissue biopsies. In a grossly oversimplified manner, the extent to which one produces and utilizes lactate during training indicates one’s overall fitness. Could we use some of those same tools, the less invasive ones, to provide a broad indicator of mitochondrial health?  Yes, we can.

Indeed, those same aerobic/anaerobic processes that occur in our body occur in the brain. Even though the brain is a huge consumer of glucose as its preferred fuel, recent evidence suggests that it also produces and consumes lactate in parallel to the body during exercise and other stressors. Beyond just the production of lactate in brain trauma, where oxygen and glucose are depleted rapidly and chronically, brain lactate levels appear to correspond with shifts in aerobic/anaerobic metabolism.

My thought, and what began this entire adventure, couldn’t measures of aerobic/anaerobic metabolism be adapted to compare healthy mitochondrial functioning versus non-healthy mitochondrial functioning? Wouldn’t a skew towards anaerobic metabolism and excess lactate, especially during rest and low exertion, indicate, at least broadly, mitochondrial damage?  The answer is yes; measures of respirometry, along with body and brain lactate could broadly indicate mitochondrial functioning.

But wait, there’s more. Instead of tissue biopsies, and perhaps even instead of the blood tests, researchers have figured out how to image lactate metabolism within the brain and presumably the body. Enter the lactate doublet.

Imaging Lactate with Magnetic Resonance Spectroscopy

Magnetic resonance spectroscopy (MRS) is like a magnetic resonance imaging (MRI) except that instead of simply taking pictures of the tissue, through a myriad of complicated calculations, the MRS measures the relative concentrations of specific metabolites in the brain and other tissues. The MRS can measure lactate metabolism in the brain and researchers around the world have begun to look at brain lactate as markers of different disease process, like autism, aging and brain injury. It is not without technical difficulties (machine calibration is complicated) and controversy, especially around the clinical interpretation, but I surmise it will open up a whole new area of diagnostic possibilities once the early glitches are worked out.

What is a Lactate Doublet?

The lactate molecule has two, weakly coupled, signals or resonances. When viewed on the MRS the lactate doublet presents as a double peak in the signal algorithm.

Lactate Doublets in Cerebral Mitochondrial Dysfunction

The presence of lactate can be diagnostic of specific types of brain tumor or stroke. Since lactate is elevated in mitochondrial disease, evidence of lactate doublets from MRS, even when MRI imaging shows no irregularities, can point to cerebral mitochondrial dysfunction. More specifically, in patients with genetic mitochondriopathies researchers have been able to delineate the regional differences in brain lactate corresponding to the neurological and clinical symptomotology associated with each mitochondriopathy. As was indicated previously, lactate doublets have been recognized in autism, aging (although mechanisms remain contended) and other mitochondrial disease processes.

Using MRS and Respirometry to Detect Post Medication or Vaccine Induces Mitochondrial Damage

Dynamic and functional changes to mitochondria are emerging as culprits in the more complicated adverse reactions we observe post medication and post vaccine. Recognizing the potential for mitochondrial damage post reaction is difficult, especially those impacting the nervous system. Conventional MRI’s and other imaging tests rarely detect visible lesions that can be attributable to clinical symptoms and standard blood tests are often normal, leaving the doctor and the patient without recourse. In advance of genetic testing and the measurement of each co-factor required for proper mitochondrial functioning, respirometry and MRS could be used to identify potential deficits in mitochondrial functioning. Measuring respiratory efficiency and lactate production and usage efficiency could be an easily detectable marker to rule in or out mitochondrial dysfunction. Those results could then be used to determine the need for additional testing that would identify more specific causes of mitochondrial dysfunction.

 

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

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Lisa Bloomquist

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.

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Your Mighty Mitochondria

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Lisa Bloomquist

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.

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.

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References

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

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

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The Paradox of Modern Vitamin Deficiency, Disease, and Therapy

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calorie rich versus nutrient rich

In order to understand why this article is about “paradox”, the concept of vitamin therapy must be appreciated. Hence, the explanation of the title is deferred to the end. Although vitamin deficiency disease is believed by most physicians to be only of historical interest, this is simply not true. When we think of a vitamin deficiency disease, we envision an individual living in a third world country where starvation is common. Such an individual is imagined as being skeletal, whereas an obese person is considered to be well fed with vitamin enriched foods. For this reason, common diseases, some of which are associated with obesity, are rarely, if ever, seen as potentially vitamin deficient.

