thiamin deficiency

SIDS and Vaccination

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Posted on Child Health and Safety on January 13, 2015 was an announcement that vaccines had been proven to cause sudden death in children (SIDS). The announcement indicated that death in 67 cases was only explicable as caused by vaccines. Drug safety regulators were said to have had the information for over two years. In this post, I am going to contest vaccination as the sole cause and try to explain why I think it is a much more complex problem.

In 2001, I published a paper that hypothesized the requirement of three variables: Sudden infant death syndrome requires genetic predisposition, some form of stress and marginal malnutrition. I have just published another paper on the same subject: Thiamin and Magnesium Deficiencies: Keys to Disease.

What History Tells Us about SIDS

Back in the seventies, I was working at Cleveland Clinic in Cleveland Ohio in the Department of Pediatrics. At that time there was a great deal of professional interest in SIDS. In the course of my research, I had found a paper written in a prestigious medical journal in 1944 by a British Medical Officer of Health by the name of Lydia Fehily. Readers will remember that Hong Kong was then a British protectorate and Fehily was sent out from England in order to investigate a common form of sudden death in breast fed infants of Chinese mothers in the colony.

A little bit of history is important to the final solution. Before World War II, the Japanese had invaded China. The rice ration was cut to starvation levels, thus cutting down the calorie intake. Although the symptoms of starvation prevailed in the mothers and the infants, the sudden infant death had disappeared. After the Japanese were driven out, the pregnant mothers in Hong Kong had as much rice as they wished. The calorie intake had been restored, overwhelming the required concentration of vitamin B1 for adequate oxidation of the calories. The sudden death in the breast fed infants immediately reappeared.

Fehily had discovered that the reemergence of SIDS was due to infantile beriberi because the infants were fed by vitamin B1 deficient breast milk (Human milk intoxication due to B1 avitaminosis). Those affected were almost always regarded by their mothers as the healthiest appearing infants in the family prior to their death. These events were rare under two months and after six months of age. It occurred almost always at night, was often associated with a runny nose interpreted as a mild cold and was more common in winter months. The epidemiology of this is almost exactly like that of modern SIDS. Although the modern interpretation is related to the positioning of the infant in the crib, it is certainly not the whole story. I came across the report of a meeting of beriberi researchers held at that time. A statement in that report had said that:

“any sudden otherwise inexplicable infancy death is a guarantee of infantile beriberi. No other disease has a similar outcome”.

Predicting SIDS

During the early part of the seventies it was thought that SIDS could not be predicted, that there were no symptoms to provide a warning. Later on in the decade, it was shown that there was such a thing as “threatened SIDS” judged by a few non-specific symptoms. Coincidentally, an alarm system had been invented that an infant could wear in the crib. It indicated when breathing stopped for a given interval or when the heart slowed. If and when such a thing happened, it was very easy to resuscitate the infant by a simple slap on the buttock.

SIDS, Thiamine and Brain Development

I began to admit infants with this kind of history to the hospital and place them on an alarm system. Believe it or not, by giving thiamine by injection to these infants, the alarms ceased to be initiated. I found this to be very exciting and I continued my research. I even went to Australia to do sabbatical research with the late Dr. Read at the University of Sydney who had evidence of implication of thiamine metabolism in SIDS. I found that there were families where SIDS had been occurring in more than one related infant. There was no pattern that indicated a direct genetically determined outcome and I concluded that it was a genetic risk rather than a genetically determined disease.

The overall logical conclusion to this series of facts was as follows:

  1. That genetic risk implied an unusually well developed brain that required a great deal of energy to function. The only means by which this could be acquired was through pristine nutrition for the mother during pregnancy.
  2. That calories from simple carbohydrate with insufficient thiamine was extremely dangerous. (Note that rice rationing had stopped the infancy deaths in Hong Kong).  The brain of an infant in the first six months of life grows at a tremendous rate and the oxidation of glucose to provide the required energy is crucial. Vitamin B1 is essential to that oxidation. This had been shown by Dr. Peters in Cambridge, England as early as 1936.
  3. That some form of stress may or may not be necessary, depending on the state of biochemistry in the brain. The infant is already at risk at birth because of the nature of nutrition supplied by the mother during pregnancy. A state of marginal malnutrition in the infant is insufficient to meet the energy demands of adapting to the vaccination as a stress factor.

