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Manifestations of Thiamine Deficiency: Another Case of Beriberi in America

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Why Publish Another Case?

Just last week, we published a case of classic beriberi in a 23 year old man, and now, yet another case comes to our attention. Most in the medical profession are under the false impression that beriberi, thiamine deficiency, has been eradicated in Western cultures. It has not. In fact, a number of factors in modern Western culture have aligned to make thiamine sufficiency more precarious than ever. High calorie malnutrition and toxicant exposures are top among them. For a detailed look at thiamine deficiency in modern cultures, see our new book: Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition.

Kaleidoscope of Symptoms Associated with Thiamine Deficiency

There are a colossal number of symptoms associated with thiamine deficiency. The symptoms are confusing and not being seen for what they represent. First of all, let me make it clear: we are oxygen consuming animals and anything that interferes with oxygen utilization in the body will produce symptoms that are called to our attention by the brain and demand explanation. Any adverse sensation whether it be pain, itching or any other symptom is expressly a result of brain action. Joint pains are not perceived in the joints. They are perceived in the brain, even though the joint is actually the location of the inflammation.

The body consists of 70 to 100 trillion cells, all of which have to cooperate in producing human function. Each of these cells requires energy that is developed in specialized organelles within each cell. These organelles are called mitochondria and the way that they produce the required energy is by the combination of oxygen with glucose. Known as oxidation, thiamine is a major catalyst in this process and can be compared to a spark plug in a car cylinder. No gasoline (glucose), no function. No oxygen, no function. No spark plug (thiamine), no function. If oxidation in the mitochondria is compromised, the function of the cell in which they reside is also compromised. Because the brain and heart are the highest oxygen consuming organs in the body, it is not particularly surprising that these organs are the most affected in the disease called beriberi.

Please remember that this is an extremely ancient disease for which no cause was known for centuries. The word beriberi, according to the Oxford English dictionary, comes from a Sinhalese phrase meaning “weak, weak” or “I cannot, I cannot”, the word being duplicated for emphasis. I think of the body as being like an orchestra. Every organ knows exactly what it has to do, but its action must be monitored by the brain which acts as the conductor in playing “the Symphony of Health”.

A Case of Unrecognized Beriberi

The woman whose symptoms are discussed here is 38 years of age. During childhood she experienced what she called a great deal of pain, repeated episodes of candida infection (yeast) breathing trouble with swimming and running, reactive hypoglycemia, chest pain, panic attacks and nausea. She has recently experienced dizziness.

How Was She Treated?

Because the many physicians that she has seen were unable to find significant laboratory changes, the symptoms were usually explained as “it is all in your head”. This is really a pejorative diagnosis because it is assuming that the unfortunate patient is either inventing the symptoms or experiencing them in her imagination. The paradox is that the symptoms are produced in the brain by abnormal signals between the brain and body organs. They are just as real as any other symptom where there is physical evidence of its cause.

Modern medicine seems to think in extraordinarily limited terms and prednisone is offered for many different symptoms as it was in this case. Prednisone made her symptoms worse as indeed it often does. Dizziness was treated by a chiropractor by an “adjustment of the Atlas” (the first bone in the neck that supports the skull) and made her worse. She was found to have scoliosis of the spine and without going into details, this is because of compromised oxidation in the brainstem. It results in asymmetric motor signals to the muscles on either side of the spine, producing the typical curvature.

Understanding the Clinical Clues

The symptoms in childhood indicated even then oxidation was inefficient.

Difficulty breathing. She had breathing trouble when swimming or running, indicating that the breathing control mechanisms in the brain were affected.

Reactive hypoglycemia. She consumed a great deal of sugar and reported reactive hypoglycemia, a classical effect of thiamine deficiency caused by the excessive sugar. It results in overproduction of insulin, hence the drop in blood sugar.

Digestive problems. She reported “stomach problems” in pregnancy, gastritis and GERD, all of which can occur with thiamine deficiency.

