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Thiamine, Fibromyalgia and Chronic Fatigue

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thiamine deficiency in fibromyalgia and chronic pain

Fibromyalgia affects roughly six million Americans, mostly women. Its symptoms include all-over muscle and tendon pain, increased pain sensitivity, chronic fatigue, sleep disturbances and brain fog. Fibromyalgia is often reported as feeling like a flu that never leaves. Similarly, symptoms of Chronic Fatigue Syndrome (CFS) overlap with many of those of fibromyalgia and the two conditions are often co-morbid. With chronic fatigue, however, the predominant symptom is a fatigue that never lets up versus all-over muscle and tendon pain.

Both fibromyalgia and chronic fatigue are co-diagnosed frequently in women with endometriosis, especially those who have had Lupron treatments. Similarly, we are finding a high incidence of chronic fatigue and fibromyalgia post Gardasil/Cervarix and post fluoroquinolone. All over muscle and tendon pain, coupled with never-ending tiredness seem to be common symptoms post medication or vaccine reaction. Could they be linked to a broader problem, specifically, thiamine deficiency?

What is Thiamine?

Thiamine or vitamin B1 is necessary for cellular energy. It is a required co-factor in several enzymatic processes, including glucose metabolism and interestingly enough, myelin production. We can get thiamine only from diet. When diet suffers, as in the case of chronic alcoholism where most of the research on this topic is focused, when nutritional uptake is impaired (leaky gut and other GI disturbances), or when other factors inhibit the enzymes necessary to carry out intracellular reactions, thiamine deficiency ensues. And thiamine deficiency can elicit a whole host of problems that are consistent with the current definitions of chronic fatigue and fibromyalgia.

Thiamine and Fibromyalgia – A Few Hints

A recent case study suggests that what is currently diagnosed as fibromyalgia and/or chronic fatigue may be attributable to thiamine deficiency. A very small case study (n =3) from Italian physicians found a significant reduction in fibromyalgia symptoms in patients given high dose thiamine. Researchers found:

  • Patient 1:  71.3% reduction in fatigue; 80% reduction in pain.
  • Patient 2:  37% reduction in fatigue; 50% reduction in pain.
  • Patient 3:  60.7% reduction in fatigue; 60% reduction in pain.

Thiamine and Chronic Fatigue

In a little bit larger study – 17 patients with Chronic Fatigue, researchers found a functional reduction of the enzymes involved in vitamin B metabolism (aspartate aminotransferase -pyridoxine, glutathione reductase and transketolase) compared to healthy controls, suggesting thiamine deficiency.

What This Means

It’s way too early to tell if thiamine deficiency is at root of fibromyalgia and/or chronic fatigue symptoms, or if adverse reactions to medications and vaccines can elicit the symptoms of fibromyalgia and chronic fatigue, but there are hints pointing in that direction. Much more research should be done. In the meantime, if you suffer from fibromylagia or chronic fatigue or undiagnosed neuromuscular pain, why not consider testing for thiamine.  And while you’re at it, since many of these symptoms overlap with those of hypothyroidism, particularly of the autoimmune Hashimoto’s sort, why not get tested for that too. If you test positive for either of these, tell us about it, it will help other patients find solutions. To learn more about thiamine deficiency and other topics, search our growing library of research and patient stories here on Hormones Matter.

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This article was first published on Hormones Matter in October, 2013.

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The Sugar – Thiamine Connection in Adverse Reactions

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

What Does Thiamine do in the Body?

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

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

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

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

The Reptilian Brain and the Limbic Nervous System

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

Autonomic and Endocrine Systems

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

Explanation of Symptoms in Reference to Thiamine Deficiency

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

Published Effects of Gardasil Vaccination

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

Sugar, the Autonomic Nervous System and the Liver

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

Interpretation of Technical Language

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

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

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

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

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Addendum

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

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

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

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More About Eosinophilic Esophagitis

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Eosinophilic Esophagitis

Seeing some of the comments following the appearance of my post Eosinophilic Esophagitis May Be a Sugar Sensitive Disease, it seemed that it was necessary to provide a little more explanation for how the conclusions were reached. Hopefully this may produce less misunderstanding.

Compartmentalized Medicine

The present model for disease is being rapidly outdated, so let me first of all review how a diagnosis is made in modern medicine. When a patient pays a visit to a physician, a medical history is recorded. The history begins by the patient describing symptoms, the sensory afflictions experienced since the loss of health began. This is followed by a physical examination when the physician is looking for evidence of malfunction. For example, this may include finding enlargement of a given organ, point tenderness when pain is elicited or a neurological deficit. Family history and the history of previous illnesses are both taken into account. The physician may or may not have a working idea of the nature of the disease process at this stage and a series of laboratory tests are requested. All of this is put together and the physician then has to consider what is generally referred to as a differential diagnosis. Which part of the physical examination, combined with the tests, all point conclusively to a diagnostic category?

