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

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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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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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Poor Nutrition Stress: The Enemy of Health

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Stress and Diet

In previous posts, I have indicated that stress can initiate or exacerbate disease and medication or vaccine adverse reactions. Read that statement, you might think I am attributing the onset of serious disease and adverse reactions to a psychosocial cause. That is not the case. Stress comes in a myriad of forms, some external, some internal, and although much of what we call stress relates to psychosocial responses to perceived threats, I think stress encapsulates so much more. At its most fundamental level, stress represents a physical state where the body is performing less than optimally. Let me explain.

What is Stress?

I define the word “stress” as a physical or mental force that is acting upon you. An example of mental or psychosocial stress might be an insult from a person, meaning that the stress comes from a source outside the body. On the other hand, it might be the realization that a deadline has to be met, a mental source from within. Any form of injury is an obvious source of physical stress. Physical action such as shoveling snow is another form of stress, demanding energy consumption imposed by the individual who wishes to get rid of the snow. Being infected with a virus or by bacteria is a form of stress that demands a defensive reaction. In each of these instances, the body reacts to the inflicting stressor. Sometimes, when the resources are available, it reacts efficiently. Other times, when the resources are not available or when additional factors intercede, the body’s response to the stress is ill-adapted.

Your Body is Your Fortress, Your Immune System the Soldiers

Perhaps an analogy might help to provide an explanation for the remarks that follow. I imagine the body as being like an old fashioned fortress. The people living within it go into action when the fortress is attacked by an enemy from outside. It would be of little use if the defense soldiers went to the eastern battlements if the attack came from the west and so there had to be a central figure that would coordinate the defensive reaction. The nature of the attack would be spotted by a guard on duty and the central figure informed by messenger.

The body represents the fortress and the lower part of the brain represents the central figure that coordinates the defense. The cells in the blood known as white cells can be thought of as soldiers, armed with the necessary weapons to meet the nature of the enemy. Suppose, for example, a person’s finger is stuck by a splinter carrying a disease bearing germ. The pain, felt in the brain, recognizes its source and interprets it as a signal that an attack has occurred. White cells in the area can be regarded as the “militia under local command” and a “beachhead” is formed to wall off the attack. The white cells sacrifice themselves and as they die, they form what we call pus. If the beachhead is broken and the germs manage to get into the bloodstream, it is then called septicemia and the brain/body goes into a full defensive reaction where high fever is the most obvious result. Such an illness is an attack/defense battle.

The symptoms that develop from such an infection represent the evidence for this defense, feeling ill, pain and developing a fever are excellent examples. Micro-organisms are most efficient at 37° C, the normal body temperature. The rise in body temperature, initiated by the brain, makes the microorganisms less efficient and may kill some of them. One therefore has to question the time honored method of reducing the fever, during illness, as being an example of good treatment. While reducing fever improves the symptoms caused by the infection, it also reduces the efficiency of the immune battle raging within.

The outcome against the stressor is death or recovery; although it is possible sometimes to end up in a kind of stalemate, represented by prolonged symptoms of ill health. Chronic illness may be viewed as the immune system’s inability to eradicate fully the stressor.

Poor Nutrition and Stress

As I have emphasized in previous posts, the autonomic (automatic) nervous and endocrine systems are used to carry the messages between the body and the brain that enable the defense to be coordinated. This demands a colossal amount of cellular energy, no matter the nature of the stress. That energy to fight stress comes from oxidation of the fuel that is provided from nutrition. Of course, the greater the stress the greater the energy demand, but in the end the equation is quite simple. If the energy required to meet the stress is greater than the energy that is supplied, there must be a variable degree of collapse within the defensive system. That collapse presents as intractable symptoms, where the body is unable provide the energy needed to sustain health. This is the secret of the autonomic dysfunction in the vitamin B1 deficiency disease, beriberi. It is also the secret behind the initiation of POTS because both conditions are examples of defective oxidation. You can read more details regarding thiamine deficiency, beriberi, POTS and other health issues from previous posts on this website

High Energy Demands Equal High Nutritional Demands

Nutrient density of diet might appear to be perfectly adequate for a given individual, but inadequate to meet the self-initiated energy demands of a superior brain/body combination in a highly active individual such as an actively engaged student or athlete. Our genetic characteristics, the quality of nutrition and the nature of life stresses each represent a factor that all combine together to give us a profile for understanding health and its potential breakdown.