Panic attacks. Chest pain, panic attacks and nausea are all related to brain oxygen compromise.

Nystagmus. Her dizziness, reported to be associated with “vertical downbeat nystagmus” are both typical of beriberi.

Yeast infections and Brewer syndrome. She had repeated episodes of yeast infection. This is an opportunist organism, meaning that it is detecting a body situation which is favorable to it and not to its host. Of course, yeast is used to create alcohol from sugar and the squeaks and bubbles experienced by the patient represent the effects of ongoing fermentation in the bowel. So her complaint of “constantly feeling drunk” is quite real and is known as the Brewer syndrome.

Connecting the Dots: The Myriad Manifestations of Thiamine Deficiency

The history in this woman indicates that her health problems existed in childhood and may well have started because of her mother’s pregnancy. She indicated that she consumed a great deal of sugar, by far and away the easiest way to produce thiamine deficiency. The nystagmus and dizziness are manifestations of oxidative dysfunction in the brain and indicate the ongoing problem. There may well be a genetic mechanism involved. However, the genetic mechanism can be mild enough not to result in symptoms unless nutrition and stress events are involved. She reported that she had experienced a number of surgical interferences, each one of which may have been sufficient stress to initiate downgrading in her thiamine deficiency. We now know that a marginal deficiency can be converted into full-blown deficiency as a result of the energy consumption required in meeting the stress.

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Just Released: Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition

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Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition

Together with Dr. Lonsdale, I am proud to announce the release of our new book: Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition.

If you have followed our blog, Hormones Matter, for any amount of time, you’ll know that we spend a lot time writing about mitochondrial distress. Mitochondria are the engines that fuel our cells and sit at the nexus of health and disease. Healthy mitochondria do much to stave off disease, allowing the body to survive all manner of modern stressors, from illness to toxicant exposures, and everything in between. Unhealthy mitochondria, on the other hand, can set into motion a series of reactions leading to complex, multisystem illnesses that modern medicine often has no earthly idea how to treat. This book is about those illnesses and the mitochondrial cascades that allow their existence.

We cover the chemistry of illness from the mitochondria upwards through the autonomic system, to the symptoms and back again. It is a chemistry that we seem to have forgotten in recent years, a chemistry we like to ignore when it contradicts our presumptions about pharmaceutical medicine and diet, and a chemistry that kicks us in the butt when we deny its importance. The chemistry is complicated on its surface, but a deeper dive reveals what Dr. Lonsdale refers to as ‘the exquisite simplicity‘ of health and disease. This book will teach you that chemistry and much more.

Why Thiamine? Why Now?

Thiamine takes center stage in this book, not because it is a magic vitamin that cures all, but because it sits atop the mitochondrial energy pathways. It is a gatekeeper of sorts, determining if or how other downstream mitochondrial functions proceed. For some inexplicable reason, amid all the research on the importance of other nutrients, we seem to have forgotten thiamine. Over and over again, we are presented with cases on Hormones Matter of overt thiamine deficiency, and yet, rarely do physicians consider it. More often than not, it is the patients or their caregivers that figure it out.

Why don’t we consider one of the most fundamental units of health? The short answer, if we are honest with ourselves, pharmacology and surgery are far sexier than nutrition. Unfortunately, however, disease processes do not develop because of drug deficiencies or a lack of surgical prowess. In the Western world, they develop in large part because of nutrient deficiencies within the context of high calorie malnutrition and in conjunction with other stressors. Understanding the chemistry that decides health or disease is critical to achieving health. A key component of that chemistry involves thiamine. This book details how to recognize, evaluate, treat, and understand thiamine deficiency. It is a complicated topic, but written for a broad audience.

Buy Now and Receive a Discount

For a limited time, the publisher is offering a 30% discount off of the list price and free shipping if the book is ordered from their site. Just click the link below enter the promotional code ATR30 at checkout.

Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition

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A Case of Classic Beriberi in America

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thiamine deficiency beriberi in america

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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Adverse Reactions, Hashimoto’s Thyroiditis, Gait, Balance and Tremors

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Gait, tremors with adverse medication vaccine reactions

One of the things I most love about social media and health research is the opportunity to identify patterns of illness across different patient groups. Here is an example of finding research from one patient group, ThyroidChange, that likely spans many others (Gardasil injured, post Lupron Hashimoto’s, and Fluoroquinolone reactions – to name but a few) and offers clues to a perplexing array of symptoms. The research, is about a little known association between movement and balance disorders and Hashimoto’s thyroiditis: Ataxia associated with Hashimoto’s disease: progressive non-familial adult onset cerebellar degeneration with autoimmune thyroiditis.  Some background.

Hashimoto’s Disease

Hashimoto’s is the most common causes of hypothyroidism afflicting women at a rate of 10 to 1 compared to men. It is an autoimmune disorder in which antibodies attack the thyroid gland and destroy its ability to maintain normal thyroid hormone concentrations. The most common symptoms include: fatigue, muscle pain, weight gain, depression, cognitive difficulties, cold intolerance, leg swelling, constipation, dry skin. If left untreated, goiter – a swollen thyroid gland, appears. If left untreated for an extended period, cardiomyopathy (swelling of the heart muscle), pleural (lung) and pericardial (heart) effusion (fluid), coma and other dangerous conditions develop.

Hashimoto’s and Cerebellar Degeneration

A little known risk in Hashimoto’s is cerebellar degeneration. The cerebellum is the cauliflower looking section at the base of the brain that controls motor coordination – the ability to perform coordinated tasks such as walking, focusing on a visual stimuli and reaching for objects in space. The walking and balance disturbances associated with cerebellar damage or degeneration have a very distinct look, a wide gait, with an inability to walk heel to toe. Cerebellar ataxia looks like this:

In recent years, cerebellar involvement in attention and mood regulation have also been noted. The physicians reporting the Hashimoto’s – ataxia connection present case studies of six patients with Hashimoto’s disease, presumably controlled with medication and a progressive and striking shrinkage of the cerebellum (see report for MRI images) along with progressively debilitating ataxia (walking and balance difficulties) and tremors. Here’s where it becomes interesting.

Hashimoto’s: Medication Adverse Reaction and Misdiagnosis

Hashimoto’s disease is prevalent in our research into medication adverse reactions for Gardasil and Cervarix and Lupron, with some indications it may develop post Fluoroquinolone injury as well. The symptoms are difficult to distinguish from other neurological and neuromuscular diseases such as chronic fatigue syndrome, fibromyalgia, multiple sclerosis and an array of psychiatric conditions, and so Hashimoto’s often goes undiagnosed or is misdiagnosed and mistreated for some time.

Hashimoto’s, Demyelination and Cerebellar Damage

In some of the more severe adverse reactions to medications and vaccines that would lead to Hashimoto’s, the tell tale cerebellar gait disturbances have been noted and documented, along with a specific type of tremor (discussed below).

Research from other groups shows a strong relationship between thyroid function and myelin/demylenation patterns in nerve fibers in animals. Specifically, insufficient T3 concentrations demyelinates nerve axons, while T3 supplementation elicits myelin regrowth. Myelin is the white sheathing, the insulation that protects nerves and improves the electrical conduction of messages in sensory, motor and other neurons. Like co-axial cable in electrical wiring, when the protective sheathing is lost, electrical conductance is disrupted. The early symptoms of a demyelinating disease neuromuscular pain, weakness, sometimes tremors. These can be misdiagnosed as multiple sclerosis, fibromyalgia, chronic pain, when in reality, the culprit is a diseased thyroid gland.

Back to the Cerebellum

The cerebellum is a focal point of white matter axons – myelinated sensory and motor nerves. The cerebellum is where input becomes coordinated into motor movements or movement patterns. White matter damage in the cerebellum causes cerebellar ataxia, the movement and balance disorders displayed above. Hashimoto’s elicits white matter disintegration. Adverse reactions to medications and vaccines can elicit autoimmune Hashimoto’s disease. See the connection?

