thiamin - Page 2

Of Oxygen, Spark Plugs, and Mitochondria

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Everyone knows that we need oxygen to live. Few know or care what the body does with it. Although everyone knows that it is extracted from the air by the lungs and carried by the blood to body tissues, it is left to scientists to understand what happens to it in the 50 to 100 trillion cells that make up an adult human body. The reaction that makes it possible for oxygen to maintain life is called oxidation. This reaction takes place in the mitochondria and produces energy that is used by each cell to carry out its program of function.  Perhaps we can understand this better by using an analogy.

Car Engines and Human Engines: Each Need Fuel

A car uses gasoline as a fuel. It is ignited by a spark plug that causes a controlled explosion in a cylinder. This drives a piston that passes the energy through a series of mechanical levers known collectively as the transmission. It is the conversion of chemical energy in gasoline to what Newton called kinetic energy that enables the car to move. The machine that does this is an engine. Perhaps it stretches the imagination to state that the body works on exactly the same principles. It is the details that make the difference. Oxidation is the equivalent of explosion in the cylinder. In other words, it is combustion. Now we have to compare it to the relatively simple mechanism of explosion.

First, combustion is merely the union of oxygen with a fuel. If we do not carry the reaction out in some controlled way, the energy is dissipated as heat into the surrounding air. In a car, the cylinder encloses the combustion and forces the energy into the transmission. In the body it is controlled in a much more complex way. Yes, heat is produced and is used to make us “warm blooded creatures” but there is no noise, fire or smoke as in the car engine. The energy is guided through an ingenious series of chemical reactions in what we might term “the engines of the cell”.

Mitochondria: The Engines in Our Cells

Each cell has a whole series of “engines” called mitochondria and it is in these organelles where oxidation occurs. A mitochondrion is so small that its structure can only be seen with the aid of an electron microscope and yet it is in each of the millions of cellular mitochondria where energy is produced for the use of each cell to perform its designed function. The usual fuel for this is glucose and it is not surprising that people have concluded that the consumption of sugar provides “quick energy”.

Good Sugar and Bad Sugar: Mitochondria Know the Difference

When sugar is ingested in its proper form, meaning as it is found in nature, it is stored in the liver and muscles as glycogen, a complex substance built up by sticking glucose molecules together, making something that looks like a miniature tree. As fuel is required, the glycogen is broken down and released as glucose into the blood. This requires an enzyme and there is an inborn error of metabolism where this enzyme is missing. The affected infant is found to have an enlarged liver stuffed with glycogen, together with low blood sugar, a situation that is not compatible with life and the patient dies in infancy.

Blood glucose is absorbed from the blood into cells under the influence of insulin and then goes into an ingenious “pipeline” that processes it. The beginning of this process requires a number of B group vitamins. There is a well known nutritional disease known as beriberi where the carbohydrate load is too great for this action to occur efficiently. It is now known that vitamin B1 is insufficient to meet the caloric demand and is the key to understanding the disease and how it is treated, a discovery that took many years to unravel.

Let us look again at the simpler method by which gasoline is ignited in a car. An electrically energized spark plug is used to ignite the fuel as it is passed into the cylinder by carefully controlled mechanisms. Some people will remember that cars once had a gadget called a choke, used for starting the cold engine. This allowed gasoline to flow into the cylinder with a relative deficiency of air, the so-called “rich” mixture. When the engine was warm the choke was automatically removed and the mixture weakened by allowing more air and less gas into the cylinder. If the choke mechanism stuck, there would be an excess of black smoke issuing from the exhaust pipe and the engine would not run properly. The smoke represents the hydrocarbons in gas that have not been ignited and a simple equation shows us why:

Fuel + Oxygen + Catalyst = Energy

empty calories

The Figure shows the ratio of calories to B vitamins in a healthy diet. The line AB represents the calorie intake (protein, fat and carbohydrate) and the line ED the vitamin intake that enables its efficient processing. If the line AB is extended to C (line AC) without the increase in vitamin intake, the triangle BCE represents “empty calories” equivalent to a “choked engine”. The remedy is obvious: we can extend line DE to F, thus restoring the ratio as in line FC, reduce the calories back to line AB, or meet each other half way (not shown).

Beriberi: Bad Sugar and Empty Calories

Beriberi is caused by consuming empty calories (triangle BCE), where the line AC represents carbohydrate calories and ED the corresponding ingestion of vitamin B 1. (thiamin).  The disease, throughout history, has been primarily in Eastern countries where the diet has been white rice based, particularly in times of greater affluence. This is because the grain in rice is starch and the cusp contains the necessary vitamins. When the Chinese peasants became more affluent they would take their rice to a rice mill where white rice was produced by removing the cusps. This was because it looked better when served to their friends, thus demonstrating their new found affluence. Outbreaks of beriberi were always associated with an increase in consumption of white rice.

What is the lesson to be learned from this in our modern age where diseases like beriberi have been thought to be of only historical interest?  Think of the enormous load of simple carbohydrate consumed by millions in the U.S. Everything supplied by the food industry is sweetened or it would not sell. White bread (the equivalent of white rice), cookies, pastry in general, ice cream, soft drinks, desserts, tomato ketchup——— the list goes on and on! Even the vitamin enrichment indicated on the label is insufficient. Obesity, often associated with inflammatory disease, is affecting millions. Our health bills are threatening us with national bankruptcy and we wonder why we are being “hit” with so many diseases and health catastrophies. Pockets are being lined with money made from a variety of reducing diets and pills.

Diet is Everything: Feed your Mitochondria

That is why I have a standard answer to every query that I get about diet. Eat only nature made food and the less that it is handled by mankind the better. The balance of calories and vitamins is automatically produced. If the food had not been available when life started on Earth animal evolution could not have occurred and we would never have survived. Granted, unfortunately with population explosion, fresh food of this nature is expensive and we have all given up back yard gardening The First Lady has shown the example. Will we take a “leaf from her book” and acknowledge that a lot of our health is in our own hands.

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

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The Paradox of Modern Vitamin Deficiency, Disease, and Therapy

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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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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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