Epigenetics and Mitochondria: The Stress of Our Parents

Epigenetics, the science of how our genes are influenced by diet and lifestyle, is relatively new. Epigenetics considers the possibility that genes can be activated and deactivated by nutrition and lifestyle. Stress can come in many forms, from psychosocial trauma, poor nutrition, environmental and medical toxin exposures, to infections. Stress impacts how our genes behave. Even though one may inherit a hard-coded genetic mutation from a parent, that mutation may not be activated unless exposed to a particular type of stress. Similarly, an individual who may have no obvious illness-causing genetic abnormalities but stress, in the form of nutritional depletion, exposures or trauma, can turn on or turn off a set of genes that induce illness. What is remarkable about epigenetics is the transgenerational nature of the stressors. The memories of stressors affecting our parents and even our grandparents can affect our health by activating or deactivating gene programs.

We also have to consider the state of our mitochondria, the “engines” in each of our cells that produce the energy for cellular function (to learn more about mitochondria and health, see previous posts on this website). Mitochondria have their own genes that are inherited only from the mother. Damage to the DNA that makes up these genes sometimes explains the similarity of symptoms that affect a given mother and any or all of her children. For example, although this damage may be inherited, we also have scientific evidence that thiamine deficiency, known to be the result of poor diet, can damage mitochondria. A bad gene might be the solitary cause of a given disease, but even where this is known as the cause, the symptoms of the disease are sometimes delayed for many years, suggesting that other variables must play a part. A minor change in cellular genetic DNA might be alright to meet the demands of normal living, but impose a risk factor that could be impacted by prolonged stress or poor nutrition, and disease emerges.

Nutrition is the Only Factor that We can Control

The imposition of stress on any given individual is variable, most of which is accidental and out of our control. Therefore, if we represent these three factors, genetics, stress and nutrition as three interlocking circles, all of which overlap at the center of such a figure, there is actually only one circle over which we have control and that is nutrition. We now know from the science of epigenetics that nutritional inadequacy can affect our genes. By examining the mechanism by which we defend ourselves against stress, we can also see the effect of poor nutrition.

Poor Nutrition Equals a Poor Stress Response

Using these three variables, perhaps we can begin to understand several unanswered questions. Why does a vaccination negatively affect a relatively small percentage of the total population vaccinated? Or why do some medications negatively impact only some individuals? It might be because of a genetic risk factor or because of a collapse of the coordinated stress response related to quality of nutrition or a combination of both. Why does a vaccination tend to “pick off” the higher quality students and athletes? Again, the same kind of answer; high quality machinery demands high quality fuel. Since the limbic system of the brain has a high energy demand and represents the computer that coordinates a stress response we can understand the appearance of beriberi or POTS and cerebellar ataxia, all examples of a deviant response to stress. Nutrition, therefore, should not be looked at as supplement to good health, but as the foundation of health. When disease or medication and vaccine reactions emerge, efforts to identify and then restore nutritional deficiencies must be the first line of immune system health. Without critical nutrients, the body simply cannot mount a successful stress response and the battlefield will expand and eventually fall.

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How Dietary Mayhem Causes Disease: The Choked Engine Syndrome

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Dietary mayhem and thiamine deficiency with simple sugars

Over the past year, I have written extensively about thiamine deficiency post Gardasil vaccination (here, here, here, here). We now have five cases where thiamine deficiency was identified and clinical symptoms remediated with supplementation. Many more are suspected but recognition and testing have been slow. Thiamine deficiency may not be limited to the post Gardasil population, although that is where we first recognized it. Symptoms of thiamine deficiency and dysfunctional oxidative metabolism have been observed amongst the post fluoroquinolone and post Lupron populations and likely other populations adversely affected by a vaccine or medication, though data are limited. For the current paper, I should like to offer an explanation of the effect of thiamine deficiency in relationship to the stress of the vaccination or medications.

Thiamine Deficiency and Diet

With the widespread ingestion of simple carbohydrates that is almost a hallmark of Western civilization I suggest that the Gardasil vaccination and certain other medications represent “the last straw to break the camel’s back”.  I have included a case report, from my clinical practice, as an example of the effect of a simple nutritional stressor – sugar – imposed on an individual who’s oxidative metabolism was marginal at the time. I have included the references for anybody that wishes to check on how much of this is published.