The Thiamine – Gut Connection

It gets even more interesting when we add another component of systemic medication adverse reactions – nutritional malabsorption, specifically thiamine deficiency. Almost across the board, patients with medication or vaccine adverse reactions report gut disturbances, from leaky gut, to gastroparesis, constipation, pain and a myriad of other GI issues that make eating and then absorbing nutrients difficult. Gut issues are common in thyroid disease too.

As we learn more, and as individuals are tested, severe nutrient deficiencies are noted, in vitamin D, Vitamin B1, B12, Vitamin A, sometimes magnesium, copper and zine. We’ve recently learned of the connections between Vitamin B1 or thiamine deficiency and a set of conditions affecting the autonomic nervous system called dsyautonomia or Postural Orthostatic Tachycardia Syndrome (POTS) linked to thiamine deficiency in the post Gardasil and Cervarix injury group. It may be linked to other injured groups as well, but we do not know yet.

Thiamine and Cell Survival

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 (the Hashimoto’s – cerebellar connection). 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, or when nutritional uptake is impaired, thiamine deficiency ensues. Thiamine deficiency can elicit cell death by three mechanisms:

  1. Mitochondrial dysfunction (reduced energy access) and cell death by necrosis
  2. Programmed cell death – apoptosis
  3. Oxidative stress – the increase in free radicals or decrease in ability to clear them

Thiamine deficiency in and of itself can elicit a host of serious health symptoms. The cell death and disruption of cellular energy balance can be significant and lead to a totally disrupted autonomic system.

Thiamine and Myelin Growth

Add to those symptoms, the fact that thiamine is involved in the growth myelin sheathing around nerves, and we have a whole host of additional neuromuscular symptoms masking as fibromyalgia, multiple sclerosis, chronic fatigue. Like with MS, limb and body tremors are noted in dysautonomic syndromes such as POTS. (Video of POTS tremors, note the uniqueness of the POTS tremor and the similarity between it and the foot tremor shown above along with cerebellar ataxia).

Let thiamine deficiency continue unchecked for period and we get brain damage, as white matter – the myelin disintegrates in the brainstem, the cerebellum and likely continues elsewhere. One of the most prominent areas of damage in thiamine deficiency, is the cerebellum, and hence, the cerebellar ataxia (movement disorders) noted in chronic alcoholics who are thiamine deficient, but also observed post medication or vaccine adverse reaction.

The Double Whammy on Myelin and Cerebellar Function

In the case medication or vaccine adverse reactions, particularly those that reach the systemic level, we have a double whammy on myelin disintegration: from a diseased thyroid gland and a diseased gut. Hashimoto’s and the reduction of thyroid hormones, particularly T3, impairs nerve conduction by shifting from a constant and healthy remyelinating pattern to one of demyelination, while the lack of thiamine further impairs myelin regrowth, because it is a needed co-factor. Both deficiencies affect peripheral nerves, but both also hit the brainstem, the cerebellum and likely other areas within the brain.

Take Home Points

The science of adverse reactions is new and evolving and much of what I am reporting here remains speculative. However, it has become abundantly clear through our research that to address medication adverse reactions or vaccine adverse reactions in a simplistic fashion, by region, or in an organ specific manner, is to miss the broader implications of the compensatory disease processes that ensue. Moreover, to look for symptoms of adverse reactions simply by the drug’s mechanism of action and/or by the standard outcome variables listed in adverse event reporting systems, again misses the complexity of the human physiological response to what the body is perceiving as a toxin. I believe that the entire framework for understanding the body’s negative response to a medication must be shifted to a much broader, multi-system, and indeed, multidisciplinary approach. In the mean time, we will continue to collect data on adverse reactions and offer our readers points of consideration in their quests for healing. I should note, that finding these connections is entirely contingent on the input our community of patients and health activists, both via the personal health stories that so many of you have been willing to share and the data we collect through our research. You know more about your health and illness than we do.