The Calorie Rich and Nutrient Sparse Modern Diet

Our food is made up of two different components, the caloric and the non-caloric nutrients.  When we ingest high calorie foods (e.g. a doughnut) without even a vestige of non-caloric nutrients, we refer to this as “empty” or “naked” calories.  For our food to be processed into energy that enables the body and brain cells to function, there must be a ratio of the calorie bearing component to that of the non-caloric nutrients.  When we load the calories together with an insufficiency of non-caloric nutrients, we alter this ratio and produce a relative vitamin deficiency.  The trouble with this is that it does not result in the formation of the classic vitamin deficiency diseases as recorded in the medical literature. There is a gradual impairment of function, resulting in many different symptoms. Because modern medicine seeks to make a diagnosis by the use of imaging techniques and laboratory data and because of the physician’s mindset, if the tests used are normal, the possibility of a relative vitamin deficiency is ignored.

The Brain as a Chemical Machine

We have two different nervous systems. One is called “voluntary” that enables us to do things by will-power.  This is initiated and controlled by the upper brain, the part of the brain that thinks. The other system is known as the autonomic nervous system (ANS).  This is initiated and controlled by the lower part of the brain, the limbic system and brainstem.  This system is controlled automatically.  Although it collaborates with the other system, it is not normally under voluntary control. The limbic system and brainstem are highly sensitive to oxygen deficiency, but since the oxygen is useless without the non-caloric nutrients, their absence would produce the same kind of phenomena as oxygen deficiency. Thiamine (vitamin B1) has been found to be of extreme importance as a member of the non-caloric nutrients. The brain, and particularly the limbic system and brainstem, is highly sensitive to its deficiency.

Since the ANS is automatic, we are forced to think of the limbic system and brainstem as a computer.  For example, when it is hot, you start to sweat.  Evaporation of the sweat from the skin produces cooling of the body, representing an adaptive response to environmental hot temperature. When it is cold, you may start to shiver. This produces heat in the muscles and represents an adaptive response to environmental low temperature. If you are confronted by danger, the computer will initiate a fight- or- flight reflex.  This is a potential lifesaving reflex.  It is designed for short term use, consumes a vast amount of energy and prepares you to kill the enemy or flee from the danger.  Any one of these reflexes may be modified by the thinking brain. For example the lower brain, also known as the reptilian system, initiates the urge to copulate.  It is modified by the upper brain to “make love”.  The reptilian system, working by itself, can convert us into savages. There is an obvious problem here because our ancestors were faced with the dangers of short term physical stress associated with survival.  In the modern world the kind of stress that we face is very different for the most part.  We have to contend with traffic, paying bills, business deadlines and pink slips. The energy consumption, however is enormous, continues for a long time and it is hardly surprising that it is associated with fatigue, an early sign of energy depletion. It has been shown in experimental work that thiamine deficiency causes extensive damage to mitochondria, the organelles that are responsible for producing cellular energy.

Autonomic Function

The autonomic nervous system, controlled by the lower brain, uses two different channels of neurological communication with the body. One is known as the sympathetic system and the other is the parasympathetic. There are also a bunch of glands called the endocrine system that deals with the brain-controlled release of hormones.

We can think of the sympathetic branch of the ANS as the action system. It governs the fight-or-flight reflex for personal survival and the relatively primitive copulation mechanisms for the survival of the species. It accelerates the heart to pump more blood through the body.  It opens the bronchial tubes so that the lungs may get more oxygen. It sends more blood to the muscles so that you can run faster and the sensation of fear is a normal part of the reflex. When the danger is over and survival has been accomplished, the sympathetic channel is withdrawn and the parasympathetic goes into action. Now in safety and under its influence, body functions such as sleep and bowel action can take place.  That is why I refer to the parasympathetic as the “rest and be thankful system”.

Dysautonomia, Dysfunctional Oxidation and Disparate Symptoms 

When there is mild to moderate loss of efficiency in oxidation in the limbic system and/or brainstem they become excitable. This is most easily accomplished by ingesting a high calorie diet that is reflected in relative vitamin deficiency.  The sympathetic action system is turned on and this can be thought of as a logical reaction from a design point of view.  For example, if you were sleeping in a room that was gradually filling with carbon dioxide, the gradual loss of efficiency in oxidation would be lifesaving by waking you up and enabling you to exit the room. In the waking state, this normal survival reflex would be abnormal.

