thiamine POTS

How Can Something As Simple as Thiamine Cause So Many Problems?

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I have read a criticism that thiamine deficiency is “too simple” to explain the devastating nature of the post Gardasil illnesses or the systemic adverse reactions to some medications. Sometimes, it is the simple and overlooked elements that are the most problematic.

Understanding Thiamine’s Role in Complex Adverse Reactions – The Limbic System

The lower part of the brain, called the brainstem, is a like computer, controlling the most basic aspects of survival, from breathing and heart rate, hunger and satiety, to fight or flight and reproduction. This computer-like function within the brainstem is called the autonomic system (ANS). The ANS together with the limbic system act in concert to regulate our most basic survival functions and behaviors. Both require thiamine to function.

Postural Orthostatic Tachycardia Syndrome or POTS , a type of dysautonomia (dysregulation of the autonomic system) seems to be the among the commonest manifestations of the Gardasil effect. Many cases have been diagnosed already, while others present all of the symptoms but have yet to receive a diagnosis. Dysautonomia and POTS have also been observed with adverse reactions to other medications, as well. Dysautonomia and POTS, at the most basic level, represent a chaotic state of the limbic-autonomic system. Let me explain.

Fragmented Fight or Flight

The brainstem autonomic system together with the limbic system enable us to adapt to our environment, presiding over a number of reflexes that allow us to survive. For example, fight-or-flight is a survival reflex, triggered by perception of a dangerous incident that helps us to kill the enemy or escape. This kind of “stress event” in our ancestors was different from that we experience today. Wild animal predators have been replaced by taxes/business deadlines/rush hour traffic etc. These are the sources of modern stress. The beneficial effect is that the entire brain/body is geared to physical and mental response. However, it is designed for short term action and consumes energy rapidly. Prolonged action is literally exhausting and results in the sensation of fatigue. In the world of today where dietary mayhem is widespread, this is commonly represented as Panic Attacks, usually treated as psychological. They are really fragmented fight-or-flight reflexes that are triggered too easily because of abnormal brain chemistry.

Thiamine and Oxidative Metabolism: The Missing Spark Plug

Our brain computers rely completely on oxidative metabolism represented simply thus:

Fuel + Oxygen + Catalyst = Energy

Each of our one hundred trillion body/brain cells is kept alive and functioning because of this reaction. It all takes place in micro “fireplaces” known as mitochondria. Oxygen combines with fuel (food) to cause burning or the combustion – think fuel combustion engine. We need fuel, or gasoline, to burn and spark plugs to ignite in order for the engines to run.

In our body/brain cells it is called oxidation. The catalysts are the naturally occurring chemicals we call vitamins (vital to life). Like a spark plug, they “ignite” the food (fuel). Absence of ANY of the three components spells death.

Antioxidants like vitamin C protect us from the predictable “sparks” (as a normal effect of combustion) known as “oxidative stress”.  Vitamin B1, is the spark plug, the catalyst for these reactions. As vitamin B1, thiamine, or any other vitamin deficiency continues, more and more damage occurs in the limbic system because that is where oxygen consumption has the heaviest demand in the entire body. This part of the brain is extremely sensitive to thiamine deficiency.

Why Might Gardasil Lead to Thiamine Deficiency?

We do not know for sure how Gardasil or other vaccines or medications have elicited thiamine deficiency, but they have. We have two girls and one boy, tested and confirmed so far. More testing is underway. Thiamine deficiency in these cases may not be pure dietary deficiency. It is more likely to be damage to the utilization of thiamine from as yet an unknown mechanism, affecting the balance of the autonomic (automatic) nervous system. It is certainly able to explain POTS (one of the many conditions that produce abnormal ANS function) in two Gardasil affected girls. Beriberi, the classic B1 deficiency disease, is the prototype for ANS disease. Administration of thiamine will not necessarily bring about a cure, depending on time since onset of symptoms, but it may help.