What we Know So Far – Tests to Consider

If you have had an adverse reaction to a medication or vaccine and neuromuscular difficulties, like pain, numbness, motor coordination problems, tremors etc., consider testing for Hashimoto’s thyroiditis. Also, consider thyroid testing when fatigue, depression, mood lability (switching moods), constipation, attentional and focus difficulties are present. In fact, I would consider thyroid testing, specifically for autoimmune thyroid disease like Hashimoto’s, as one of the first disease processes to rule out.

If you have had an adverse reaction to a medication that includes gut disturbances, consider the possibility that you are deficient in key micronutrients such as Vitamin D, the B’s, Vitamin A, magnesium, copper, zinc. And given the modern diet, consider that you were probably borderline deficient even before experiencing the adverse reaction. These nutrients are critically important to health and healing (and no, I do not have an association with vitamin companies or testing companies). Some tests for these nutrients are more accurate than others, so be sure to do your homework first.

If you have symptoms associated with autonomic systems dysregulation such as those associated with POTS, dysautonomia and its various permutations, consider thiamine testing, especially, transkelotase testing.

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Postscript: This article was published originally on Hormones Matter on October 15, 2013. 

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What is Thiamine to Energy Metabolism?

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thiamine energy

What is Energy?

Energy is an invisible force. The aggregate of energy in any physical system is a constant quantity, transformable in countless ways but never increased or diminished. In the human body, chemical energy is produced by the combination of oxygen with glucose. This reaction is known as oxidation. The chemical energy is transduced to electrical energy in the process of energy conservation. This might be thought of as the “engine” of the brain/body cells. We have to start thinking that it is electrical energy that drives the human body. The production of chemical energy is exactly the same in principle as the burning of any fuel but the details are quite different. The energy is captured and stored in an electronic form as a substance known as adenosine triphosphate (ATP) that acts as an energy currency. The chemical changes in food substances are induced by a series of enzymes, each of which combine together to form a chain of chemical reactions that might be thought of as preparing food for its ultimate breakdown and oxidation. Each of these enzymes requires a chemical “friend”, known as a cofactor. One of the most important enzymes, the one that actually enables the oxidation of glucose, requires thiamine and magnesium as its cofactors. Chemical energy cannot be produced without thiamine and magnesium, although it also requires other “colleagues”, since all vitamins are essential. A whole series of essential minerals are also necessary, so it is not too difficult to understand that all these ingredients must be obtained by nutrition. The body cannot make vitamins or essential minerals. There is also some evidence that thiamine may have a part to play in converting chemical energy to electrical energy. Thus, it may be the ultimate defining factor in the energy that drives function. If that is true, its deficiency would play a vital role in every disease.

Energy Consumption

Few people are aware that our lives depend on energy production and its efficient consumption. A car has to have an engine that produces the energy. This is passed through a transmission that enables the car to function. In a similar manner, we have discussed how energy is produced. It is consumed in a series of energy requiring chemical reactions, each of which requires an enzyme with its appropriate cofactor[s]. This series of reactions can be likened to a transmission, enabling the human body to function. If energy is consumed faster than it can be synthesized, or energy cannot be produced fast enough to meet demand, it is not too difficult to see that it would produce a fundamental change in function. Lack of function in body organs affects our health. The symptoms are merely warning the affected individual that something is wrong. The underlying cause has to be ascertained in order to interpret how the symptoms are generated.

Why Focus on Thiamine?

We have already pointed out that thiamine does not work on its own. It operates in what might be regarded as a ”team relationship”. But it has also been determined as the defining cause of beriberi, a disease that has affected millions for thousands of years. Any team made up of humans requires a captain and although this is not a perfect analogy, we can regard thiamine as “captain” of an energy producing team. This is mainly due to its necessity for oxidation of glucose, by far and away the most important fuel for the brain, nervous system and heart. Thus, although beriberi is regarded as a disease of those organs, it can affect every cell in the body and the distribution of deficiency within that body can affect the presentation of the symptoms.