This method of making a diagnosis was derived from the Flexner report initiated by Rockefeller in 1910. It was adopted from the German method in which laboratory confirmation was emphasized. This gave rise to the methodology that we now call “scientific medicine”. The symptoms, signs and laboratory reports are then put together and a given disease is named as the most likely fit.

So let us examine for a moment how this confuses us. All sensations are perceived in the brain and symptoms are merely a method by which the brain/body provides a warning that something is wrong. The “wrongness” has to be interpreted. In the present model, each constellation of symptoms, signs and laboratory reports are then given a name. For example, because somebody by the name of Parkinson was the first to describe a given constellation, it is called Parkinson’s disease, even though the underlying cause is completely unknown. Research has been aimed at finding a cure for that disease without giving full recognition to the fact that the constellation of findings overlaps with the constellations exhibited in other brain diseases, each being named separately. Furthermore, if the constellation points to an organ as the seat of a given problem (such as the intestine), the patient is referred to a specialist (a gastroenterologist) whose practice is confined to diseases of that organ (organic disease). An attempt to improve the symptoms by prescribing drugs is the chosen method, without considering the complex connection of the sick organ with the brain. An “anti-inflammatory” drug is prescribed, without asking why or what caused the organ to become sick.

In the case that I wrote about previously, the disease process called eosinophilic esophagitis or EoE, results from ingesting food. The presently accepted cause is “food allergy”.

Understanding Disease Differently: A Connected System

Let me provide an example to illustrate the change in perspective that occurs if the whole person is considered. On one of these posts a mother reported that her daughter had eosinophilic esophagitis, “associated with idiopathic gastroparesis” (partial or complete paralysis of the intestine). The word idiopathic stands for the simple sentence “the cause is unknown”. Evidently, no attempt had been made to connect the two conditions together. Is it likely that two unusual conditions will exist at the same time in one individual? By recognizing that the brain is always involved with body disease and brain disease is always involved with the body, it is possible to provide a solution for a connection between eosinophilic esophagitis and gastroparesis. It depends completely on an understanding of the profound genius of the brain/body interconnection.

The post that led to all of these comments asks the question, is this disease caused by the ingestion of sugar? We know that ingestion of sugar can easily induce thiamine deficiency because we have the ancient model of beriberi where white rice (without its surrounding cusp) ingestion, consumed as a staple, was found to be the cause. (Rice grain is starch and is broken down in the body to glucose. The cusp around the grain contains the vitamins. When the cusp of the rice is removed, as it is in white rice, the vitamins are removed leaving only the starch, which is converted to glucose.)

Digestion: Where Mechanical Meets Chemical

The vagus nerve is the 10th cranial nerve. Its action, initiated in the lower part of the brain, is to send outgoing messages to the spleen, an important organ that is used for controlling inflammation. The vagus nerve uses a neurotransmitter called acetylcholine and it also deploys messages to the esophagus and the entire intestinal tract. The wave pattern in the respective parts of the intestine that is induced by this nerve is called peristalsis. It pushes the contents along while the complex process of digestion occurs. Without going into details, the synthesis of acetylcholine depends on vitamin B complex, dominated by thiamine. Without thiamine, there is less acetylcholine and without this vital neurotransmitter, the control of inflammation and peristalsis in the esophagus, the intestinal tract, or both, are all compromised.

Eosinophilic Esophagitis and Food Allergy

In EoE, food sensitivity, occurring for whatever reason and known as food allergy, is causing inflammation that might occur in either the esophagus or any other part of the intestinal tract. When it occurs in the intestine it is called eosinophilic enteritis. Although the mechanism is the same, the locality differs but the esophagus is more commonly the affected part. The inflammatory response gets out of control because the vagus nerve, lacking acetylcholine to transmit the necessary information, is failing to suppress esophageal inflammation by sending a proper message to the spleen. The association of eosinophilic penetration into the intestinal tissue is part of the inflammation and it is interesting that a similar event has been associated with asthma in bronchial tubes. Asthma was a recurrent problem in the history of my patient.

Like the famous poem:

“for the want of a nail a shoe was lost; for the want of a shoe a horse was lost; for the want of a horse a battle was lost; for the want of a battle a kingdom was lost”.

To paraphrase this in biochemical terms “for the want of thiamine (vitamin B1), action of the citric acid cycle (engine of the cell) was lost; for the want of the citric acid cycle, acetylcholine (neurotransmitter) was lost; for the want of acetylcholine, suppression of inflammation was lost; for the want of acetylcholine, normal peristalsis (wavelike action) in the esophagus and intestinal tract was lost.

The loss of the peristaltic wave in the intestine was given the name “idiopathic gastroparesis”, a clear indication by the diagnostician that “its cause is unknown”. Like the blind men and the elephant the present medical model looks at a segment of the problem and fails to see the big picture. The trouble with this failure to understand the full nature of the problem is because we have divided brain disease from body disease. If it is suspected that the brain is the cause of the problem and all laboratory studies are negative, it is assumed that the symptoms are psychosomatic in nature and have been “imagined by the patient”. When the patient is told that it is “psychological”, it naturally induces anger.