High calorie malnutrition, by upsetting the calorie/vitamin ratio, causes the ANS to become dysfunctional. Its normal functions are grossly exaggerated and reflexes go into action without there being any necessity for them. Panic attacks are merely fragmented fight-or-flight reflexes.  A racing heart (tachycardia) may start without obvious cause.  Aches and pains may be initiated for no observable reason. Affected children often complain of aching pain in the legs at night. Unexplained chest and abdominal pain are both common. This is because the sensory system is exaggerated. One can think of it as the body trying to send messages to the brain as a warning system.

Nausea and vomiting are both extremely common and are usually considered to be a gastrointestinal problem rather than something going on in the brain. Irritable bowel syndrome (IBS) is caused by messages being conveyed through the nervous system of the bowel, increasing peristalsis (the wave-like motion of the intestine) and often leading to breakdown of the bowel itself, resulting in colitis.  Of course, the trouble may be in the organ itself but when all the tests show that “nothing is wrong”, the symptoms are referred to as psychosomatic. The patient is often told that it is “all in your head”.

Emotional instability seems to be more in keeping with psychosomatic disease because emotional reactions are initiated automatically in the limbic system and thiamine deficient people are almost always emotionally unstable. A woman patient had been crying night and day for three weeks for no observable reason. A course of intravenously administered vitamins revealed a normal and highly intelligent person.  Intravenously administered vitamins are often necessary for serious disease because the required concentrations cannot be reached, taking them by mouth only.

The Vitamin Therapy Paradox

The body is basically a chemical machine.  But instead of cogwheels and levers, all the functions are manipulated through enzymes that, in order to function efficiently, require chemicals called “cofactors”. Vitamins are those essential cofactors to the enzymes.  If a person has been mildly to moderately deficient in a given vitamin or vitamins for a long time without the deficiency being recognized, the enzyme that depends on the vitamin for its action appears to become less efficient in that action.  A high concentration of the vitamin is required for a long time in order to induce its functional recovery.

Although the reason is unknown, doctors who use nutritional therapy with vitamins have observed that the symptoms become worse initially.  Because patients expect to improve when a doctor does something to them and because drugs have well-known side effects, it is automatically assumed by the patient that this worsening is a side effect of the vitamins. If the therapy is continued, there is a gradual disappearance of those symptoms and overall improvement in the patient’s well being. Unless the patient is warned of this possibility he or she would be inclined to stop using the treatment, claiming that vitamins have dangerous side effects and never getting the benefit that would accrue from later treatment.  This is the opposite effect that the patient expects. This is the paradox of vitamin therapy. 

If we view dysautonomia as an imbalance in the functions of the ANS and the vitamin therapy as assisting the functional recovery by stimulating energy synthesis, we can view this initial paradoxical as the early return of the stronger arm of the ANS before the weaker arm catches up, thus worsening an existing imbalance. However, this is mere speculation. I did not learn of the “paradox” until I actually started using mega dose vitamins to treat patients.

The Paradox and Thiamine

In this series of posts, we are particularly concerned with energy metabolism and the place that thiamine holds in that vital mechanism.  It is, of course, true that worsening of serious symptoms is a fact that has to be contended with and vitamin therapy should be under the care of a knowledgeable physician. The earlier the symptoms of thiamine deficiency are recognized, the easier it is to abolish them. The longer they are present the more serious will be the problem of paradox and a clinical response will also be much delayed and may be incomplete.

Beriberi and Thiamine Deficiency

I will illustrate from the early history of beriberi when thiamine deficiency was found to be its cause.  Many of the patients had the disease for some time before thiamine was administered, so the danger of paradox was increased. It was found that if the blood sugar was initially normal, the patient recovered quickly. If the blood sugar was high, the recovery was slow.  If the blood sugar was low, the patient seldom recovered.  In the world of today, an abnormal concentration of glucose in the blood would make few doctors, if any, think of thiamine deficiency as a potential cause. It is no accident that diabetes and thiamine metabolism are connected. Education of the doctor and patient are both absolutely essential. I believe that the ghastly effects of Gardasil, and perhaps some other medication reactions covered on Hormones Matter, can only be understood by thinking of the body as a biochemical machine and that the only avenue of escape is through the skilled use of non caloric nutrients.

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Dysautonomia and Hypoxia

Every profession has its jargon that enables its practitioners to communicate relatively easily but is incomprehensible to those outside the

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