thiamine deficiency gardasil

Adverse Reactions, Hashimoto’s Thyroiditis, Gait, Balance and Tremors

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Gait, tremors with adverse medication vaccine reactions

One of the things I most love about social media and health research is the opportunity to identify patterns of illness across different patient groups. Here is an example of finding research from one patient group, ThyroidChange, that likely spans many others (Gardasil injured, post Lupron Hashimoto’s, and Fluoroquinolone reactions – to name but a few) and offers clues to a perplexing array of symptoms. The research, is about a little known association between movement and balance disorders and Hashimoto’s thyroiditis: Ataxia associated with Hashimoto’s disease: progressive non-familial adult onset cerebellar degeneration with autoimmune thyroiditis.  Some background.

Hashimoto’s Disease

Hashimoto’s is the most common causes of hypothyroidism afflicting women at a rate of 10 to 1 compared to men. It is an autoimmune disorder in which antibodies attack the thyroid gland and destroy its ability to maintain normal thyroid hormone concentrations. The most common symptoms include: fatigue, muscle pain, weight gain, depression, cognitive difficulties, cold intolerance, leg swelling, constipation, dry skin. If left untreated, goiter – a swollen thyroid gland, appears. If left untreated for an extended period, cardiomyopathy (swelling of the heart muscle), pleural (lung) and pericardial (heart) effusion (fluid), coma and other dangerous conditions develop.

Hashimoto’s and Cerebellar Degeneration

A little known risk in Hashimoto’s is cerebellar degeneration. The cerebellum is the cauliflower looking section at the base of the brain that controls motor coordination – the ability to perform coordinated tasks such as walking, focusing on a visual stimuli and reaching for objects in space. The walking and balance disturbances associated with cerebellar damage or degeneration have a very distinct look, a wide gait, with an inability to walk heel to toe. Cerebellar ataxia looks like this:

In recent years, cerebellar involvement in attention and mood regulation have also been noted. The physicians reporting the Hashimoto’s – ataxia connection present case studies of six patients with Hashimoto’s disease, presumably controlled with medication and a progressive and striking shrinkage of the cerebellum (see report for MRI images) along with progressively debilitating ataxia (walking and balance difficulties) and tremors. Here’s where it becomes interesting.

Hashimoto’s: Medication Adverse Reaction and Misdiagnosis

Hashimoto’s disease is prevalent in our research into medication adverse reactions for Gardasil and Cervarix and Lupron, with some indications it may develop post Fluoroquinolone injury as well. The symptoms are difficult to distinguish from other neurological and neuromuscular diseases such as chronic fatigue syndrome, fibromyalgia, multiple sclerosis and an array of psychiatric conditions, and so Hashimoto’s often goes undiagnosed or is misdiagnosed and mistreated for some time.

Hashimoto’s, Demyelination and Cerebellar Damage

In some of the more severe adverse reactions to medications and vaccines that would lead to Hashimoto’s, the tell tale cerebellar gait disturbances have been noted and documented, along with a specific type of tremor (discussed below).

Research from other groups shows a strong relationship between thyroid function and myelin/demylenation patterns in nerve fibers in animals. Specifically, insufficient T3 concentrations demyelinates nerve axons, while T3 supplementation elicits myelin regrowth. Myelin is the white sheathing, the insulation that protects nerves and improves the electrical conduction of messages in sensory, motor and other neurons. Like co-axial cable in electrical wiring, when the protective sheathing is lost, electrical conductance is disrupted. The early symptoms of a demyelinating disease neuromuscular pain, weakness, sometimes tremors. These can be misdiagnosed as multiple sclerosis, fibromyalgia, chronic pain, when in reality, the culprit is a diseased thyroid gland.

Back to the Cerebellum

The cerebellum is a focal point of white matter axons – myelinated sensory and motor nerves. The cerebellum is where input becomes coordinated into motor movements or movement patterns. White matter damage in the cerebellum causes cerebellar ataxia, the movement and balance disorders displayed above. Hashimoto’s elicits white matter disintegration. Adverse reactions to medications and vaccines can elicit autoimmune Hashimoto’s disease. See the connection?

The Thiamine – Gut Connection

It gets even more interesting when we add another component of systemic medication adverse reactions – nutritional malabsorption, specifically thiamine deficiency. Almost across the board, patients with medication or vaccine adverse reactions report gut disturbances, from leaky gut, to gastroparesis, constipation, pain and a myriad of other GI issues that make eating and then absorbing nutrients difficult. Gut issues are common in thyroid disease too.