Thiamine Deficiency Appetite and Eating Disorders

Using beriberi as a model, let us take appetite as an example of one of its many symptoms. When we put food into the stomach, it automatically sends a signal to a “satiety center” in the computer. As we fill the stomach, the signals crescendo and the satiety center ultimately tells us that we have eaten enough. Thiamine deficiency affects the satiety center, wrecking its normal action. Paradoxically it can cause anorexia (loss of appetite) or the very opposite, a voracious appetite that is never satisfied and may even go on to vomiting. It can also shift from anorexia to being voracious at different times within a given patient. That is why Anorexia Nervosa and Bulimia represent one disease, not two.

Thiamine Deficiency, Heart Rate and Breathing

The autonomic nervous system, responsible for fight or flight, regulates heart activity, accelerating or decelerating according to need. So heart palpitations are common in thiamine deficiency. Its most vital action is in control of automatic breathing and thiamine deficiency has long been known to cause infancy sudden death from failure of this center in brainstem.

Thiamine Deficiency and Sympathetic – Parasympathetic Regulation

The hypothalamus is in the center of the brain computer and it presides over the ANS, as well as the endocrine (hormone) system. The ANS has two channels of communication known as sympathetic (governs action) and parasympathetic (governs the body mechanisms that can be performed when we are in a safe environment: e.g. bowel activity, sleep, etc.). When the ANS system is damaged, sometimes by genetic influence, but more commonly by poor diet (fuel), our adaptive ability is impaired. A marginal energy situation might become full blown by a stress factor. In this light, we can view vaccines and medications as stress factors. From false signal interpretation, we may feel cold in a warm environment, exhibiting “goose bumps on the skin”, or we may feel hot in a cold environment and experience profuse sweating. The overriding fatigue is an exhibition of cellular energy failure in brain perception.

Sometimes, it really is the simple, overlooked, elements that cause the most devastating consequences to human health. Thiamine deficiency is one of those elements.

To learn more about thiamine testing: Thiamine Deficiency Testing: Understanding the Labs.

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

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This article was published originally in October 2013.

 

It All Comes Down to Energy

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The Threat Around Us

Animals, including Homo Sapiens, survive in an essentially toxic environment, surrounded by microorganisms, potential poisons, the risk of trauma, and adverse weather conditions. Evolutionary development has equipped us with complex machinery that provides defensive mechanisms when any one of these factors has to be faced. Before the discovery of microorganisms, medical treatment had no rhyme or reason, but killing the microorganisms became the methodology. The research concentrated on ways and means of “killing the enemy”, the bacteria, the virus, the cancer cell. The discovery of penicillin reinforced this approach. We are now facing a period of potential impotence because of bacterial resistance, failure of attempts to kill viruses, and the resistance to chemotherapeutic agents in cancer. Louis Pasteur is purported to have said on his deathbed, “I was wrong, it is the terrain that matters”, meaning body defenses.

Hans Selye, whose research into how animals defend themselves when attacked by any form of stress, led to his description of the General Adaptation Syndrome (GAS). He recognized the necessity of energy in initiating the GAS and its failure in an animal that succumbed to stress. He labeled human disease as “the diseases of adaptation”. In Selye’s time, there was little information about energy metabolism but today, its details are fairly well-known. The suggestion of a new approach depends on the fact that our defenses are metabolic in character and require an increase in energy production over and above that required for homeostasis. If the GAS applies to human physiology and that we are facing the “diseases of adaptation”, it is hypothesized that research should be applied to methods by which energy metabolism can be stimulated and mobilized to meet the stress.