Readers of this website may or may not be aware of a series of posts on the relationship of post Gardasil postural orthostatic tachycardia syndrome (POTS) with thiamine deficiency. I believe that this post on SIDS bears comparison with the logical reasoning applied in that post.  Also, Dr. Marrs has repeatedly pointed out the relationship between drugs and seemingly unrelated disease caused by them.

Does Thiamine Deficiency Underlie Post Vaccination SIDS?

The epidemiology (study of cause) of infantile beriberi (vitamin B1 deficiency) is sudden death. The commonest time for this is between three and four months and more commonly in male infants. Although this is almost the exact epidemiology of modern SIDS, this well researched truth is ignored. The classical vitamin deficiency diseases (beriberi, pellagra, scurvy) are considered to be of only historical interest because vitamin enrichment of foods has abolished them. This is simply not true.  A high intake of sugar in the form of simple carbohydrate, empty calories is widespread in America and other Westernized countries, automatically overwhelming the insufficient concentration of vitamin B1, the equivalent of a choked engine in a car. “Soft” drinks are all too well advertised and encouraged in opposition to the consumption of “hard” alcohol that is regarded as more dangerous. Although the dangers of alcohol are well known, the danger of “soft” and “Diet” drinks, particularly during pregnancy, is almost totally unknown to consumers who erroneously believe they are preventing weight gain and contributing to personal health.  The advertising is misleading.

Looking again at history, we also know that the very first symptoms of beriberi could occur in a group of patients when exposed to sunlight. We now know that ultra violet light is very stressful to the human body, demanding an adaptive “stress” response that is automatically initiated by the lower part of the brain, the limbic system and brainstem. The word “stress” must be used in its proper connotation. It must be defined as a mental or physical force to which we have to adapt. For an infant, stress would include weather changes, infection, trauma, vaccination, partial suffocation from being placed in the prone position, inhalation of chemicals in the crib mattress and other possible variables. This part of the brain is particularly sensitive to thiamine deficiency, diminishing the supply of energy required by the cells in order to perform this complicated adaptive process.

We live in a hostile environment to which we have to adapt automatically 24 hours a day by brain/body mechanisms initiated by the lower brain. Damaging the brainstem affects the nervous control of automatic breathing and control of heart rhythm. Thus, breathing or heart beat may cease in an infant during sleep when thiamine deficiency prevails. During the first six months of life brain growth is tremendously fast, requiring an enormous amount of energy. I am proposing that the infant with the highest, genetically determined brain energy requirement is more at risk. If this is true, the tragedy of SIDS may be removing the most superior future citizens. Obviously, the mother’s diet must provide a proper balance between the calories that provide the fuel and the capacity of the cell to burn the calories by means of the appropriate vitamins. Because we now know that sufficient thiamine or vitamin B1 is critical to prevent beriberi and I have published evidence for deficiency of this vitamin in threatened SIDS, it makes sense to consider the interplay of three variables in SIDS. The three variables are as follows:

  1. Genetic risk, “e.g. a high brain energy requirement”
  2. A non specific stress factor, “e.g. vaccination”
  3. Marginal high carbohydrate calorie malnutrition

It also makes sense to consider the possibility that the stress of vaccinations is too great a risk for infants who are genetically and/or environmentally predisposed to oxidative damage in the brainstem.

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This article was published originally on Hormones Matter on January 21, 2015.

 

A Case of Classic Beriberi in America

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A desperate mother sent me an email about her 23-year-old son and it was easy to recognize that this young man had full-blown beriberi. You may or may not know that beriberi is well known as a vitamin B1 deficiency disease. Because the medical profession is convinced that this disease never occurs in America, it is usually not recognized for what it is. He had seen many physicians without success. I want to record the majority of his symptoms to show that they are surprisingly common and are usually ascribed to a “more modern” diagnosis. I have christened beriberi as the “great imitator” and I am sure that the reader will readily recognize the common nature of these symptoms, presented below in the form of a Table. It is important also to understand that these symptoms can occur for other reasons, but thiamine deficiency is widespread.