Cellular Energy and Diet

Present knowledge indicates that cellular energy arises only from oxidation of food sources. The prevalently common form of nutritional mayhem in the U.S. is a high calorie content from simple carbohydrates with insufficient vitamin/mineral content to catalyze efficient oxidation. This form of malnutrition might be compared with functional decline in a choked internal combustion engine. Evidence presented in this case report presented below indicates that simple carbohydrate ingestion can have far-reaching consequences.  A review indicates that a common manifestation of its effect is oxidative stress in the brain, particularly in the limbic system where emotional reflexes originate and where the controls of the autonomic and endocrine systems react automatically to sensory input. Beriberi is the classic example of high calorie carbohydrate malnutrition and is the prototype for dysautonomia (abnormal function of the autonomic nervous system [ANS] ) in its early stages. A later stage results in degeneration of autonomic ganglia and irreversible disease. Symptoms arising from thiamine deficiency or abnormal homeostasis are protean and diverse in nature.

Dysautonomia, Oxidative Stress and Thiamine

Dysautonomia, a common presentation of functional disease and often associated with variable organic diseases caused by loss of oxidative efficiency in the brain, has been reviewed. A hypothesis was presented that there is a combination of genetic risk, different forms of sensory input defined as stress, particularly those imposed by present civilization, and high calorie malnutrition that are collectively responsible. This was presented diagrammatically by the degree of overlap in the “three circles of health, named genetics, stress and nutrition” (1).  It is also known that mitral valve (a heart valve) prolapse (MVP) is widespread in the population and is associated with dysautonomia, although the cause and effect relationship is said to be unknown (2-4). MVP is associated with adrenergic overdrive (the well-known adrenalin rush) in the normally balanced adaptive reactions of the autonomic/endocrine axis (5-8). (The autonomic nervous system and the glands of the endocrine system are under the control of the brain).  Panic disorder, also sometimes associated with MVP, is seen as an example of falsely triggered fight-or-flight reflexes engendered in the limbic brain.  Pasternac and associates (6) showed that symptomatic patients with MVP demonstrated increased resting sympathetic tone and that supine bradycardia (slow heart rate) suggested increased vagal (the vagus is a nerve that runs from the brain to many parts of the body) tone at rest. Davies and associates (7) demonstrated physiologic and pharmacologic hypersensitivity of the sympathetic system in a group of patients with MVP. Sympathoadrenal responses were noted in rats exposed to low oxygen concentration (9) and impaired cerebral autoregulation has been reported in obstructive sleep apnea in human subjects (10). It has also been shown that thiamine deficiency produces traditionally accepted psychosomatic or functional disease (11,12).  A low oxygen concentration results in changes in brain structures similar to those induced in thiamine deficiency (13).

A Case Study of Thiamine Deficiency and Dietary Influence: The Sugar Problem

The Table below shows laboratory results from an 84-year old man who had begun to experience severe insomnia for the first time in his life. He also had painful tenosynovitis (also known as “trigger finger”) in the index finger of the left hand.  He had edited a journal for some 14 years and for several years, had been a member of a bell choir in which he played a heavy base bell in each hand, involving repetitive trauma to the index fingers.  He did not crave sugar, his ingestion of simple carbohydrates being minimal to moderate. The only treatment offered was complete withdrawal from all forms of simple carbohydrates.

Serial laboratory studies revealed a gradual improvement over six months and his weight decreased from 182 to 170 pounds without any other change in diet. Insomnia and tenosynovitis gradually improved. The Table shows that serial laboratory tests over a period of six months, from February to August, showed continued gradual improvement. In September, the day after a minimal ingestion of simple carbohydrate, there was an increase in triglycerides and TPPE.

Understanding the Labs

Notice that the triglycerides dropped from 206 in February to 124 in August, then rose again in September only one day after a minimal amount of sugar.  Triglycerides are part of the routine lipid profile test done by doctors and are well known to be related to the ingestion of simple carbohydrates.  Fibrinogen and HsCRP are both recognized as markers of inflammation.  Notice that both of them decreased between February and August but HsCRP rose again in September like the triglycerides.  The TPPE is the important part of the transketolase test.  The higher the percentage, the greater is the degree of thiamine deficiency.  Notice that it dropped from 35% to zero between February and August, but that it jumped to 8% in September, the day after the ingestion of sweets.  I have provided the normal laboratory values for the discerning reader.