Energy Deficiency, Defective Immunity, and COVID-19

There is evidence that energy deficiency applies to each of the diseases described here. It may be the unrecognized cause of defective immunity in Covid-19 disease. Although in coronavirus disease the clinical manifestations are mainly respiratory, major cardiac complications are being reported involving hypoxia, hypotension, enhanced inflammatory status, and arrhythmic events that are not uncommon. Past pandemics have demonstrated that diverse types of neuropsychiatric symptoms, such as encephalopathy, mood changes, psychosis, neuromuscular dysfunction, or demyelinating processes may accompany acute viral infections or may follow infection by weeks, months, or longer in viral recovered patients. Electrocardiographic changes have been reported in Covid-19 patients. The authors suggest that it may be attributed to hypoxia as one possibility. Because the total body stores of thiamine are low, acute metabolic stress can initiate deficiency. Thiamine deficiency has a clinical expression similar to that observed in hypoxic stress and the authors referred to it as pseudo-hypoxia. It is therefore not surprising that defective energy metabolism can express itself clinically in many different ways.

The present medical model regards each disease as having a separate cause, but the large variety of symptoms induced by thiamine deficiency suggest the ubiquitous nature of energy deficiency as a cause in common. Obesity, a reflection of high calorie malnutrition, has been published as a risk factor for patients admitted to intensive care with Covid-19. Thiamine deficiency was reported in 15.5-29% of obese patients seeking bariatric surgery. Hannah Ferenchick M.D. an emergency room physician commented online that many of her patients with Covid-19 had what she called “silent hypoxemia”. These patients had an arterial oxygen saturation of only 85% but “looked comfortable” and their chest x-rays “looked more like edema”  It has long been known that patients with beriberi had low arterial oxygen and a high venous oxygen saturation. All that would be needed to support the hypothesis of thiamine deficiency in some Covid victims would be finding a high venous oxygen saturation at the same time as a low arterial saturation. Also, edema is a very important sign of beriberi, and thiamine deficiency has been noted in critical illness.

Disrupted Autonomic Function

There have been many articles in medical journals describing dysautonomia, mysteriously in association with a named disease, but with no suggestion that the dysautonomia is part of that disease. More recently, there is increasing evidence that dysautonomia is a feature of chronic fatigue syndrome (CFS), manifested primarily as disordered regulation of cardiovascular responses to stress. Manipulating the autonomic nervous system (ANS) may be effective in the treatment of CFS. Dysautonomia is also a characteristic of thiamine deficiency. Patients with Parkinson’s disease begin to lose weight several years before diagnosis and a study was undertaken to investigate this association with the ANS. Costantini and associates have shown that high dose thiamine treatment improves the symptoms of Parkinson’s disease, although the plasma thiamine concentration was normal. They have also shown that high dose thiamine treatment decreases fatigue in inflammatory bowel disease, Hashimoto’s disease, after stroke, and multiple sclerosis. As already noted, it is also an important consideration in critically ill patients.

Multiple System Atrophy is a devastating and fatal neurodegenerative disorder. The clinical presentation is highly variable and autonomic failure is one of its most common problems. Dysautonomia was found to be a clinical entity in Ehlers-Danlos syndrome, a musculoskeletal disease, and this syndrome frequently coexists with Postural Orthostatic Tachycardia Syndrome (POTS), a disease that is included in the group of diseases under the heading of dysautonomia. Some cases of POTS have been reported to be thiamine deficient. This common condition often involves chronic unexplained symptoms such as inappropriate fast heart rate, chronic fatigue, dizziness, or unexplained “spells” in otherwise healthy young individuals. Many of these patients have gastrointestinal or bladder disorders, chronic headaches, fibromyalgia, and sleep disturbances. Anxiety and depression are relatively common. Not surprisingly the many symptoms are often unrecognized for what they represent and the patient may have a diagnosis of psychosomatic disease.

Immune-Mediated Inflammatory Diseases (IMIDs) is a descriptive term coined for a group of conditions that share common inflammatory pathways and for which there is no definite etiology. These diseases affect the elderly most severely with many of the patients having two or more IMIDs. They include type I diabetes, obesity, hypertension, chronic pulmonary disease, coronary heart disease, inflammatory bowel disease, rheumatoid arthritis, Sjogren’s syndrome, systemic lupus, psoriasis, psoriatic arthritis, and multiple sclerosis. The recent recognition of small fiber neuropathy in a large subgroup of fibromyalgia patients reinforces the dysautonomia-neuropathic hypothesis and validates fibromyalgia pain. These new findings support the disease as a primary neurological entity.