 

collapsing fatigue confusion
panic attacks loss of balance
blurred vision cluster headaches
hair loss jaundice at birth
infantile colic migraines
poor intestinal motility bloating
severe calf pain joint pains
weakness salt craving
cold extremities chemical sensitivity
POTS severe pain sensitivity

 

I want now to describe some of the features reported by this mother that were extremely important major clues. She described her son, when in good health, as 6’2”,  175 pounds, extremely athletic with “amazing hand-eye coordination and finishing college with high honors”.

As a result of his undiagnosed illness, his weight had dropped to 133 pounds. Because thiamine governs energy metabolism, an intelligent brain consumes a great deal. Of course, compromised energy production can occur for reasons other than thiamine deficiency. But there were very strong clues for beriberi. The mother described how her son

“…went out drinking with friends. The next day he could barely sit up in the car or stand. We were all commenting on why he was having such an extreme hangover”.

Alcohol would certainly exaggerate an existing thiamine deficiency. It is a well-known association. The symptoms were intermittent, rising and falling “for no apparent reason”. For example, she said that he was

“able to play sports, then lose his balance, become weak and complain of blurred vision”.

The reason for this is because the physical activity was demanding energy that could not be supplied because of the thiamine deficiency. He had jaundice at birth, now known to be because of inefficient oxygen utilization. This would indicate poor maternal diet in pregnancy or a genetic mechanism involving thiamine absorption. So-called panic attacks are common in the modern world and are absolute indicators of poor oxygen utilization in the brain. Under these conditions the reflex known as fight-or-flight would be initiated and this is what is being called panic attacks. The blurred vision would go along with this too.

Beriberi is a Form of Dysautonomia

We have two nervous systems. One maintains what we call willpower and is known as the voluntary system. The other one is known as autonomic and is entirely automatic and outside willpower. This system controls all the organs within the body. It explains why there are so many symptoms involving many parts of the body. This is because of the loss of signaling power between the organs and the brain. A lot of energy is required to run this system and explains why the autonomic nervous system is affected in beriberi. POTS is one variety of dysautonomia. This young man craved salt and that too is a form of dysautonomia is known as cerebral salt wasting syndrome, explaining the natural craving.

Thiamine deficiency beriberi in America

Is there a help from the laboratory?

The answer to this is no, as long as physicians refuse to recognize that beriberi is common in America. This unfortunate young man was diagnosed almost certainly as psychosomatic. The disease has a very long morbidity with symptoms shifting up and down according to the state of energy metabolism on a day-to-day, week-to-week and month-to-month basis. The laboratory has to look for it because the standard tests done only provide distant clues. It is the absence of the abnormal results that make it easy to conclude that this is “a psychologic disease”. For example, it was reported that this young man had an elevated vitamin B12 and a mildly elevated CRP. I cannot give the complex details here, but both are peculiarly related to energy metabolism and require understanding in order to fit them into the pattern of diagnostic clues. I have reported these facts elsewhere.

What is the hope of normal health in this person?

It stands to reason that the first thing is proper diagnosis and a knowledge of the widespread symptomatology, including their fluctuation. As long as he continues to take alcohol and sugar, he will never get his health back even if he supplements with thiamine. He is in danger of developing the classical brain disease known as Wernicke’s Encephalopathy. This state of the disease almost certainly involves cellular damage that cannot be repaired. It is therefore very urgent to understand the self-responsibility that is required. He has to learn that alcohol is potentially lethal for him. There is undoubtedly a genetic relationship between alcoholism and sugar craving and it is probably true that a search for the genetic relationship would at least be helpful in understanding the nature of this disease.

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Diabetes and Thiamine: A Novel Treatment Opportunity

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Underlying all diabetic conditions is poor sugar control or hyperglycemia. Hyperglycemia can be due to a lack of insulin as in Type 1 diabetes or insulin resistance as in Type 2 diabetes. In either case, the corresponding diabetic complications that evolve over time in many diabetics, the cardiovascular disease, retinopathy, peripheral nerve and vascular damage, represent the effects of sustained hyperglycemia. Until recently, the mechanisms by which diabetic vascular damage developed eluded researchers. Although multiple, seemingly discrete biomarkers had been identified, no single, unifying mechanism was understood. It turns out that diabetics, both Type 1 and Type 2, are severely deficient in thiamine or vitamin B1 and that thiamine is required for glucose control at the cell level. Why is thiamine deficient in diabetics and how does thiamine manage glucose control? The answers to those questions highlight the importance of micronutrients in basic cellular functioning, particularly mitochondrial functioning, and the role of excessive sugar in disease.