As we learn more, and as individuals are tested, severe nutrient deficiencies are noted, in vitamin D, Vitamin B1, B12, Vitamin A, sometimes magnesium, copper and zine. We’ve recently learned of the connections between Vitamin B1 or thiamine deficiency and a set of conditions affecting the autonomic nervous system called dsyautonomia or Postural Orthostatic Tachycardia Syndrome (POTS) linked to thiamine deficiency in the post Gardasil and Cervarix injury group. It may be linked to other injured groups as well, but we do not know yet.

Thiamine and Cell Survival

Thiamine or vitamin B1, is necessary for cellular energy. It is a required co-factor in several enzymatic processes, including glucose metabolism and interestingly enough, myelin production (the Hashimoto’s – cerebellar connection). We can get thiamine only from diet. When diet suffers as in the case of chronic alcoholism, where most of the research on this topic is focused, or when nutritional uptake is impaired, thiamine deficiency ensues. Thiamine deficiency can elicit cell death by three mechanisms:

  1. Mitochondrial dysfunction (reduced energy access) and cell death by necrosis
  2. Programmed cell death – apoptosis
  3. Oxidative stress – the increase in free radicals or decrease in ability to clear them

Thiamine deficiency in and of itself can elicit a host of serious health symptoms. The cell death and disruption of cellular energy balance can be significant and lead to a totally disrupted autonomic system.

Thiamine and Myelin Growth

Add to those symptoms, the fact that thiamine is involved in the growth myelin sheathing around nerves, and we have a whole host of additional neuromuscular symptoms masking as fibromyalgia, multiple sclerosis, chronic fatigue. Like with MS, limb and body tremors are noted in dysautonomic syndromes such as POTS. (Video of POTS tremors, note the uniqueness of the POTS tremor and the similarity between it and the foot tremor shown above along with cerebellar ataxia).

Let thiamine deficiency continue unchecked for period and we get brain damage, as white matter – the myelin disintegrates in the brainstem, the cerebellum and likely continues elsewhere. One of the most prominent areas of damage in thiamine deficiency, is the cerebellum, and hence, the cerebellar ataxia (movement disorders) noted in chronic alcoholics who are thiamine deficient, but also observed post medication or vaccine adverse reaction.

The Double Whammy on Myelin and Cerebellar Function

In the case medication or vaccine adverse reactions, particularly those that reach the systemic level, we have a double whammy on myelin disintegration: from a diseased thyroid gland and a diseased gut. Hashimoto’s and the reduction of thyroid hormones, particularly T3, impairs nerve conduction by shifting from a constant and healthy remyelinating pattern to one of demyelination, while the lack of thiamine further impairs myelin regrowth, because it is a needed co-factor. Both deficiencies affect peripheral nerves, but both also hit the brainstem, the cerebellum and likely other areas within the brain.

Take Home Points

The science of adverse reactions is new and evolving and much of what I am reporting here remains speculative. However, it has become abundantly clear through our research that to address medication adverse reactions or vaccine adverse reactions in a simplistic fashion, by region, or in an organ specific manner, is to miss the broader implications of the compensatory disease processes that ensue. Moreover, to look for symptoms of adverse reactions simply by the drug’s mechanism of action and/or by the standard outcome variables listed in adverse event reporting systems, again misses the complexity of the human physiological response to what the body is perceiving as a toxin. I believe that the entire framework for understanding the body’s negative response to a medication must be shifted to a much broader, multi-system, and indeed, multidisciplinary approach. In the mean time, we will continue to collect data on adverse reactions and offer our readers points of consideration in their quests for healing. I should note, that finding these connections is entirely contingent on the input our community of patients and health activists, both via the personal health stories that so many of you have been willing to share and the data we collect through our research. You know more about your health and illness than we do.

What we Know So Far – Tests to Consider

If you have had an adverse reaction to a medication or vaccine and neuromuscular difficulties, like pain, numbness, motor coordination problems, tremors etc., consider testing for Hashimoto’s thyroiditis. Also, consider thyroid testing when fatigue, depression, mood lability (switching moods), constipation, attentional and focus difficulties are present. In fact, I would consider thyroid testing, specifically for autoimmune thyroid disease like Hashimoto’s, as one of the first disease processes to rule out.