My patient’s symptoms, recurring through infancy to the age of 8 years, were thought to be psychosomatic until endoscopy revealed the esophagitis. The “psychosomatic symptoms” were resulting from thiamine deficiency affecting the brain. His dramatic growth spurt during treatment strongly suggested that the autonomic (automatic) nervous system was at the seat of the complex problem. That conclusion can be supported by the medical literature concerning a well known genetically determined disease called Familial Dysautonomia, a disease whose clinical course results in growth failure. In the case of my patient, the dysautonomia was reversible and the result of thiamine deficiency, hence the growth spurt.

Nobody is looking for evidence of a vitamin deficiency because it has been assumed that that kind of disease is of only historical interest. This idea is so impregnated in the modern medical psyche that we can actually miss such a diagnosis when it is staring us in the face! That was the case here and may be the case in many other instances of eosinophilic esophagitis or enteritis.

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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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Very high magnification micrograph of eosinophilic esophagitis.

Nephron, CC BY-SA 3.0, via Wikimedia Commons.

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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 loss, cardiac dysregulation,  GI 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.

We Need Your Help

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

Yes, I would like to support Hormones Matter. 

Image by Tesa Robbins from Pixabay.

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

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The Flu Vaccine, Molecular Mimicry, Narcolepsy: Clues to Gardasil Injury

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molecular mimicry vaccine

What do molecular mimicry, the H1N1 Flu vaccine and the HPV vaccines Gardasil or Cervarix have to do with the brain neurons involved in narcolepsy or hypersomnia? Plenty. Researchers are learning that vaccine induced immune reactions can destroy innate cells via molecular mimicry and in the case of the flu vaccine, the hypocretin/orexin neurons responsible for maintaining wakefulness are attacked. Idiopathic hypersomnia, a derivative of narcolepsy is one of the many side effects reported by post Gardasil girls and women. Could the HPV vaccine be attacking those same neurons? Is molecular mimicry at play in the HPV vaccine too? The answers are yes and possibly, but with the HPV vaccine, the molecular mimicry is more widespread and the research only beginning to delineate its effects.

What is Molecular Mimicry?

Molecular mimicry is the notion that foreign pathogens like bacteria, viruses and vaccines can be so similar in structure or function to innate, ‘self’ peptide sequences that they evoke an autoimmune response in the exposed individual.  Molecular mimics are thought to be involved in the onset of Type 1 Diabetes, Lupus, Multiple Sclerosis and other diseases, including some neurological disease processes.

Molecular mimics are snippets of protein code embedded within the pathogen that are either functionally similar and contain sequences of identical code to those found innately in humans, or structurally similar and because of their shape can bind to and activate an immune cell receptor. The protein codes, called motifs, are instructions that govern all aspects of the cell’s activity levels, and indeed, our very health and survival. Some codes tell the cell to live and how to function, others tell the cell to die and even how to die. The thought is that when external pathogens contain protein motifs that mimic internal and innate protein motifs, our immune system recognizes the foreign invader and attacks not only the dangerous pathogen, but the innate molecules that contain those same protein motifs too, evoking all sorts of damage to potentially many different tissues and organs. When there is structural similarity between the pathogen and immune cells, the process for immune activation is quite easy. The pathogen slips in, binds to a receptor and initiates the inflammatory immune response. In either case, the immune response to the environmental pathogen results in a disease process identified as autoimmune – the immune system attacking itself. It should be noted that connection between molecular mimicry and autoimmune disease onset is hotly debated.

Narcolepsy or Hypersomnia, the Immune System and the Flu Vaccine

In 2010, amidst the fears of the H1N1 swine flu pandemic, citizens in Scandinavia and Europe were given the adjuvanted (MF-59 a squalene based adjuvant plus ASO3 – squalene-α-tocopherol mix) flu vaccine called Pandemrix. Shortly thereafter physicians began noting an increase in new onset cases of narcolepsy, especially in Scandinavian children.

Narcolepsy is the lifelong disorder characterized by excessive sleepiness with abrupt and sudden transitions to REM sleep.  It affects approximately ~ 1 in every 3000 individuals worldwide. Individuals with narcolepsy/hypersomnia have sudden and very strong urges to sleep throughout the day, though at night insomnia may develop. Patients may fall asleep as many as 20-30 times per day, for brief periods, making regular functioning difficult without wake stimulating medications.

Often co-occurring with narcolepsy is a condition called cataplexy. Cataplexy denotes the muscle tone and behavioral changes that precede the narcoleptic sleep incident. Cataplexy symptoms can range from the barely perceptible loss of facial muscle tone or twitches to full muscle paralysis and collapse. Approximately 70% of patients with narcolepsy also have cataplexy.