Thiamine

Thiamine (thiamin) or vitamin B1 is an essential nutrient for all living organisms. The body cannot synthesize thiamine by itself and so it must be obtained from diet. Thiamine is present in yeast, pork, fish, various nuts, peas, asparagus, squash and grains (unprocessed) and because of the severity of the illnesses that thiamine deficiency evokes, many processed foods have been fortified with thiamine. Nevertheless, thiamine deficiencies thought resolved by modern nutritional technologies, are emerging once again. Modern thiamine deficits appear to be caused by diets of highly processed, carbohydrate and fat laden foods, exposures to thiamine blocking factors such as alcohol and those found in many medications (fluoroquinolones, possibly others) and vaccines (Gardasil, possibly others), environmental toxicants and some foods. Thiamine deficiency is also common after bariatric surgery and in disease processes like AIDS and cancer. Over the course of our research, thiamine deficiency has been observed in previously healthy, young, non-alcoholic patients, post medication or vaccine, along with symptoms of dysautonomia.

Thiamine Deficiency Symptoms

Thiamine deficiency at its worst is linked to severe decrements neurological functioning, like Wernicke’s Encephalopathy that include noticeable ataxic and gait disturbances (loss of voluntary control of muscle movements, balance and walking difficulties), aphasias (language comprehension and/or production difficulties), and if it persists, Korsakoff’s Syndrome (severe memory deficits, confabulations and psychosis). Early on though and as the deficiency is evolving, thiamine deficiency presents much like the mitochondrial disease that it is – with the myriad of seemingly unrelated symptoms, that are not typically attributed to thiamine deficiency, such as fatigue and excessive sleeping, hair losscardiac dysregulationGI disturbances such as gastroparesis and others, autonomic instability, demyelinating syndromes and hormone irregularities, especially thyroid, but also reproductive hormones. In diabetics, thiamine deficiency may present as ketoacidosis, lactic acidosis, hyperglycemia and persistent encephalopathy. Thiamine deficiency attacks the mitochondria. Mitochondrial dysfunction presents diversely. In fact, with mitochondrial dysfunction, symptoms are as varied as the individuals who experience them. Diabetes, may be just one more phenotype of among many.

Thiamine Deficits in Diabetes

With diabetes, thiamine deficiencies are common, though likely under-recognized. Diabetics are susceptible to thiamine deficiencies mediated by diet and exposures like most of the Western world, but also have added risk factors associated with the disease itself. In diabetics, kidney function is altered which decreases thiamine reabsorption while increasing thiamine excretion. In some people, diabetic and non-diabetic alike, thiamine deficiency can be exacerbated even further by a mutation in the thiamine transporter protein that brings thiamine into the cells.

How thiamine deficient are diabetics? One study found that in comparison to non-diabetics, individuals with Type 1 and Type 2 diabetes had 75% and 64% less thiamine, respectively. Think about this for a moment. If diabetes predisposes individuals to thiamine deficiency without any other intervening factors, imagine what happens when diabetics are nutritionally thiamine deficient, exposed to the myriad of environmentally or medically thiamine-depleting substances currently on the market, or worse yet, carry the thiamine transporter mutation. Alone, but especially in combination, thiamine deficiency diseases, many of which align with diabetes-related complications, could be magnified exponentially. The remarkable thing about this new research is that treatment is easy, it requires only dietary changes and high dose thiamine therapy alongside normal diabetes interventions. (Although one suspects with Type 2 diabetes at least, dietary changes and thiamine supplements could replace other medications entirely). Backing up a bit though, let us look at the research and mechanisms by which thiamine moderates sugar exposure at the cell level and how thiamine modifies those processes.