  TABLE 1
Month

Cholesterol

Triglycerides

Fibrinogen

HsCRP

TKA

TPPE
February

169

206

412

7

65

35%
March

155

165

55

25%
May

160

152

312

0.9

85

2%
August

166

124

0.3

59

0%
September*

169

165

220

1

62

8%

Consecutive laboratory blood tests
Cholesterol N <200 mg/dL. Triglycerides N< 150 mg/dL. Fibrinogen N 180-350,g/dL
HsCRP N 0.1-1.0 mg/L. TKA 42-86mU. TPPE 0-18%. *Next day after ingestion of simple carbohydrate.

 

The abnormal TPPE indicated thiamine deficiency in this patient (14). The increased triglycerides and their steady decrease over time indicated that sugar ingestion was a potent cause of his symptoms. An increase in fibrinogen and hypersensitive CRP are both laboratory markers of inflammation, although the site is not indicated.  Recent studies in mice (15) have shown that high calorie malnutrition activates a normally silent genetically determined mechanism in the hypothalamus, causing either obesity, inflammation or both. The potential association of thiamine with electrogenesis (formation of electrical energy) (16) may have some relationship with brain metabolism and the complex functions of sleep.

Compromised Oxidative Function: Thiamine Deficiency, Beriberi and Diet

It has long been known that beriberi is a classic disease caused by high consumption of simple carbohydrate with insufficient thiamine to process glucose into the citric acid cycle. (This complex chemistry represents the engine of the cell, meaning that it produces the energy for function).  Widespread thiamine deficiency has been reported in many publications(17-20), producing the same brain effects as low oxygen concentration (13,21). In rat studies, this produces an imbalance in the autonomic nervous system (9). Thiamine  deficiency is easily recognized in a clinical laboratory by measuring TKA and TPPE (14).

Thiamine and the Brain

Thiamine triphosphate (TTP) (this is synthesized from thiamine in the brain) is known to be important in energy metabolism. Although its action is still unknown, the work with electric eels has revealed that the electric organ has a high concentration of TTP and may have a part to play in electrogenesis, the transduction of chemical to electrical energy (16,22). The energy for its synthesis from thiamine comes from the respiratory chain. This is also complex chemistry in the formation of energy synthesized within mitochondria, the “engines” of the cell (23), so that any form of disruption of mitochondria would be expected to reduce adequate synthesis of this thiamine ester. Although slowing of the citric acid cycle appears to be the main cause of the biochemical lesion in brain thiamine deficiency (24), the part played by TTP is not yet known. Alzheimer’s disease has been helped by the use of therapeutic doses of thiamin tetrahydrofurfuryl disulfide (TTFD) (25), a more efficient method of administering pharmacologic doses of thiamine (26).

Acetylcholine, the neurotransmitter used by both branches of the autonomic nervous system, is generated from glucose metabolism, requiring  B vitamins, particularly thiamine. Choline is a “conditional nutrient”, meaning that it is derived mainly from diet but is also made in the body. The presence of all these nutrients leads to the synthesis of this neurotransmitter.  It’s depletion would affect both branches of the autonomic nervous system, resulting in dysautonomia.

There is evidence that high-dose thiamin increases the effect of acetylcholine (27). Animal studies have shown that TTFD improves long term memory in mice (28) and it has been shown that it extends the duration of  neonatal seizures in DBA/J2 mice, seizures that normally cease in a few days with normal maturation (29).  These seizures are naturally related to a prolonged effect of this neurotransmitter in this strain of mouse.  The experimental prolongation of the seizures by administration of TTFD indicated that it enhanced the effect of the neurotransmitter. A pilot study in autistic spectrum disorder showed clinical improvement in 8 of the 10 children treated with TTFD (30), a disease that has been shown to have reduced  parasympathetic activity in the heart (31,32). Neural reflexes regulate immunity (33).  Dysautonomia was found in a large number of patients with cancer at Mayo Clinic (34).