Thiamine exists only in naturally occurring foods and it is now easy to see that its deficiency, arising from an inadequate ingestion of those foods, results in slowing of energy production. Because the brain, nervous system and heart are the most energy requiring tissues in the body, beriberi produces a huge number of problems primarily affecting those organs. These changes in function generate what we call symptoms. Lack of energy affects the “transmission”, giving rise to symptoms arising from functional changes in the organs thus subserved. However, it must be pointed out that an enzyme/cofactor abnormality in the “transmission” can also interrupt normal function.

In fact, because of inefficient energy production, the symptoms caused by thiamine deficiency occur in so many human diseases that it can be regarded as the great imitator of all human disease. We now know that nutritional inadequacy is not the only way to develop beriberi. Genetic changes in the ability of thiamine to combine with its enzyme, or changes in the enzyme itself, produce the same symptoms as nutritional inadequacy. It has greatly enlarged our perspective towards the causes of human disease. Thiamine has a role in the processing of protein, fat and carbohydrate, the essential ingredients of food.

Generation of Symptoms

Here is the diagnostic problem. The earliest effects of thiamine deficiency are felt in the hindbrain that controls the automatic brain/body signaling mechanism known as the autonomic nervous system (ANS). The ANS also signals the glands in the endocrine system, each of which is able to release a cellular messenger. A hormone may not be produced in the gland because of energy failure, thus breaking down the essential governance of the body by the brain. Hypoxia (lack of oxygen) or pseudo-hypoxia (thiamine deficiency produces cellular changes like those from hypoxia) is a potentially dangerous situation affecting the brain and a fight-or-flight reflex may be generated. This, as most people know, is a protective reflex that prepares us for either killing the enemy or fleeing and it can be initiated by any form of perceived danger. Thus, thiamine deficiency may initiate this reflex repeatedly in someone that seeks medical advice for it. Not recognizing its underlying cause, it is diagnosed as “panic attacks”. Panic attacks are usually treated by psychologists and psychiatrists with some form of tranquilizer because of the anxiety expressed by the patient. It is easy to understand how it is seen as psychological, although the sensation of anxiety is initiated in the brain as part of the fight-or-flight reflex and will disappear with thiamine restoration. It may be worse than that: because the heart is affected by the autonomic nervous system, there may be a complaint of heart palpitations in association with the panic attacks and the heart might be considered the seat of the disease, to be treated by a cardiologist. The defining signal from the ANS is ignored or not recognized. Because it is purely a functional change, the routine laboratory tests are normal and the symptoms are therefore considered to be psychological, or psychosomatic. The irony is that when the physician tells the patient “it is all in your head”, he is completely correct but not recognizing that it is a biochemical functional change and that it has nothing to do with Freudian psychology.

A Sense of Pleasure

A friend of mine has become well aware that alcohol, in any form, or sugar, will automatically give him a migraine headache. He still will take ice cream and suffer the consequences. I have had patients tell me that they have given up this and that “but I can’t give up sugar: it is the only pleasure that I ever get”. They still came back to me to treat the symptoms. We have come to understand that we have no self-responsibility for our own health. If we get sick, it is just bad luck and the wonders of modern medicine can achieve a cure. The trouble is that a mild degree of thiamine deficiency might produce symptoms that will make it more difficult to make the necessary decisions for our own well-being. Let me give some examples of symptoms that are typically related to this and are not being recognized.