The Hyperglycemic Cascades

Under normal conditions, with appropriate dietary nutrients and physiological concentrations glucose, dietary sugars are converted to ATP in the mitochondria. The byproduct of that reaction is the production of free radicals also known as oxidative stress or reactive oxygen species (ROS). ROS are neither good nor bad, but too much or too little ROS wreaks havoc on cellular functioning. The cells can clear the ROS and manage oxidative stress via activating antioxidizing pathways and shuttling the excess glucose to secondary, even tertiary processing paths. However, under conditions of chronic hyperglycemia, mediated by diet or diabetes, the conversion of glucose to ATP becomes dysregulated, the production of ROS become insurmountable and a cascade of ill-effects are set in motion.

Too much ROS cause the mitochondria to produce high concentrations of an enzyme called superoxide dismutase (SOD) in the endothelial cells of both the small and large blood vessels. SOD is a powerful antioxidant, however, like everything else, too much for too long causes problems. Superoxide then upregulates the five known chemical pathways that alone and together perturb vascular homeostasis and cause the diabetic injuries that have become commonplace. Technically speaking, hyperglycemia causes:

  1. Increased activation of the polyol pathway
  2. Increased intracellular formation of advanced glycation end products (AGEs)
  3. Increased AGE receptor expression and ligands
  4. Upregulated protein kinase C (PKC)
  5. Enhanced hexosamine pathway activity

In non-technical terms, elevated concentrations of circulating glucose increase the production of ROS and superoxide, but also, and as a compensatory survival reaction to maintain cellular health, secondary and tertiary glucose processing pathways come online. These backup pathways are not nearly as efficient and so produce additional, negative metabolic byproducts which can damage blood vessels if not cleared. The body is capable of clearing these byproducts, but only when the reactions are short term and the nutrient substrates feeding those reactions are present. If, however, the nutrients are deficient and/or the hyperglycemia is chronic, or both, those clearance mechanisms are insufficient to remove the toxins. The toxic byproducts build up and diabetic vascular diseases ensue.

High Dose Thiamine Therapy and Diabetes

Over the last decade or so, researchers have found that thiamine normalizes each of these five aberrant processes activated by sustained hyperglycemia and implicated in diabetic vascular complications. High dose thiamine (300mg/day) reduces the biochemical stress of hyperglycemia human subjects. Additionally, thiamine can prevent and/or offset incipient vascular damage in diabetic patients. Finally, in rodent models of Type 1 diabetes, thiamine transporters have been identified and emerging research shows that thiamine moderates pancreatic insulin secretion significantly. In rats fed a thiamine deficient diet, glycolysis (sugar processing and conversion to ATP by mitochondria) was inhibited by 41%, utilization of fatty acids (secondary energy processing pathway) declined by 61% in just 30 days and insulin production diminished by 14%. The connection between pancreatic downregulation of fatty acid utilization and thiamine is particularly interesting considering the recent discovery of a thiamine dependent enzyme in fatty acid regulation, the HACL1.

Diabetes and Modern Medicine

Diabetes and the destruction it causes affects every cell, tissue and organ system in the body. As such, some researchers have postulated that diabetes represents a model for the paradigm shift in modern medicine. If diabetes is the model for chronic, multi-system illness that marks modernity, then thiamine, and likely other nutrients, are the markers by which the new model of medicine must be drawn. Diabetes is, at its root a mitochondrial disorder. Whether diabetes is inherited, as in Type 1 or induced environmentally as in Type 2, diabetes exemplifies how we convert food to fuel to power cellular functions. When that food is deficient in vital nutrients, the power conversion processes adapt for survival. The compensatory actions have consequences, especially when sustained beyond their capacity to meet the needs of the body. Disease erupts, first gradually then explosively.

Consider the implications of thiamine deficiency, a single micronutrient available in food, on cellular health, and indeed, physical health. In addition its role in mitochondrial functioning, thiamine controls sugar metabolism through multiple pathways. Inefficient sugar metabolism leads to disease. Thiamine also regulates the metabolism of fatty acids and provides the necessary substrates for the neurotransmitters acetylcholine and GABA. Thiamine, much like other critical nutrients, is not only absent from the largely processed diets of modernity, but at every turn, can be depleted by medications and environmental toxicants. Against the backdrop of nutrient depleted and damaged mitochondria, accommodating  medications, vaccines and environmental toxicants that also damage mitochondria, increase oxidative stress and further deplete critical nutrients, it is no wonder we are living sicker and dying younger than ever before. The depletion of critical nutrients is causing disease; diseases no medication can treat.

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

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

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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