Hypersomnia, or more specifically, idiopathic hypersomnia, is a central nervous system disorder similar to narcolepsy. Like with narcolepsy, the brain is unable to regulate sleep-wake cycles, only here instead of bouts of uncontrollable sleepiness and periods of sudden onset sleep, with idiopathic hypersomnia, the sleepiness is severe, excessive and continuous. Both narcolepsy and idiopathic hypersomnia have long been thought to be autoimmune in nature, triggered by environmental factors. Bacterial infections such as streptococcus pyogenes, the bacteria responsible for strep throat/pharyngitis and skin infections like impetigo can elicit narcolepsy in some individuals, as well as autoimmune rheumatic fever and kidney disease in others.

Hypocretin/Orexin Neurons Damaged in Patients with Narcolepsy/Hypersomnia

From an autoimmune standpoint, key to triggering narcolepsy in some individuals, is presence of a particular gene variant in immune cells called human leukocyte antigens (HLA). The variant is labeled HLA -DQB1*0602.  Fully 98% of patients with narcolepsy exhibit the DQ0602 haplotype (DQA1*0102/DQB1*0602) versus 18-25% of the general public who have the mutation but do not experience narcolepsy. DQ0602 impairs and often destroys the brain neurons that secrete a peptide hormone that is required to maintain wakefulness. The wake-promoting hormone released from the hypothalamus, is called orexin or hypocretin.  Orexin and hypocretin are the same molecule that was discovered simultaneously by two separate research groups and then named independently.  Readers will see research articles on both orexin and hypocretin linked to narcolepsy (and the flu vaccine, migraine, glucose metabolism, feeding behavior, to name but a few other areas of research).

Molecular Mimics in the Flu Vaccine Attack Hypocretin Neurons and Induce Narcolepsy

Researchers from Stanford found molecular mimics in the adjuvanted Flu vaccine, Pandemrix, both sequence code and structural similarities that initiated immune system attacks on the hypocretin/orexin system in narcolepsy patients but not healthy controls. It should be noted in this particular study, only the adjuvanted version of the flu vaccine was studied, as that was the product distributed in Europe and Scandinavia. The non-adjuvanted version of the Flu vaccine sold in the US was not tested.

For the present study: CD4+T Cell Autoimmunity to Hypocretin/Orexin and Cross-Reactivity to a 2009 H1N1 Influenza A Epitope in Narcolepsy, the researchers used confirmed narcolepsy patients and controls who were all positive for the DQB1*0602 gene variant associated with narcolepsy. Here, despite having the variant, only the patients had a reactivation of the immune attack on the hypocretin neurons. The control group, who were also positive for the variant, but who had no active symptoms or diagnoses of narcolepsy, did not demonstrate the same immune response.  This suggests that other factors in addition to the molecular mimics and a personal predisposition must align to initiate the immune response or, in this case, what is deemed the autoimmune response. It also suggests, that in predisposed individuals, vaccine introduced molecular mimics can trigger immune system attacks and initiate disease states that may or may not have been symptomatic pre-exposure.

What this research does not explain is whether the new onset cases observed in the Scandinavian population post vaccine exposure were solely in individuals with the pre-disposing genetic variant. Was the increase in narcolepsy post flu vaccine exposure indicative of a latent disease state simply triggered by the vaccine? Or is it possible that there are other molecular mimics embedded within the flu vaccine, not yet identified, that might also trigger narcolepsy? Finally, and most importantly, could there be additional factors native to this and other vaccines, to the individual, or with the combination thereof, that evoke an attack on the neurons responsible for regulating wakefulness and inducing narcolepsy, or evoke an attack on other cells and elicit different disease processes? If the answer is yes to any of these questions, then our approach to vaccines ought to be rethought.

Molecular Mimicry and the HPV Vaccines Gardasil and Cervarix

Here is where it gets interesting for those interested in post Gardasil injury. The flu study, as limited and focused as it was, provides important clues to how and why the HPV vaccine might also induce an array of side effects, including, but not limited, to hypersomnia in some individuals but not in others.

Researchers have begun investigating molecular mimics in the HPV vaccines Gardasil and Cervarix. Thus far, they have identified 82 pentamer (5) level  mimics and 34 heptamer (7) level mimics in the HPV 16L component. The offending motifs control a variety of cell behaviors related to cardiac functioning, cell permeability and cell death. An immune system attack on any of these motifs could elicit serious illness. Indeed, the researcher postulates that the mimicked motifs controlling cardiac functioning could be culprits in the post HPV vaccine incidences of sudden death.

To my knowledge, the full HPV vaccine to human proteome has not been mapped and so how or if there are mimicked protein motifs within the HPV vaccine that are capable of attacking the hypocretin/orexin neurons is not known. Nevertheless, idiopathic hypersomnia, a derivative of narcolepsy, is one of the core symptoms of post Gardasil injury, though it is sometimes misdiagnosed and mischaracterized as excessive fatigue and sleepiness. Additionally, a number of other symptoms post Gardasil are influenced by the hypocretin/orexin system, including feeding behavior, gastroparesis (perhaps via galanin) migraine, and all over pain (via dynorphin) – more on this in subsequent posts. Since we now know that molecular mimics can evoke reactions, it is only a matter of time before researchers match the vaccine protein motifs and structural homologies to individual gene variants, environmental predispositions and the clinical symptoms/syndromes that develop.

