gardasil thiamine deficiency

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 Wild animal predators have been replaced by taxes/business deadlines/rush hour traffic etc.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.

We Need Your Help

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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Photo by Robina Weermeijer on Unsplash.

This article was published originally in October 2013.

 

Post Gardasil Heart Failure, Ragged Red Fibers and Thiamine

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

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

Mitochondria

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

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

Mitochondrial Disorders are Multi-Systemic

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

Thiamine Deficiency Post Gardasil

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

Thiamine is Critical for Mitochondrial Functioning

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

The Gardasil Thiamine Relationship

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

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

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

Ragged Red Fibers and Cardiomyopathy

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

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

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

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

Thiamine Deficiency and Ragged Red Fibers: Experimental Evidence

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

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

Case Studies: Ragged Red Fibers, Thiamine and Mitochondrial Disease

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

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

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

Mitochondrial Dysfunction in Myocardial Infarction and Sudden Death

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

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

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

Connecting the Dots

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

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

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

Yes, I would like to support Hormones Matter.

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

Nephron, CC BY-SA 3.0, via Wikimedia Commons

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

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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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.

Yes, I would like to support Hormones Matter. 

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References

  1. Lonsdale D. Dysautonomia, a heuristic approach to a revised etiology for disease. eCAM 2009;6(1):3-10.
  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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More Ideas on Gardasil Toxicity and the Thiamine Connection

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

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

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

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

Puzzling Symptoms Post HPV Vaccine

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

Oxidative Metabolism 

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

Thiamine and the Brain

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

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

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

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

How Could Gardasil Induce Thiamine Deficiency?

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

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

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

Additional Reference

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

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 (we hope to launch the male version soon), please take this important survey. The Gardasil Cervarix HPV Vaccine Survey.

To take one of our other surveys, click here.

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

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My Son’s Gardasil Story and Thiamine Deficiency

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On June 16th 2012 my son complained of ear pain, so I took him to his doctor thinking he had an ear infection. He had no infection but his doctor suggested doing a physical exam since he had not been in for a couple of years. My son had just turned 18 years old three weeks prior and just graduated from high school. He was happy, healthy, and active. After the exam I was called into the room. His doctor said he was in good health and observed no problems, but since he would be going off to college in the fall, he recommended that he should receive the meningococcal vaccine along with the Gardasil vaccine. In his words, “HPV is rampant in colleges and he should have this vaccine.” This had been my son’s physician since birth, and having no prior knowledge of the Gardasil vaccine controversy, I trusted him and agreed to these two vaccines that day.

There was absolutely no discussion of possible harmful side effects.

My son did not have any immediate reactions that I can remember, but on July 30th 2012 that all changed. We were out to lunch and when his food arrived he looked at me with a very strange look on his face and said that he just didn’t feel right, something was wrong. He could not eat that day even though he was hungry just prior. He would complain of severe stomach pain that came and went over the next few weeks.

On August 7th 2012 he received the second dose of Gardasil. His stomach pain increased in severity, but we still did not make the Gardasil connection. Who would think that a vaccine for HPV would cause stomach aches?

Just nine days after that second injection, he felt he needed to go in and see his doctor. The pain was becoming unbearable. The doctor prescribed antacids but this only made his problem worse, so he then suggested an endoscopy. The endoscopy came back completely normal. At this point his doctor felt that his stomach pain was due to stress and anxiety because he was going off to college. The doctor suggested that he should “go talk to someone.” I knew for a fact that the pain was not in his head or simply due to stress. It was real. Now, almost a year later, and with the knowledge of the possible side effects of the Gardasil vaccine, I am very angry that his doctor did not recognize “severe stomach aches” as being one of the Gardasil side effects. How did he not connect those dots, especially given the fact that my son was in his office just nine days after receiving the second dose complaining of that very thing? This recognition would have prevented him from getting that dreadful final dose.

My son left for college and soon after began developing other symptoms, mainly extreme fatigue and brain fog. He made it through the quarter and came home for Winter break. On December 27th he received the 3rd and final dose of Gardasil. The very next evening he became extremely sick. All the symptoms he had been experiencing along with many others became instantly worse. I was finally able to make the Gardasil connection. Since then he has had more symptoms than I can list, sinus headaches, pain at the base of his skull, fever, chills, hair loss, vision changes, gallbladder pain/gallstones, sleep disturbances, tingling, numbness, no appetite, weight loss, anxiety, excessive thirst, salt cravings, kidney issues, liver issues, heart palpitations, slow heartbeat, fast heartbeat, dizzy, rashes, mouth sores, yeast issues, low stomach acid… the list goes on. To this day he still suffers from many of these symptoms.

What has followed are many doctors and  many, many tests; most of which have come back normal with the exception of his most recent test. After reading Dr. Lonsdale’s article on thiamine deficiency and his recommendation for Gardasil injured to have a red cell transketolase blood test,  I immediately requested one for my son. I researched the symptoms of thiamine deficiency and he pretty much had every single one. The test came back strongly positive. He was severely thiamine deficient.

This is where we are today. We started immediate supplementation with oral alliathiamine and we are looking into possible IV supplementation, for perhaps, a quicker, more thorough improvement. I sincerely hope that this discovery might be the key to my son finally being well again and that this devastating nightmare may finally come to an end.

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 (we hope to launch the male version soon), 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 and research participation opportunities click here.

To share your health story with our community, click here.

If you think what we do at Hormones Matter is worthwhile, contribute to our research programs and our continued health research reporting. Hormones Matter is totally unfunded and can use your help to continue operations. Crowdfund Hormones Matter – Buy an Unsubscription.