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The Paradox of Modern Vitamin Deficiency, Disease, and Therapy

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calorie rich versus nutrient rich

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

The Calorie Rich and Nutrient Sparse Modern Diet

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

The Brain as a Chemical Machine

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

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

Autonomic Function

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

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

Dysautonomia, Dysfunctional Oxidation and Disparate Symptoms 

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

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

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

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

The Vitamin Therapy Paradox

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

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

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

The Paradox and Thiamine

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

Beriberi and Thiamine Deficiency

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

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How Dietary Mayhem Causes Disease: The Choked Engine Syndrome

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Dietary mayhem and thiamine deficiency with simple sugars

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

Thiamine Deficiency and Diet

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

Cellular Energy and Diet

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

Dysautonomia, Oxidative Stress and Thiamine

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

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

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

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

Understanding the Labs

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

  TABLE 1
Month

Cholesterol

Triglycerides

Fibrinogen

HsCRP

TKA

TPPE
February

169

206

412

7

65

35%
March

155

165

55

25%
May

160

152

312

0.9

85

2%
August

166

124

0.3

59

0%
September*

169

165

220

1

62

8%

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

 

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

Compromised Oxidative Function: Thiamine Deficiency, Beriberi and Diet

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

Thiamine and the Brain

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

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

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

Dysautonomia and Thiamine Deficiency         

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

The Role of Nutritional Stress in Post Vaccination and Medication Reactions

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

Conclusion

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

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

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References

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

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

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

The Case Details: Acute Cerebellar Ataxia Post HPV Vaccine

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

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

Treatment Options for Acute Cerebellar Ataxia

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

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

Immunoglobulin G (IgG) and Cerebellar Ataxia Symptoms

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

HPV16L and Post HPV Vaccine Reactions and Death

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

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

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

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

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

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

Mitochondrial Injury, Thyroid, Thiamine and Cerebellar Ataxia

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

Final Thoughts

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

Participate in Research

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

We are also conducting research adverse reactions associated with the fluoroquinolone antibiotics, Cipro, Levaquin and Avelox: The Fluoroquinolone Antibiotics Side Effects Study.

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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.

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Thiamine Deficiency Testing: Understanding the Labs

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Thiamine Deficiency Blood test

It has recently been found that a number of individuals who have experienced adverse reactions to the Gardasil or Cervarix vaccines and some medications have had a blood test that indicated thiamine deficiency (TD), or its abnormal chemistry (TAC) in the body. This article reviews the methods by which TD or TAC can be detected.

Blood Thiamine – Vitamin B1 Concentrations

Measuring blood thiamine or B1 concentrations is the laboratory test that is commonly offered by doctors. It is only helpful in extreme cases and is usually in the normal range even when there is clinically demonstrable abnormal body chemistry. The reason for this is that thiamine does its work inside cells and has no effect outside them. When we get this vitamin from our natural food, it goes through a very important genetically determined process to enter our cells. There can be something wrong with this system so that even a dietary sufficiency will not be effective and the concentration in the blood will be in the “normal” range. When the B1 is inside a cell, it has to be treated by a biochemical process known as phosphorylation to become an active vitamin. Failure of this mechanism will result in a “normal” blood level but no vitamin activity. We therefore have to use a method that actually detects this “vital” activity.

Erythrocyte Transketolase: The Test of Choice for Assessing Thiamine Deficiency

Erythrocyte is the technical name for red cells. These are the cells that carry oxygen to our tissues and they contain a complex mechanism that depends on a series of biochemical processes, each of which requires an enzyme. Transketolase is one of these enzymes. Its activity can be detected by a laboratory test and measuring transketolase is the only way of showing that the activity of thiamine is normal. The reason for this is that all the enzymes in body and brain cells require one or more “cofactors” that enable the enzyme to function properly. Vitamins and some minerals are cofactors and that is why they are so important. We have long known that they have to be obtained from our diet, but the reasons given above make it clear that dietary intake may be normal and still result in poor function of the enzyme in question.

Transketolase requires two cofactors, thiamine and magnesium and the laboratory test is designed to show their deficiency or abnormal chemistry by detecting the activity of the enzyme. Because thiamine is vital to cellular energy production, its deficiency affects first the tissues that are the most active oxygen using tissues, the brain, nervous system and heart.

Method of Performing Erythrocyte Transketolase Test

First, the baseline (as it exists in the patient’s red cells) activity of the enzyme is detected by measuring the rate at which it synthesizes its product, the chemical substance next in line in the series of biochemical reactions that are referred to as a “pathway” to the final end product. This is reported as TKA and it has a normal range. In moderate thiamine deficiency the TKA can still be in the normal range but if it is low it indicates that the enzyme is not doing its job efficiently.

The next step is to repeat the test after the addition of thiamine pyrophosphate (the biologically active form of the vitamin) to the test tube reaction. If there is an acceleration of the product synthesis, it indicates that the enzyme needed its cofactor to become efficient in its job. This is reported as a “percentage increase in activity over baseline”. This is called TPPE (thiamine pyrophosphate effect); the higher the TPPE, the greater the deficiency.  A “normal” range for TPPE is allowed up to 18% and this was drawn from people that were supposedly “healthy”, meaning free of symptoms.

In essence the TPPE should be zero, indicating that the enzyme is fully saturated with its cofactor. If a person is (unknowingly) sensitive to sugar, this test may be abnormal and show the effect of sugar in that individual. This is because thiamine is vitally necessary to metabolism of ALL simple sugars. That is the reason why sugar caused disease is so common in our world today.

In order to test thiamine deficiency, one must request transketolase testing. Not all labs can perform this test and so many will substitute the simple blood vitamin B1 testing. This test is insufficient for detecting thiamine deficiency for the reasons stated above. In this case, you may have to advocate on your own behalf and find the appropriate lab testing service.

Additional Labs

Since the publication of this article, the US lab performing these tests has closed. We have just learned a lab in London offers transketolase testing: Biolab Medical Unit. As we learn of additional labs offering the appropriates tests we will post them here.

Health Diagnostics and Research Institute in New Jersey also apparently will test for thiamine pyrophosphate (TPP) and erythrocyte transketolase (ETKA), but these tests are not listed on their menu and have to be requested.

In Germany – SYNLAB MVZ Leinfelden-Echterdingen GmbH
Labor Dr. Bayer
Nikolaus-Otto-Str. 6
70771 Leinfelden-Echterdingen / Germany

In Spain – Estudios Analiticos – Avenida nuevo mundo 11 (Madrid)
http://www.eaac.es
Email: info@eaac.es
Telephone: 916334223
Fax: 91 533 10 44 / 91 632 44 17
Information: Monday to Friday: 8:00 a.m. to 8:00 p.m. Saturdays: 9:00 a.m. to 10:30 a.m.

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Post Gardasil POTS and Thiamine Deficiency

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Autonomic nervous system

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

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

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

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

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

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

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

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

Publications and resources from Dr. Lonsdale:

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

Resources for Understanding Thiamine Deficiency

Molecular Mechanism of Thiamine Utilization

Participate in Research

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

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

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

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

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

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

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

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

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

Participate in Research

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

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

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

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