If you have had an adverse reaction to a medication that includes gut disturbances, consider the possibility that you are deficient in key micronutrients such as Vitamin D, the B’s, Vitamin A, magnesium, copper, zinc. And given the modern diet, consider that you were probably borderline deficient even before experiencing the adverse reaction. These nutrients are critically important to health and healing (and no, I do not have an association with vitamin companies or testing companies). Some tests for these nutrients are more accurate than others, so be sure to do your homework first.

If you have symptoms associated with autonomic systems dysregulation such as those associated with POTS, dysautonomia and its various permutations, consider thiamine testing, especially, transkelotase testing.

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Image Source: Pixabay.

Postscript: This article was published originally on Hormones Matter on October 15, 2013. 

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Thiamine Deficiency and Aberrant Fat Metabolism: Clues to Adverse Reactions

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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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More Ideas on Gardasil Toxicity and the Thiamine Connection

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I am in constant touch with the mother of the Gardasil treated daughter whose personal research suggested that her daughter had beriberi after she received the HPV vaccine.  As has been previously posted on this web site, thiamine deficiency, the basic cause of beriberi, was proved in this girl by a blood test called transketolase. It led to the test being done on two other girls and a boy, all of whom had been Gardasil vaccinated. All proved to have thiamine deficiency through this test.  Each of these young people, who have had the HPV vaccination and have succumbed to prolonged illness, have a variety of symptoms that have defied diagnosis and treatment.

As the original post on this subject pointed out, Postural Orthostatic Hypotension Syndrome (POTS), an apparently common post Gardasil illness, is a form of dysautonomia [damage to the autonomic nervous system] as is beriberi in its early stages. More recently, cerebellar ataxia has also been reported as a post Gardasil phenomenon. I have already pointed out on a previous post that the first case of thiamine dependency to be reported was in a six year old boy who suffered repeated attacks of cerebellar ataxia (see below for reference). Thus, thiamine plays a vital part in the brain.

As an analogy, the effect of its deficiency can roughly be compared with a defective spark plug in the engine of a car, thus killing the engine. It has been difficult for a number of Gardasil affected families to accept this proven fact because it seems so simple. It is not at all simple, for thiamine deficiency is a very serious problem in the brain. Believe it or not, it is capable of explaining all the symptoms that have been described to me.

The mother, whose research had led to the belief that beriberi was the cause of her daughter’s illness, has notified me of a number of symptoms that have been the subject of many questions from other mothers of Gardasil affected individuals. For example, one of the most classical signs of beriberi is swelling of tissues from fluid under the skin. This is called edema, a phenomenon that occurs in what is generally known as “wet” beriberi.  In dealing with a complex subject where technical knowledge is required, it was one of the observations in her daughter that convinced the mother that this was in fact beriberi.

Puzzling Symptoms Post HPV Vaccine

One of the puzzles that the mothers have discussed is that the vaccination seems to pick off the brightest and the best students who are usually also excellent athletes.  Another puzzle they have discussed is that symptoms seem to get worse when there is an abrupt change in the weather. Severe reactions to food and histamine related skin problems seem to be common to many of these affected individuals. Naturally, these have been passed on to me to try to provide an explanation, based on the proof that has been shown by the transketolase test.

Oxidative Metabolism 

We all understand that our lives depend upon the consumption of oxygen.  The brain uses 20% of the oxygen that you intake with every breath. This is because the metabolism in nervous tissue and the brain is very rapid. The same is true for the heart and that is why beriberi predominantly affects the nervous system, the brain and the heart. Thiamine “ignites” (spark plug) the fuel (glucose) by causing the glucose to combine with oxygen (combustion). This is what is called oxidative metabolism and why I refer to thiamine as “the spark of life”.  It is how we generate energy in every one of our 70 to 100 trillion cells that enable them to function.

Thiamine and the Brain

The lower part of the brain is highly sensitive to thiamine deficiency, interrupting the normal course of oxidative metabolism. If this part of the brain (the computer) is made to be inefficient from mild to moderate thiamine deficiency, it becomes irritable. If the deficiency persists or is more severe, structural damage begins and is irreversible. When the brain is healthy, all the physical and mental stimuli that we encounter on a daily basis are passed into the computer through our senses.

With the aid of the “thinking brain”, a decision is made as to how we will respond to the input stimulus, including our emotional responses which are generated in the limbic system and modified by the upper “thinking brain”. This is how we continuously adapt to both the mental and physical “stress factors” that we encounter in our daily lives.  But if the computer is made irritable, it will over-react to a stimulus and create an exaggerated response. For example, a normal response to an insult would be anger.