Energy Deficiency During Pregnancy: The Cause of Many Complications

Irwin emphasized the energy requirements of pregnancy in which the maternal diet and genetics have to be capable of producing energy for both mother and fetus. He found that preventive megadose thiamine, started in the third trimester, completely prevented all the common complications of pregnancy. Hyperemesis gravidarum is the most common cause of hospitalization during the first half of pregnancy and is second only to preterm labor for hospitalization in pregnancy overall. This disease has been associated with Wernicke’s encephalopathy, well known to be due to brain thiamine deficiency. The traditional explanation is that vomiting is the cause, but since vomiting is a symptom of thiamine deficiency, it could just as easily be the cause rather than the effect. In spite of the fact that migraines are one of the major problems seen by primary care physicians, many patients do not obtain appropriate diagnoses or treatment. Migraine occurs in about 18% of women and is often aggravated by hormonal shifts. A complex neurological disorder involving multiple brain areas that regulate autonomic, affective, cognitive, and sensory functions, it occurs also in pregnancy. Features of the migraine attack that are indicative of altered autonomic function include nausea, vomiting, diarrhea, polyuria, eyelid edema, conjunctival injection, lacrimation, nasal congestion, and ptosis.

The Proteopathies: Disorders Involving Critical Enzymes

The earliest and perhaps best example of an interaction between nutrition and dementia is related to thiamine. Multiple similarities exist between classical thiamine deficiency and Alzheimer’s disease (AD), in that both are associated with cognitive deficits and reductions in brain glucose metabolism. Thiamine-dependent enzymes are critical components of glucose metabolism that are reduced in the brains of AD patients. Senile plaques and neurofibrillary tangles are the principal histopathological marks of AD and other proteopathies. The essential constituents of these lesions are structurally abnormal variants of normally generated proteins (enzymes). The crucial event in the development of transmissible spongiform encephalopathies is the conformational change of a host-encoded membrane protein into a disease associated, fibril forming isoform. A huge number of proteins that occur in the body have to be folded into a specific shape in order to become functional. When this folding process is inhibited, the respective protein is referred to as being mis-folded, nonfunctional, and causatively related to a disease process. These diseases are termed proteopathies and there are at least 50 different conditions in which the mechanism is importantly related to a mis-folded protein. Energy is required for this folding process. Because of their reported relationship with thiamine, it has been hypothesized that mis-folding might be related to its deficiency on an energy deficiency basis.

It All Comes Down to Energy

A hypothesis has been presented that the overlap of symptoms in different disease conditions represents cellular energy failure, particularly in the brain. If this should prove to be true, the present medical model would become outdated. An attack by bacteria, viruses or an oncogene might be referred to as “the enemy”. The defensive action, organized and controlled by the brain, may be thought of as “a declaration of war” and the illness that follows the evidence that “a war is being fought”. This concept is completely compatible with the research reported by Selye. It underlines his concept that human diseases are “the diseases of adaptation”, dependent on energy for a successful outcome in a “war” between an attacking agent and the complex defensive actions of the body. Killing the enemy is a valid approach to treatment if it can be done safely. Unfortunately, the side effects of most medications sometimes makes things worse and that is offensive to the Hippocratic Oath. We badly need to create an approach to research that explores ways and means of supporting and stimulating the normal mechanisms of defense.

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

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This article was published originally on May 11, 2020.