  • Occasional headache
  • Occasional heartburn or abdominal pain
  • Occasional diarrhea or constipation
  • Allergies
  • Fatigue
  • Emotional lability
  • Insomnia
  • Nightmares
  • Pins and needles
  • Hair falling out
  • Heart palpitations
  • Persistent cough for no apparent reason
  • Voracious or loss of appetite

The point is that thiamine governs the energy synthesis that is essential to our total function and it can affect virtually any group of cells in the body. However, the brain, heart and nervous system, particularly the autonomic (automatic) nervous system (ANS) are the most energy requiring organs and are likely to be most affected. Since the brain sends signals to every organ in the body via the ANS, a distortion of the signaling mechanism can make it appear that the organ receiving the signal is at fault. For example, the heart may accelerate because of a signal from the brain, not because the heart itself is at fault. Hence, heart palpitations are often treated as heart disease when a mild degree of thiamine deficiency in the brain is responsible. We have known for many years that sugar in all its different forms can and will precipitate mild thiamine deficiency. It is probably the reason why sugar is considered to be a frequent cause of trouble. If thiamine deficiency is mild, any form of minor stress may precipitate a much more serious form of the deficiency.

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Post Gardasil Heart Failure, Ragged Red Fibers and Thiamine

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

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

Mitochondria

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

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

Mitochondrial Disorders are Multi-Systemic

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

Thiamine Deficiency Post Gardasil

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

Thiamine is Critical for Mitochondrial Functioning

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

The Gardasil Thiamine Relationship

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

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

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

Ragged Red Fibers and Cardiomyopathy

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

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

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

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

Thiamine Deficiency and Ragged Red Fibers: Experimental Evidence

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

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

Case Studies: Ragged Red Fibers, Thiamine and Mitochondrial Disease

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

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

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

Mitochondrial Dysfunction in Myocardial Infarction and Sudden Death

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

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

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

Connecting the Dots

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

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

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

Nephron, CC BY-SA 3.0, via Wikimedia Commons

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

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Connecting the Symptom Dots: Discovering My Thiamine Deficiency

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As a registered dietitian nutritionist (RDN), I was surprised to find out that I had a thiamine deficiency in December 2015. My diet wasn’t perfect, but it was close. I never imagined I’d spend so much time trying to treat my own deficiency, but it’s been over a year the first lab work showed the deficiency and I’m still struggling with it. I’ve been asked to share my symptoms and experiences, so I’ll start back around the initial diagnosis.

Let me preface my story by sharing some information about myself. I’m a 46 year old female and I’ve always considered myself fairly healthy. I’m active, and I complete a minimum of 12,000 steps/day and often much more. That includes some form of aerobic activity daily. I’ve dealt with some annoying health problems, but nothing I considered major. I’ve had issues with insomnia, depression, nerve problems, migraines, hypoglycemia and GI distress (mostly diarrhea) for years or decades. I’ve also had some discomfort on the left side of my chest, on and off, which goes unexplained. I’ve seen many different types of doctors, including cardiologists, neurologists, gastroenterologists, psychiatrists, sleep specialists, endocrinologists, allergists, etc. Also, I have very early visual symptoms of glaucoma, but my doctor said there aren’t any signs of disease in my eye. No familial history of glaucoma, and I’ve never been diagnosed with diabetes. Separately, all of these symptoms seemed minor. Only within the last few years or so, did I begin to wonder if there was some sort of connection.

In the fall of 2014, I started a post-bachelors program in dietetics. I had returned to school almost two decades after completing my bachelors, and the road to this program was a long one. My insomnia seemed to be severe the night before exams. Sleep eluded me, even with the prescription sleeping pills. Anxiety, right? It never occurred to me that it was something else. After all, I’ve had insomnia issues for at least a decade. Sometime during the semester, I had seen a neurologist for some nerve testing. I had numbness and tingling in my feet, hands and arms. It would wake me up at night. I began seeing a doctor of osteopathy for manipulations to help with the nerve problems, too. Also, I had noticed some garbled speech and numbness in my tongue, but thought I was imagining it.