Dysautonomia and Thiamine Deficiency         

Evidence has been presented that a common connection exists between dysautonomia, inefficient oxidative metabolism produced mainly by high calorie malnutrition, and organic disease (1). Thiamine enters the equation in terms of its relationship with carbohydrate ingestion and its use by the brain as fuel (35). Decreased transketolase activity in brain cells induced by thiamine deficiency contributes to impaired function of the hippocampus (36) each, part of the limbic system control mechanisms that affect autonomic sympathetic/parasympathetic balance. Erythrocyte (red cells) transketolase indicates abnormal thiamine homeostasis that is commonly achieved by carbohydrate ingestion and deficiency of vitamin B (14).  Beriberi gives rise to functional changes in the autonomic nervous system in its early stages and produces irreversible degeneration in its later stages (37). This, because it represents a largely forgotten aspect of disease, might equate with the wide use of simple carbohydrates in Western civilization. Deficiency of other essential non-caloric nutrients has been associated with dysautonomia (1).

The Role of Nutritional Stress in Post Vaccination and Medication Reactions

Two results of post- Gardasil vaccination have been reported, Postural Orthostatic Tachycardia Syndrome (POTS) and cerebellar ataxia.  POTS, a disease easily confused with beriberi, is one of the many syndromes reported under the general heading of dysautonomia and stress related intermittent episodes of cerebellar ataxia were reported in thiamin dependency (38).  Since the inflammatory reflex has recently been found to be involved with the sympathetic branch of the ANS (39), enhancement of its dysfunction by TD might explain some of the Gardasil affected illnesses.

Conclusion

Thiamine deficiency is now accepted as the major cause of the ancient scourge of beriberi. The underlying mechanisms are still not fully understood for we do not yet know the complete roles of thiamine. The clinical effects are protean and unpredictable. It is, however, clear that thiamine has a vital effect on many aspects of oxidative metabolism and its deficiency can be used as a model for the clinical effects produced by disruption in energy synthesis. It can be summed up under the general heading of dysoxegenosis and thiamine is certainly not the only component that governs this vital life process. The example of beriberi indicates that the brain, peripheral nervous system and the heart are the tissues most affected by the disease, the tissues that rapidly consume oxygen.

The limbic system is a complex computer that organizes all our adaptive survival reflexes and its sensitivity to hypoxia is well known. It is evident that non-caloric nutrient deficiency, especially thiamine, gives rise to the same symptoms and histopathology as mild to moderate hypoxia (oxygen deficiency) and that the leading symptomology is that of dysautonomia. Since the limbic system gives rise to emotional reflexes and mild to moderate hypoxia enhances sympathoadrenal response, it can be expected that an affected individual would be more aggressive and more likely to experience exaggerated fight-or-flight reflexes. A “nursed” emotional grievance might be expected to explode in violence that would otherwise be curtailed or suppressed by normal brain metabolism. It suggests that high calorie malnutrition, particularly that provided by excessive consumption of simple carbohydrates, gives rise to uncontrolled pathophysiological actions that might explain some of the widespread incidence of emotional and psychosomatic disease in contemporary society. It may also explain some of the “hot” juvenile crime and vandalism, much of which is poorly understood in our present civilization. It is also hypothesized that a marginal state of oxidative metabolism, perhaps asymptomatic or with only mild symptoms that are ignored, might be precipitated into clinical expression with a mild degree of stress imposed by a vaccination. The individual in the case reported above appeared to be unusually sensitive to sugar ingestion and this may be an additional genetically determined risk.