Perhaps even more interesting, when we dig into the hypocretin/orexin system we see that the neurons are especially susceptible to changes in ATP. Intracellular ATP in hypocretin/orexin neurons must be maintained at much higher levels than in other cells. Diminished ATP stores inhibits hypocretin/orexin firing and thereby reduces sustained wakefulness. We know from other research and patient reports that severe thiamine deficiencies are present in post Gardasil injury (whether the deficiencies existed pre-Gardasil, but were asymptomatic is not clear). Thiamine is a required co-factor in the production of ATP. Reduced thiamine would impair functioning in the hypocretin/orexin neurons and induce the hypersomina and hypophagia and many of the other symptoms we see post vaccine.

In subsequent papers, I will explore the myriad functions the hypocretin/orexin neurons regulate and how damage to those neurons, either directly as indicated in the flu vaccine study, or indirectly, via targeting critical co-factors provides clues to the constellation of post Gardasil injuries. Additionally,  I will address the molecular mimicry debate and how it will reshape the framework for understanding autoimmunity.

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Thiamine Deficiency and Aberrant Fat Metabolism: Clues to Adverse Reactions

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Over the last several months, the writers and researchers at Hormones Matter have posted a number of articles about mitochondrial dysfunction and thiamine deficiency.  Thiamin, or thiamine as the internet search engines prefer, is critical to mitochondrial function. We’ve learned that thiamine deficiency can emerge gradually due to dietary inadequacies or more suddenly as a result of a medication, environmental or surgical insult. Regardless of the cause, deficits in thiamine evoke devastating health issues that can be treated easily if identified. More often than not, however, thiamine deficiency is not assessed and symptoms are left to escalate, mitochondrial damage increases, and patient suffering continues. Because thiamine deficiency is rarely considered in the modern scientific era, mild symptoms are ascribed to other causes such as “an allergy” or “it’s all in the patient’s head”. If, however, the cause is not revealed, the same old dietary habits will continue and can be guaranteed to produce much more severe and difficult to treat chronic disease.

Although there are a myriad reasons why mitochondria are damaged, medication or vaccine reactions paired with latent nutritional deficiencies seem to be common. Predicting who and how the mitochondrial dysfunction might appear, however, is more complicated. Quite often, athletes and individuals considered healthy are hit harder by a stress factor such as a vaccine than those whom we might not regard as particularly healthy. There are several potential reasons for this, some of which have been outlined previously. In this post, I would like to add one more reason why highly active, high performing individuals might be hit harder and more quickly than their less active counterparts with vaccine or medication reactions that induce thiamine deficiency.

Mitochondria are the Engines of the Cell

To use an analogy, the usefulness of a car obviously depends upon its engine. Mitochondria are the “engines” of each cell within our bodies, all 70 to 100 trillion cells that make up an adult body. They are known as organelles and are so small that their structure can only be seen with an electron microscope. But we can take this analogy further by comparing each cell to a different car model. A high powered car uses more gasoline than a low powered one and there are many models of each type of car. So some cells in the body require more energy than others, depending on the special function of the cell.  The most energy consuming cells are in the brain, the nervous system and the heart, followed by the gastrointestinal system and muscles. That is why those organs and tissues are most affected in the disease known as beriberi, the thiamine deficiency disease that we have discussed previously in other posts. The function of other organs is affected by the deficiency because of the changes in the control mechanisms originating in the brain through the autonomic (automatic) nervous system.

It has been pointed out that this disease in its early stages affects the autonomic nervous system by causing POTS. Beriberi and POTS, both being examples of dysautonomia (abnormal activity of the autonomic nervous system), can only be distinguished by finding evidence of thiamine or other nutrient deficiency as a cause. Thiamine is but one factor whose deficiency causes loss of cellular energy, resulting in defective brain metabolism and dysautonomia.  Although the relationship with vaccination is conjectural, some individuals with post Gardasil POTS were found to be thiamine deficient and had some relief of symptoms by taking supplementary fat soluble thiamine, an important derivative that occurs in garlic and has been synthesized. Not all of these thiamine deficient individuals have benefited to the same degree, suggesting that other deficiencies might also be involved. This post is to provide some information about more recent knowledge concerning the action of thiamine and the incredible, far-reaching effects of its deficiency, particularly in the brain. Experimental work in animals has shown that thiamine deficiency will damage mitochondria, a devastating effect for an acquired rather than a genetic cause. Far too much research has been devoted to genetic cause without sufficient attention to the way genes are influenced by diet and lifestyle.