An exaggerated response might be associated with violence because the thinking brain has not suppressed or modified the reflex.  It is the limbic system (computer) that generates the fight-or-flight reflex. When it is made to be irritable this reflex may be initiated without there being a reason for it. It is then called a panic attack. Or, with a trivial stimulus, it might send a signal to the cells which release histamine, the reaction being initiated by something as simple as perception of a quick change in the weather.

Like a high powered car that requires more energy, so a high IQ is more demanding of oxidative metabolism, thus perhaps explaining why superior students are at greater risk. When we put food into the stomach, it automatically sends a signal into the computer. As we fill the stomach, these signals gradually crescendo, finally telling us that we have had enough to eat.  If, however, the computer has been made to be more sensitive, a severe reaction to the food may be generated and we call it food allergy. We can begin to see that the action is in the brain, not in the stomach.

How Could Gardasil Induce Thiamine Deficiency?

The primary answer to this difficult question is – we don’t know.  For example, we do not know whether a person has an abnormal transketolase before the vaccine is given.  We know that thiamine metabolism is related to the intake of sugar in the diet.  Beriberi has been reported in Japanese students ingesting carbonated beverages, a common worldwide activity associated with social groups, particularly adolescents. We know also that our present food supply does not contain the kind of concentration of vitamins and minerals required for perfect health, again suggesting the greater risk of a high IQ in relation to the quality of diet. The only direct connection between thiamine deficiency and the action of the Gardasil vaccine is that it is a yeast based vaccine. The yeast used in its preparation contains an enzyme called thiaminase. This naturally occurring enzyme breaks thiamine into its component parts and destroys its biologic action. Thiaminase disease has been reported in Japan.

Could Any Vaccine or Medication be a Stress Factor Sufficient to Induce Thiamine Deficiency?

In a previous post I told the story of how workers in factories succumbed to their first symptoms of beriberi as a result of their exposure to sunlight. What this implies is that you can have a marginal thiamine deficiency which is asymptomatic. Some kind of stress factor such as a simple viral illness, an injury, or even an inoculation can initiate symptoms. There are many examples of this in the medical literature, where a marginal metabolic situation that affects the brain is activated in this manner. Evidence provided by an abnormal transketolase is but a beginning, providing a scientific clue that should, in a sane world, initiate further research.

Additional Reference

Lonsdale D, Faulkner W R, Price J W, and Smeby R R. Intermittent cerebellar ataxia associated with hyperpyruvic acidemia, hyperalaninemia, and hyperalaninuria. Pediatrics 1969;43:1025-34.

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Cerebellar Ataxia and the HPV Vaccine – Connection and Treatment

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Anecdotal evidence points to a connection between Gardasil and Cervarix, the HPV vaccines, and cerebellar injury. Here, from the journal Neuropediatrics comes the first published report linking the HPV vaccine to cerebellar ataxia: Association of Acute Cerebellar Ataxia and Human Papilloma Virus Vaccine: A Case Study.

I should note, from our research we’re also seeing cases of cerebellar ataxia post fluoroquinolone reaction and related to Hashimoto’s thyroiditis. The cerebellum appears to be particularly sensitive to insult from environmental toxins – to functional mitochondrial injuries, perhaps because it collects the millions of peripheral nerves coming from the body that control sensation and movement, as they pass to higher brain centers. As such, the cerebellum demands high levels of oxygen and nutrients.

For those of our readers new to neuroanatomy, the cerebellum is the cauliflower looking section at the base of the brain that controls motor coordination – the ability to perform coordinated tasks such as walking, focusing on a visual stimuli and reaching for objects in space. The walking and balance disturbances associated with cerebellar damage or degeneration have a very distinct look, a wide gait, with an inability to walk heal to toe – very much like a drunken sailor. Videos of cerebellar ataxia can be seen here.

The Case Details: Acute Cerebellar Ataxia Post HPV Vaccine

Approximately, two weeks after receiving the HPV vacccine, Cervarix, a previously healthy 12.5 year old girl developed nausea and dizziness with severe cerebellar ataxia, tremors and nystagmus. Initial tests came back normal and she was hospitalized on day 20 post HPV vaccine. Though she could sit on her own, she could not stand or walk unaided and the nystagmus prevented her from focusing on TV, reading or other activities. She had no fever. Heel-knee-shin and finger-nose tests indicated ataxia with terminal intention tremor and dysmetria (see videos: horizontal nystagmus or here for multiple types of nystagmus, heel-knee-shin test, finger-nose test).