The Sugar – Thiamine Connection in Adverse Reactions

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As published on this web site previously, we have scientific evidence that two girls and one boy were shown to be thiamine deficient (TD) after Gardasil vaccination. On the other hand, a girl who had similar symptoms to these three had not received the vaccine and her laboratory test proved that she also had TD.  On the face of this information, it suggests that the vaccination has nothing to do with the illness of these individuals.  In a previous post, however, I have suggested that the vaccine is a “stress factor”, given to an individual in a state of marginal, or even asymptomatic thiamine deficiency, thus exacerbating the first appearance of symptoms. In this light, medications and other vaccines may also be considered stress factors and evoke or exacerbate a previously asymptomatic thiamine deficiency. There are a number of facts that need to be seen collectively in order to understand the hypothesis that follows.  In order to make this clear I am going to present the material under subheadings.

What Does Thiamine do in the Body?

All simple sugars that we take in our diet are broken down to glucose, the primary fuel of the brain.  This oversimplified fact has long been used to suggest that taking sugar is the way to meet energy demands in the body.  It is, in fact, an extremely complex chemical process which is well beyond the scope of an article like this.  It can, however, be simplified by comparing glucose, as a fuel, to gasoline in a car.

Gasoline + Oxygen + Spark Plug = Energy  + (ash/oxides)

Glucose + Oxygen + Thiamine = Energy + (ash/oxides)

Each one of these equations represents combustion, a combination of fuel with oxygen.  Because combustion is always incomplete, waste products (oxides) are formed and must be got rid of as waste.  It is obvious that combustion of gasoline without oxygen and spark plug, or glucose without oxygen and thiamine, will not occur.  What is not quite so obvious is the fact that an excess of gasoline causes choking of the engine, black smoke from the exhaust pipe (unburned hydrocarbons) and loss of engine efficiency.  This could be referred to as “oxygen/spark plug deficiency” since each of the three components must be present in proper concentration to produce efficient combustion (oxidation).  The three component parts, glucose, oxygen and thiamine are the equivalents in the body.  An excess of glucose “chokes” the “engines” (mitochondria) that create energy in all of our cells. This particularly applies to the brain because of its high rate of metabolism (energy consumption), thus providing a potential explanation for why the vaccine seems to pick off the brightest and the best students.

The Reptilian Brain and the Limbic Nervous System

All animal brains are built on the same basic principle, a lower, more primitive part and a higher, increasingly complex part. The lower part of the human brain, the limbic system, also known as “reptilian”, computes all the reflex mechanisms by which we automatically adapt to our environment.  For example, we sweat when it is hot and shiver when it is cold, both adaptations to the ambient temperature.  It also controls our emotional reflexes, represented by body language that we recognize easily.  It uses two mechanisms, the autonomic nervous system and the endocrine system.

Autonomic and Endocrine Systems

We have two nervous systems. The one that we use to will our actions is controlled by the upper brain, here described as cognitive. The autonomic nervous system (ANS) automatically controls all the actions required by body organs to meet day- to- day adaptation.  It consists of two major branches, known as the sympathetic and parasympathetic components.  The sympathetic branch prepares us for mental and physical action while the parasympathetic switches us to a period of rest.  As one goes into action, the other one is withdrawn. The endocrine system is represented by a group of glands, each of which produces one or more hormones.  These are really messengers that induce actions in the cells to which they are aimed.  When either or both of these systems are not functioning in their ordained manner in the brain/body of an individual, we can refer to him/her as maladapted.

Explanation of Symptoms in Reference to Thiamine Deficiency

As explained in previous posts on this web site, the disease known as beriberi occurs as a result of TD.  The mother of a Gardasil affected girl had done her own research and had come to the unlikely conclusion that her daughter suffered from beriberiRed cell transketolase, a blood test used to depict TD, showed that she was correct in her conclusion. Her daughter did in fact have beriberi and has responded, at least partially, to thiamine supplementation.  We know, from historical data, that long term beriberi responds slowly to treatment and sometimes not at all, depending on chronicity.  Since she has had her symptoms for approximately four years, I think that it would be fair to call this chronic. When the ANS is not functioning properly, it is called dysautonomia (dys, meaning abnormal: autonomia refers to the ANS).  Beriberi in its early stages is the prototype for dysautonomia, the commonest effect being dominance of the sympathetic branch of the ANS.