The Importance of Enzymes to Mitochondrial Function

Before I provide this new information, let me remind the reader that enzymes, like cogwheels in a man-made machine, enable bodily function to occur. The importance of thiamine is that it is a cofactor to many of the enzymes that preside over energy metabolism. Without its cofactor an enzyme becomes inefficient. Perhaps it might be compared with missing teeth in a cog wheel. With missing teeth the cog wheel may still function but not nearly as well as it would with all of its component parts.

In previous posts we have discussed how thiamine deficiency can be caused by an excess of sugar in the diet. I have likened this to a “choked engine” in a car where an excess of gasoline, relative to insufficient oxygen concentration in the mixture, makes ignition of the gasoline extremely inefficient. Bad diet, one that is rich in sugary, carbohydrate laden foods may be one of the more common contributors to latent thiamine deficiencies. Excessive intake of processed fats and the concomitant changes to mitochondrial function and energy metabolism may be another important contributor.

Thiamine and Fat Metabolism

All the enzymes affected by thiamine deficiency have a vital part to play in obtaining cellular energy from food by the process of oxidation. Most of them have been known for many years but in the nineties a new enzyme was discovered. It has a very fancy name that has been simplified by calling it HACL1.  Only in recent years has it been found that HACL1 is dependent on thiamine as its cofactor. Although not reported, it may mean that it is also dependent on magnesium. This is exceedingly important because it introduces the fact that thiamine is involved in fat as well as carbohydrate metabolism, something brand new, even to biochemists.

Here I must digress again to describe another type of organelle called a peroxisome that occurs in our cells.  Like mitochondria, they are infinitesimally small. Their job is to break down fatty acids and they have a double purpose. One purpose is to synthesize very important substances that construct and maintain cells and their function: they are particularly important in the brain. The other purpose is what might be called fuel preparation. As the fatty acids, consisting of long carbon chains, are broken down, the resulting smaller fragments can be used by mitochondria as fuel to produce energy.  Failure to break down these fatty acids can result in the accumulation of natural components that may be toxic in the brain and nervous system or simply result in lack of one type of fuel. That is why feeding medium chain triglycerides by administration of coconut oil has been reported useful to treat early Alzheimer disease. They can be oxidized in mitochondria.

The Important Use of Fatty Acids in Mitochondrial Health

Here, I want to use another analogy. Imagine a lake that admits water to a river through a sluice gate that has to be opened and closed by a farmer who regulates the supply of water. If the gate is open the river will supply water to the surrounding fields. If however the gate is closed, the river will begin to dry up and the crops in the fields will suffer. Perhaps the farmer half closed the gate during a rainy period and has forgotten to open it when a dry period follows. High temperatures in the dry period results in insufficient water to meet the growth needs of the crops.

In this analogy, the lake represents food, the sluice gate is the HACL1 enzyme and the farmer who controls the gate represents thiamine. The water in the river represents the flow of fatty acids to the tissues for the double purpose of cellular construction and fuel for oxidation. The half open gate represents a minor thiamine deficiency, more or less sufficient for everyday life but not enough when there is greater demand. A high temperature that increases the water needs for crops represents Gardasil and many other medications as a stress factor, placing a greater demand on essential metabolic action.  The analogy also implicates the nature of the crops, some of which require more water than others. The crops, of course, represent body tissues and organs.

If we consider high performing individuals, whether academically or athletically, like high performance cars or crops that demand more nutrients, we can see how a previously unrecognized minor deficiency might trigger clinical disease by the stressful demands of a vaccine or medication. Some pharmaceuticals can attack thiamine directly, like Gardasil and the fluoroquinolones, while others attack different pathways within the mitochondria.

No matter the pathway, high performing individuals, with high energy needs not covered by diet, may be hit harder when a medication attacks mitochondrial energy.

The Outcome of Defective Fatty Acid Metabolism

Returning back to the HACL1 enzyme, we now know that HACL1 is the first thiamine dependent enzyme to be discovered in peroxisomes. It is research news of the highest importance, affecting us all. Its action is to oxidize a diet related fatty acid called phytanic acid and fatty acids with long carbon chains that cannot be used for fuel until they are broken down. Phytanic acid is obtained through consumption of dairy products, ruminant animal fats and some fish. People who consume meat have higher plasma phytanic acid concentrations than vegans. If the action of HACL1 is impaired because of thiamine deficiency the concentration of phytanic acid will be increased. The river in the analogy actually represents a series of enzymatic reactions that may be thought of as down-stream effects, whereas thiamine deficiency, being up-stream, affects all down-stream phenomena. One of the reasons thiamine deficiency is such an important contributor to illness is because its effects are broad.

These enzymatic reactions, known technically as alpha oxidation, involve four separate stages. It has been known for some time that if another enzyme at stage two is missing because of a gene defect, the result will be damage to the neurological system known as Refsum’s disease. Symptoms include cerebellar ataxia (also reported after Gardasil vaccination), scaly skin eruptions, difficulty in hearing, cataracts and night blindness. Other genetic mutations in alpha oxidation, resulting in various biochemical effects, result in a whole variety of different diseases. This places thiamine deficiency as a potential cause for all the down-stream effects resulting from defective alpha oxidation, for it has been shown in mice that this vitally important chemistry is totally dependent on presence of thiamine. Since its complete absence would be lethal, we have to assume that it is mild to moderate deficiency, equivalent to a partial closure of the sluice gate in the analogy.