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References

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  2. Orhan A L, Sayar N, Nurkalem Z, Uslu N, Erdem I, Erdem E C, Assessment of autonomic dysfunction and anxiety levels in patients with mitral valve prolapase. Turk Kardiyol Dern Ars 2009;37(4):226-233.
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  13. Macey P M, Woo M A, Macey K E, Keens T G, Saeed M M, Alger J R et al. Hypoxia reveals posterior thalamic, cerebellar, midbrain, and limbic deficits in congenital hypoventilation syndrome. J Appl Physiol 2005;98(3):958-969.
  14. Massod M F, McGuire S L, Werner W R. Analysis of blood transketolase activity.Am J ClinPathol 1971;55:465-470.
  15. Zhang X, Zhang G, Zhang H, Karin M, Bai H, Cai D. Hypothalamc 1KKbeta/N-kB and ER stress link overnutrition to energy imbalance and obesity. Cell   2008;135(1):61-73.
  16. Bettendorff L, Michel-Cahay C, Grandfils C, De Rycker C, Schoffeniels E. Thiamine triphosphate and membrane-associated thiamine phosphatases in the electric organ of Electrophorus electricus. J Neurochem 1987;49(2):495-502.
  17. O’Keefe S T, Tormey W P, Glasgow R, Lavan J N. Thiamine deficiency in hospitalized elderly patients. Gerontology 1994;40(1):18-24.
  18. Macias-Matos C, Rodriguez-Ojea A, Chi N, .Zulueta D, Bates C J. Biochemical evidence of thiamine depletion during the Cuban neuropathy epidemic, 1992-1993. Am J Clin Nutr 1996;64(3):347-353.
  19. Mazavet D. Vassilev K, Perrigot M. Neuropathy with non-alcoholic thiamine deficiency: two cases of bladder disorders [article in French]. Ann Readapt Med Phys 2005;48(1):43-47.
  20. Hazell A S, Butterworth R F. Update of cell damage mechanisms in thiamine deficiency: focus on oxidative stress, excitotoxicity and inflammation. Alcohol Alcohol 2009;44(2):141-147.
  21. Vortmeyer A O, Hagel C, Laas R. Hypoxia-ischemia and thiamine deficiency. Clin Neuropathol 1993;12(4):184-190.
  22. Nghiem H O, Bettendorff  L,Changeux J P. Specific phosphorylation of Torpedo 43K raspsyn by endogenous kinase(s) with thiamine triphosphate as the phosphate donor. FASEB J 2000;14(3):543-554.
  23. Gangolf M, Wins P, Thiry M. Thiamine triphosphate synthesis in the rat brain is mitochondrial and coupled to the respiratory chain. J Biol Chem 2010;285(1):583-594.
  24. Bettendorff  L, Sluse F, Goessens G,  Wins P, Grisar T. Thiamine deficiency-induced partial necrosis and mitochondrial uncoupling in neuroblastoma cells are rapidly reversed by addition of thiamine. J Neurochem 1995;65(5):2178-2184.
  25. Mimori Y, Katsuoka H, Nakamura S. Thiamine therapy in Alzheimer’s disease. Matab Brain Dis 1996;11(1):89-94.
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  27. Meador K J. Nichols M E, Franke P, Durbin M W. Evidence for a central cholinergic effect of high-dose thiamine. Ann Neurol 1993;34:724-726.
  28. Micheau J, Durkin D P, Destrade D C, Rolland Y, Jaffard R. Chronic administration of sulbutiamine improves long term memory formation in mice: possible cholinergic mediation.  Pharacol Biochem Behav 1985;23(2):1
  29. Lonsdale D. Effect of thiamine tetrahydrofurfuryl disulfide on audiogenic seizures in DBA/2J mice. Dev Pharmacol Ther 1982;4(1):28-36.
  30. Lonsdale D, Shamberger R J, Audhya T. Treatment of autism spectrum children with thiamine tetrahyhdrofurfuryl disulfide: a pilot study. Neuro Endocrinol Lett 2002;23(4):303-308.
  31. Ming X,  Julu P O O, Brimacombe M, Connor S, Daniels M L. Reduced cardiac parasympathetic activity in children with autism. Brain Dev 2005;27:509-516.
  32. Palmieri L Persico A M. Mitochondrial dysfunction in autism spectrum disorders: cause or effect? Biochem Biopys Acta 2010; May 1 [Epub ahead of print].
  33. Rosas-Ballina M, Tracey K J. The neurology of the immune system: neural reflexes regulate immunity. Neuron 2009;64(1):28-32.
  34. McKeon A, Lennon V A, Lachance D H, Fealey R D, Pittock S J. Ganglionic acetylcholine receptor autoantibody: oncological, neurological and serological accompaniments. Arch Neurol 2009;66(6)(:735-741.
  35. Elmadfa I Majchrzak D, Rust P Genser D. The thiamine status of adult humans depends on carbohydrate intake. Int J Vitam Nutr Res 2001;71(4):217-221.
  36. Zhao Y, Pan X, Zhao J, Wang Y, Peng Y, Zhong C. Decreased transketolase activity contributes to impaired hippocampal neurogenesis induced by thiamine deficiency. J Neurochem 2009;111(2):537-546.
  37. Inouye K, Katsura E. Etiology and pathology of beriberi. In: Thiamine and
  38. Beriberi. Igaku Shoin Ltd. Tokyo;1965:1-28.
  39. Lonsdale D. Faulkner W R, Price J W, Smeby R R. Intermittent cerebellar ataxia associated with hyperpyruvic academia,hyperalaninemia and hyperalaninuria. Pediatrics 1969;43:1025-34.
  40. Martelli D, Yao S T,McKinley M J,McAllen R M. Reflex control of inflammation by sympathetic  nerves, not the vagus. J Physiol 2014; Jan 13 [Epub ahead of print].