All blood tests, cerebral spinal fluid tests and imaging tests were normal, with the exception of testing positive for IgG and varicella zoster virus – chicken pox and shingles – indicating earlier exposure. Tumors, paraneoplastic disease, cardiovascular disease, metabolic conditions and labyrinthitis (inner ear disturbance) were all ruled out. Her symptoms did not remit as was expected with acute cerebellar ataxia.

Treatment Options for Acute Cerebellar Ataxia

Beginning on day 25 post HPV vaccine, pulsed IV methylprednisone (1000mg/d) was administered for three days. Her symptoms persisted. On day 44 post HPV vaccine, IV immunoglobulin (IVIG) at 400mg/kg was initiated and run for 5 days. Her symptoms persisted.

At day 65 post vaccine, with no indication of improvement, immunoadsorption plasmapharesis was begun at a rate of seven times per month. The physicians report a gradual improvement of the nystagmus after two treatments with a full resolution of symptoms after 19 courses of treatment (day 134 post HPV vaccine). The improvement was short-lived, however, and beginning at day 220 post HPV vaccine, the symptoms began to return, gradually at first with nystagmus, and then completely. Immunoadsorption plasmapharesis was begun anew on day 332 post HPV vaccine. After five courses of treatment, the patient’s symptoms again remitted.

Immunoglobulin G (IgG) and Cerebellar Ataxia Symptoms

Of interest, symptom severity corresponded to IgG levels. Her initial IgG levels were not reported, but after 19 treatments, when symptoms disappeared completely for the first time, her IgG levels were 354 mg/dL (day 134). When the symptoms appeared again (day 332) her IgG levels were elevated at 899 mg/dL. Upon treatment, her IgG levels dropped to 503 mg/dL as the nystagmus abated and then to 354 mg/dL upon complete remission, for the second time, at day 332 post HPV vaccine.

HPV16L and Post HPV Vaccine Reactions and Death

The researchers from this study, speculate a connection between the IgG response, and an as of yet, undetermined antibody. Testing for a variety of known antibodies were negative. Since the HPV16L is molecularly  similar to certain cell adhesion molecules, enzymes, transcription factors and neural antigens, it is possible that the HPV16L particles triggered the response.

In separate studies, autopsies of girls who died suddenly post HPV vaccine have found non-degrading HPV16L particles linked to the deaths. In the first case, researchers performed secondary postmortem immunochemistry of two girls who died suddenly after receiving Gardasil. They found evidence of cerebral vasculitis linked to the HPV16L particles throughout the cerebral vasculature.

Similarly, a postmortem exam of another girl who died from the HPV vaccine, found HPV16L DNA particles in the blood and spleen.  The researcher reported that the DNA fragments were found in the macrophages, and protected from degradation because of the tight binding of the HPV16L gene fragments to the aluminum adjuvant. The fragments underwent a conformational change rendering them more ‘stable’ and resistant to degredation, perhaps explaining their presence in the blood and spleen six months post vaccine. This has been contended.

Methods in both of the above studies have been controversial and questioned and should be interpreted with caution. However, researchers from Italy compared HPV16 proteome in the vaccine to the human to proteome and found 84 identical proteins involved in cell differentiation and neurosensory regulation. According to these researchers, the homology between the vaccine and the human proteome, bound to aluminum adjuvant

“make the occurrence of side autoimmune cross-reactions in the human host following HPV16-based vaccination almost unavoidable”.

Whatever the exact culprit, in this case the cerebellar ataxia was acute and temporally related to the HPV vaccine. The favorable response to immunoadsorption and consequent reduction in IgG levels, indicates an auto-immune response.

Mitochondrial Injury, Thyroid, Thiamine and Cerebellar Ataxia

With a more slowly developing cerebellar ataxia and related symptoms, it is possible a medication induced mitochondrial injury, related to a depletion of thiamine is present. Thiamine is critical for mitochondrial function. Similarly, patients have reported cerebellar ataxias related to Hashimoto’s. Generally, when testing for both thiamine deficiency and Hashimoto’s is undertaken, both are confirmed.

Final Thoughts

This report represents one of the first clear linkages between the HPV vaccine and acute cerebellar ataxia. More importantly, it suggests a treatment opportunity when caught early. With so little data available, it is not clear whether immunoadsorption would work for more chronic cases. However, there is evidence of its success in Guillian Barre, Myasthenia Gravis and other autoimmune conditions. When combined with the early data pointing to Hashimoto’s and thiamine deficiency, paths forward post injury are emerging.

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