Sources of Phytanic Acid: How Diet Affects Thiamine

In ruminant animals, our source of beef, the gut fermentation of consumed plant materials liberates phytol, a constituent of chlorophyll, which is then converted to phytanic acid and stored in fat. The major source of phytol in our diet is, however, milk and dairy products.  It raises several important questions. If thiamine deficiency is capable of causing an increase in phytanic acid in blood and urine, it might be a means of depicting such a deficiency in a patient with confusing symptoms. It might also explain why some individuals who have been shown to have thiamine deficiency by means of an abnormal transketolase test have symptoms that are not traditionally accepted as those of such a deficiency, perhaps because of loss of efficiency in HACL1.

If an excess of sugar in the diet gives rise to a secondary (relative) thiamine deficiency, we are provided with an excellent view of the extraordinary danger of empty simple carbohydrate and fat calories, perhaps explaining much widespread illness in Western civilization. Interestingly, it would also suggest that something as benign as milk could give rise to abnormal brain action in the presence of thiamine deficiency, because of phytanic acid accumulation. Our problems with dairy products may go well beyond lactose intolerance and immune dysregulation.

In sum, the discovery of HCAL1 enzyme and its dependence upon thiamine suggests one more mechanism by which thiamine deficiency affects mitochondrial functioning. As emerging evidence indicates a myriad of environmental and pharmaceutical insults impair mitochondrial functioning, thiamine deficiency ought to be considered of prime importance. Deficits in thiamine evoke devastating health issues that can be treated easily if identified.  If, however, thiamine deficiency is not identified and the same old dietary habits continue, the latent thiamine deficiency can be guaranteed to produce a much more severe and difficult to treat chronic disease. Moreover, individuals with thiamine deficiency who do not respond sufficiently to thiamine replacement might also have aberrant fatty acid metabolism. This too should be investigated and dietary changes adopted.

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Thresholds and Tipping Points in Thiamine Deficiency Syndromes

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Chandler Marrs

I recently stumbled upon on a research paper published in 1968. It was not that long ago in the overall course of modern medicine, perhaps even its heyday, when all things were still possible and before the complete fealty to pharmaceuticals arrived. To the youngsters and to those coming of age in the last 20 years, however, anything published pre 1990 is ancient history.  What could such old paper tell me about medicine that is new and useful? It turns out an awful lot.

Back in the day, research was a little simpler and more focused, not on finding out which drug could be fit to which symptoms, but on how things worked. Good experimental design, answered mechanical questions, like if we apply X to Y or if we remove X from Y what happens?

In this paper, Encephalopathy of Thiamine Deficiency: Studies of Intracerebral Mechanisms, the researchers identified a very important component about Vitamin B1/thiamine deficiency – the time course of the disease process. That is, with a diet deficient in thiamine, how long does it take before symptoms emerge, what is the corresponding level of deficiency in the brain, and at what point, after supplementation, does recovery begin; important questions clinically.

Vitamin B1 – Thiamine Deficiency

Remember, vitamin B1 or 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). Thiamine deficiency was originally observed in only chronic and severe alcoholics or with severe nutritional deficits as seen in famine. Fortification of food stuffs was thought to relieve much of the nutritional risks for deficit, especially in impoverished regions. More recent research, however, indicates that thiamine deficiency has reared its ugly head once again and this time in modern, non-impoverished, regions where the food supply is ample. How can that be?

Non-Alcoholic Wernicke’s Encephalopathies

Thiamine deficits can be mediated by a number of factors, including by less obvious nutritional deficits where food supply is abundant but nutrition is lacking (a diet of highly processed, carbohydrate and fat laden foods), with thiamine blocking factors found in medications/vaccines, environmental toxicants and some foods, after bariatric surgery and in disease processes like AIDS. 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.

What has always struck me about the thiamine deficits we observe is the differential expression and time course of the symptoms. In some people, the reaction leading to thiamine deficit appears linear, progressive and rapid. In others, the symptoms appear to wax and wane and to evolve more slowly. How is that possible? Certainly, individual predispositions come into play. Some individuals may be somewhat thiamine deficient prior to the trigger that initiates the full expression of symptoms, while others have higher baseline stores. Additionally, anti-thiamine environmental exposures and other medical conditions/medications may also come into play.  In the literature, however, the progression of symptoms from bad to worse is almost always direct and rapid, perhaps mistakenly so. Indeed, Wernicke’s Encephalopathy is a medical emergency necessitating immediate IV thiamine.  How is it then, that we see more chronic, remit and relapse patterns of thiamine deficiency, even in some cases where thiamine concentrations are being managed medically?