 

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Exercise to Alleviate Fatigue

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Chander Marrs

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

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

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

What is Fatigue?

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

Mitochondria and Fatigue

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

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

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

Exercise and Mitochondrial Biogenesis

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

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

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

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

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

*Post Script

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

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Post Gardasil POTS and Thiamine Deficiency

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Autonomic nervous system

On July 8th 2013, I received an e-mail from a mother of a 17-year old daughter who had received Gardasil vaccination in 2008 resulting in a severe reaction. Two weeks after the second injection she began to experience a “flu-like” episode that continued for about a week and was followed by facial swelling, streptococcal infection, double ear infection and a diagnosis of mononucleosis. It was initially concluded that this was coincidental, not due to the vaccination. From then on she suffered from Postural Orthostatic Tachycardia Syndrome ( POTS), severe edema and “digestion issues which have been constant since”. POTS is a multi-symptomatic disease of the lower brain that affects many aspects of brain/body control mechanisms. She reported that “30,000 girls (and some boys) have been affected by the vaccine” and of those of which she was aware,“ the majority have POTS and trouble metabolizing sugar and carbs”.

Because of the persistent edema and digestive problems, my informant had done her own research and concluded that her daughter’s symptoms were due to thiamine (vitamin B1) deficiency. She found my name in connection with this subject and requested my help. There is a blood test, known as erythrocyte (red cells) transketolase that is specific for identifying thiamine deficiency, so I suggested that this be done. It was strongly positive, proving TD. This led to the test being done on another Gardasil affected girl and this was also strongly positive.  Most of the affected girls known to her had POTS. Some had mitral valve prolapse (MVP).  About twenty five percent of POTS patients are disabled.  The symptoms often follow a virus infection. It is one of many conditions classified as dysautonomia and this includes beriberi, long known to be due to thiamine deficiency.

Dysautonomia, often associated with MVP, affects the lower brain controls of both branches of the autonomic (automatic) nervous system (ANS) that enable our adaptation to the constant changes in environment. For example, one branch, known as the sympathetic system, accelerates the heart and the other, called the parasympathetic, slows it. We sweat when it is hot and shiver when it is cold, both automatically initiated by the sympathetic branch of the ANS.

In the early stages of beriberi the ANS is unbalanced, so that either the sympathetic or parasympathetic, normally working in synchrony, dominates the reaction, adversely affecting blood pressure, pulse rate and many other adaptive mechanisms, like POTS.  It can be seen that the patient with POTS or beriberi is essentially maladapted and is unable to adjust bodily systems to meet environmental changes. Edema (swelling in parts of the body), a cardinal feature of beriberi, supported a diagnosis of thiamine deficiency in this mother’s daughter. Also, Gardasil is a yeast vaccine and an enzyme called thiaminase, whose action destroys thiamine, is known to be in the yeast. Thiaminase disease has been reported in Japan in association with dietary thiamine deficiency.

We know from the history of beriberi that exposure to the stress of ultraviolet light (sunlight) sometimes “triggers” the first symptoms of the disease when thiamine deficiency is marginal, but not severe enough to cause symptoms. Other stress factors (virus, inoculation, injury) can do the same. In effect, diet may cause an individual to be in a state of marginal vitamin deficiency. A mental or physical stress factor automatically induces a need for energy to meet this stress. If cellular energy is insufficient to drive the  mechanisms by which an adaptive adjustment is required, it results in a maladaptive response.