Published Effects of Gardasil Vaccination

Although many symptoms have been reported related to this vaccination, two resultant conditions have been nominated: POTS (Postural Orthostatic Tachycardia Syndrome) and Cerebellar Ataxia.  POTS is one of the many conditions that are described under the heading of dysautonomia and I have already reported in a post that the first case of thiamine dependency was in a six year old boy who had intermittent episodes of cerebellar ataxia, each of which was triggered by a stress episode that included mild infection, mild head injury or inoculation.  A critical enzyme that depends on thiamine for its energy producing action was able to function until some form of physical or mental stress was imposed.  The existing mechanism was insufficient to meet the energy requirement imposed by the stress.

Sugar, the Autonomic Nervous System and the Liver

New research provides one more clue to our emerging theory of thiamine deficiency in post vaccine and medication adverse reactions.  The study: The Autonomic Nervous System Regulates Postprandial Hepatic Lipid Metabolism by Bruinstroop et al. demonstrates the influence carbohydrate intake has on autonomic control of liver lipid metabolism. Triglycerides are measured in a medical laboratory as part of what is known as the “lipid profile”, that includes the various components of cholesterol. The Bruinstroop study found that when the parasympathetic system was deactivated and carbohydrates were ingested, triglyceride levels rose significantly, inducing metabolic dysregulation. Other studies have found stress, combined with diets high in refined carbohydrates can increase blood triglyceride concentrations also inducing metabolic syndrome. Indeed, stress and the concurrent increased sympathetic system activity seem key to metabolic functioning with sugar intake triggering the ill-health.

Interpretation of Technical Language

The work by Bruinstroop and associates was done in rats.  To understand what they found, it is necessary to remind the reader that the two branches of the ANS, sympathetic and parasympathetic, work synchronously.  As one branch becomes active the other one is withdrawn. This is automatically controlled by the “reptilian” brain, thus enabling us to adapt to the physical and mental changes we encounter on a day -to-day basis.  These authors were able to show that abolishing the parasympathetic input to the liver resulted in marked elevation of triglycerides in the blood. This would induce continuation of sympathetic dominance in any “stress reaction” in the animal if it was in a free living state. The effect was modulated by sugar intake. That is, when the animals were fed more, the effects were larger.

Hypothesis: High Sugar Diets Lead to Thiamine Deficiency, A Risk Factor for Adverse Reactions

I am proposing that an excess of carbohydrates in the diet, particularly fructose, results in a mild degree of thiamine deficiency.  We know, from studies done as early as 1943 (Williams R D, et al. Arch Int Med 1943;71:38-53), that this results in what is typically called psychosomatic disease, in which a large component is reflected in emotional lability (instability), so common in the modern child and adolescent.  Physical symptoms, such as unexplained “pins and needles”, in the hands or feet, may be so slight as to be ignored.  The stress of the vaccination or a medication reaction triggers an energy crisis in the “reptilian” brain, specifically evoking autonomic dysregulation, typically with sympathetic system dominance and resulting in beriberi, POTS, or cerebellar  ataxia and potentially other syndromes.  Perhaps a rise in blood triglycerides as suggested by the Bruinstroop study, indicates the partial crippling of the parasympathetic branch of the ANS and sympathetic dominance.  High blood triglycerides might well be a  mark of the early stages of underlying autonomic dysregulation and thiamine deficiency and a potential risk factor for adverse reactions to certain vaccines or medications.

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

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Addendum

A 5th case of post Gardasil thiamine deficiency has been identified; a young woman who developed severe idiopathic hypersomnia, a variant of narcolepsy, post vaccination. The patient is undergoing treatment with success. A full case study will be presented soon.

Image by 🌸♡💙♡🌸 Julita 🌸♡💙♡🌸 from Pixabay.

This article was published on Hormones Matter previously in January 2014.

How Dietary Mayhem Causes Disease: The Choked Engine Syndrome

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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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