Cerebral Thiamine Deficiency: Crossing the Black Line

It turns out, there is black line with regard to thiamine deficiency, that when crossed overt symptoms emerge, and a similar black line, that demarks recovery. It is possible then that barring a continuous blockade of thiamine, one can move above and below those lines and the corresponding symptoms may wax and wane. The paper from 1968, cited above, found those black lines, in rodents, but we can extrapolate to humans.

The research. The investigators took three groups of female rodents, a paired group of thiamine deprived and thiamine supplemented, along with a group fed ad lib (as desired) and assessed the time course and concentrations of cerebral thiamine deficiency relative to the initiation and progression of the observable neurological symptoms associated with Wernicke’s encephalopathy in rodents (ataxia, loss of righting, opisthotonos –rigid body arching). The experiment lasted about 6 weeks.

Neither the control group (thiamine supplemented) nor the ad lib group demonstrated neurological deficits at any time during the study. The thiamine deprived group, on the other hand, demonstrated symptoms that began with weight loss, progressive anorexia, hair loss (recall our observations about hair loss) and drowsiness at about 2.5 weeks into the experiment. Interestingly, no neurological signs of thiamine deficiency were seen at that time.

The results. At 4.5 weeks in, the researchers noted a rapid progression of symptoms and decline of health over the course of the next 5 days (the black line). These symptoms included: incoordination with walking, impairment of the righting reflex, reluctance to walk, walking backwards in circles, imbalance, rigid posturing and eventually a total loss of righting activity and severe drowsiness.

One can imagine, if a similar deprivation of thiamine were observed in humans, the corresponding symptoms might also include the initial hair loose and weight loss, perhaps noticeable, perhaps not depending upon the time frame and severity of the thiamine deficiency. It would also include incoordination and difficulty with walking, balance and voluntary movement, perhaps tremors, excessive fatigue or sleepiness and the myriad of neuro-cognitive disturbances noted in Wernicke’s syndrome.

In the cited experiment, one injection of thiamine reversed these symptoms to a nearly normal, or apparently normal neurological state within 24 hours.

Brain Thiamine Thresholds

Animals from each of the groups were sacrificed and examined at each of the stages of the experiment. Brain thiamine and other markers of thiamine metabolism were assayed to determine the cutoff levels of thiamine that demark symptoms and recovery.  This is really interesting and the beauty of this entire study.  Neurological symptoms become apparent when cerebral thiamine concentrations reach 20% of normal.  Recovery begins when those concentrations climb to 26% of normal. At least in rodents, one has to deplete 80% of the brain thiamine stores before overt neurological symptoms become apparent; 80% – that is a huge deficit.  Similarly, it doesn’t appear to take much to right that deficit, only a 6% increase in thiamine concentration set the course for improvement.

If we extrapolate to humans, where life span, genetic and environmental factors likely moderate the degree of thiamine stores and consumption, we still contemplate a rather large thiamine deficit needed before overt symptoms of Wernicke’s emerge. Similarly though, it is also evident that a rather small change in thiamine can have enormous effects on neurological functioning. In the case of the rodents, a mere 6% point change reversed the symptoms. One might suspect equivalent deficit/recovery thiamine parameters in humans.

Waxing and Waning Symptoms:  A Case for Persistent Thiamine Deficiency

If we consider the possible course of non-alcoholic thiamine deficiency, where no extraneous variables like bariatric surgery or thiamine deficient parenteral feeding are present and where dietary thiamine varies daily and is not held constant as it is during experimental conditions or during famine, we can begin to see how thiamine related neurological symptoms may wax and wane. Different exposures and triggers may decrease thiamine periodically, even to the point where overt neurological symptoms present. When those exposures are removed and barring deficiencies in metabolism and diet, symptoms may abate, at least temporarily, and until the next trigger or until the black line is crossed anew and thiamine deficiency becomes the medical emergency observed in overt Wernicke’s.

In contrast, the more persistent or chronic thiamine deficits that do not cross the 80% depletion cutoff (or the human equivalent), may also wax and wane and show all the core neurological symptoms expected in overt Wernicke’s though to a much lesser degree. Additionally, as we have speculated, persistent thiamine deficiency might disable mitochondrial functioning in such a way that the patient presents with a myriad of seemingly unrelated symptoms, that are not typically attributed to thiamine deficiency, such as cardiac dysregulation, gastroparesis, autonomic instability, demyelinating syndromes and hormone irregularities, especially thyroid, but also reproductive hormones. These too may be related to thiamine deficiencies. Although, we cannot and should not rule out other causes as well, sub-optimal thiamine may be involved with a host of complex disease states and medication adverse reactions where neurological symptoms are present. Thiamine deficiency should be tested for and ruled out before more invasive therapeutic options are contemplated.

We Need Your Help

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

Yes, I would like to support Hormones Matter. 

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Of Oxygen, Spark Plugs, and Mitochondria

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mitochondria spark plug

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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Image by Sumanley xulx from Pixabay.

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