The lower brain, where the ANS control mechanisms are situated, is particularly sensitive to thiamine deficiency, equivalent to a mild to moderate degree of oxygen deprivation. The commonest cause of thiamine deficiency in industrial nations is alcohol, but it is also known that sugar consumption will increase the need for thiamine. Beriberi has recently been reported in Japan in seventeen adolescents consuming carbonated soft drinks. The social life of adolescents may thus increase the risk from an inoculation that might otherwise be less threatening.

The statistics on sugar ingestion (150 pounds per person per year) suggests that marginal TD is common. The report of a “difficulty in metabolizing sugar and carbs” may be highly relevant. One of the questions asked by parents of the affected girls known to my informant is why did the vaccine seem to “pick off” the most intelligent and athletic individuals. The answer must be that the higher the IQ, the more is cellular energy required by the brain. Sugar, even at social levels of consumption, may be a greater risk for them.

It is important to understand that there are multiple factors that have to be taken into account in solving the cause of this disaster. The “fitness” of the individual implies her adaptive ability in biochemical terms, not her athletic or student prowess. Dietary indiscretion may or may not enter the equation and depends on individual sensitivity to food substances as well as the ratio of calories to the necessary vitamins for their processing in the body. The stress factor, the case in discussion being Gardasil, may be more or less stressful in its own right, perhaps related to batch number or commercial process. Lastly the genetics of an individual always enters the equation. These three factors, Genetics, Stress and Nutrition can be seen as three interlocking circles, all of which overlap at the center. Each circle must be evaluated in its contribution to the ensuing result.

Publications and resources from Dr. Lonsdale:

  1. A Review of the Biochemistry, Metabolism and Clinical Benefits of Thiamin(e) and Its Derivatives
  2. Treatment of autism spectrum children with thiamine tetrahydrofurfuryl disulfide: A pilot study.
  3. Thiamine
  4. Asymmetric functional dysautonomia and the role of thiamine.
  5. Exaggerated autonomic asymmetry: a clue to nutrient deficiency dysautonomia.
  6. Oxygen – the Spark of Life. Dr. Lonsdale’s blog.

Resources for Understanding Thiamine Deficiency

Molecular Mechanism of Thiamine Utilization

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Post Gardasil Thiamine Deficiency: A Mother’s Quest for Answers

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My daughter has struggled since she got her second Gardasil shot in December 2008. Even though she has improved immensely and was finally able to return to college after missing 3 years, she still had some problems including issues with swelling/edema, gut, thyroid, and temperature regulation.

In July, I came across a 2008 article written by Leslie Botha about the Gardasil side-effects that were being reported at the time.  A woman who was knowledgeable about thiamine deficiency because it runs in her family read the article and realized that the side effects of Gardasil were similar to thiamine deficiency. She speculated in her post that the yeast in the vaccine, or possibly the manufacturing process, might be responsible for the beriberi type reactions people were having.

The more I read about beriberi, the more I became convinced that this was causing many of my daughter’s problems. She had all the symptoms of thiamine deficiency with cardiovascular involvement including Postural Orthostatic Tachycardia Syndrome (POTS), chest pains, edema, sleep disturbance, abdominal discomfort, and  trouble digesting and processing foods, especially carbs.

I contacted Dr. Lonsdale, a long-time expert in Thiamine Deficiency, and he has been immensely helpful and willing to share his knowledge. After an erythrocyte transketolase test confirmed that my daughter was extremely thiamine deficient, she started taking a form of thiamine that crosses the blood brain barrier.  In the two months she has been on the supplement her lab tests show a substantial improvement in several areas including swelling, ability to detox, and hormone and thyroid levels. Her energy level has also improved.

Over the past five years we have tried a wide gamut of treatments including hyperbaric oxygen therapy, IV’s, supplements, infrared sauna, thyroid medications, low dose naltrexone, UV blood irradiation, homeopathic and chiropractic treatments, acupuncture and countless others. Although she improved nothing fully explained the root cause of her symptoms until I came across thiamine deficiency and talked with Dr. Lonsdale. Although he says it can take months to treat thiamine deficiency, we have already seen many good things happen.

Participate in Research

Hormones MatterTM is conducting research on the side effects and adverse events associated with Gardasil and its counterpart Cervarix. If you or your daughter has had either HPV vaccine, please take this important survey. The Gardasil Cervarix HPV Vaccine Survey.

To take one of our other Real Women. Real Data.TM surveys, click here.

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

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