During finals week in December, my insomnia became severe. My physician prescribed Xanax, but I hated the way it made me feel. I felt my anxiety actually increased.  Even after finals were over, sleep eluded me. I was piecing 3-5 hours of sleep together, if that. I had trouble eating a full meal and was losing weight. In addition, I was having discomfort on the left side of my chest, something that I had experienced in the past but was yet unexplained. All of this was attributed to anxiety. By the end of December, my physician prescribed a daily anti-anxiety medication. This medication made me nauseous and I had diarrhea. Of course, these symptoms didn’t help the weight loss. At no time did my physician do any lab work while this was happening. I was so miserable that I emailed my advisor to inquire about dropping out of the dietetics program. Fortunately, she wouldn’t entertain the idea and encouraged me to continue, noting that I could take an Incomplete if necessary.

By February of 2015, I was down to 103 pounds, (I’m 5’ 4” and 130 pounds currently). I was dragging myself to school. I had lost a lot of muscle mass, and couldn’t sit for long in class because of the lack of muscle. My face looked quite thin and my temples were hollowed out. In March 2015, I was weaned off the medications and began taking 7.5 mg Remeron, and Ambien as needed. The Remeron helped my appetite and I began regaining weight and strength. With the support of my professors, I was able to complete the semester, and even maintained a high grade point average!

Early in the fall semester, I listened to a lecture by an RDN who is an integrative and functional medicine certified practitioner (IFMCP). Based on her lecture, I knew my instincts about an underlying connection to all of my symptoms was correct. In November 2015, I had an appointment with that RDN. She recommended some blood work, which my primary care physician (PCP) reluctantly agreed to do. It was a lot of blood work, and fortunately my insurance covered it. There were many positive or problematic results, but among them was low thiamine (whole blood) at 29ug/L, a positive ANA test, TPO 693, as well as magnesium and ferritin were in the low normal range. After further autoimmune testing, it was determined that I have Hashimoto’s disease, too.

The low thiamine level could explain many of my symptoms, including, insomnia, nerve issues, migraines, precordial pain, weight loss and problems processing carbohydrate. The question is why was my thiamine level low? I had always thought my diet was relatively healthful. For years, I watched my added sugar intake because of trouble with hypoglycemia. My fiber, protein and water intake seemed adequate. I’m very careful with my fat intake because I had a cholecystectomy in 2009 and still have problems with lipid digestion. I rarely drank alcohol because of the hypoglycemia and insomnia. The only other beverage I consumed was tea, usually 1-3 cups per day. Furthermore, because of my hypoglycemia, I ate mostly whole grains and very little gluten, if any.

In January 2016, I began taking a B vitamin complex, magnesium, lipothiamine and some other supplements, including Ortho-Digestzyme to aid in lipid digestion. I made changes to my diet, including dairy free and gluten free. I began seeing some health improvements. Eventually, I added yogurt and cheese back into my diet, but remained gluten free. I was having fewer migraines and began sleeping without Ambien. That spring I was taken off the lipothiamine, but continued the B vitamin complex and magnesium. I graduated from the dietetics program in May 2016, something I feared wouldn’t happen only one year earlier.

At the end of October 2016, I had an infection (perhaps, due to an insect bite) on my outer ear which wouldn’t go away. My PCP prescribed a cephalosporin antibiotic for 10 days. Towards the end of November and into December, I was having increased nerve issues, occasional insomnia, mild apathy and anxiety, which was strange given I had nothing to be anxious about. Also, I had the same chest discomfort again. My thiamine level was tested and it was low at 32 ug/L. I was taking the B vitamin complex and magnesium all along, so my PCP was unsure what to do. I’ve since learned that some antibiotics, like the one I took, can deplete thiamine.  I saw the RDN again and began taking lipothiamine again on 12/23/2016. I was taking 50 mg, twice a do with magnesium, in addition to the B vitamin complex.

My PCP planned to retest in a month to see if it was working. However, on January 20, 2017, I had an emergency appendectomy. During the surgery, I was given a cephalosporin antibiotic, but it was only during the surgery, not afterwards. It should be noted that I only missed one day of supplements because of the surgery. By the end of the first week, I strongly suspected my thiamine level had bottomed out, because my symptoms of anxiety, insomnia, nerve pain, etc., reminded me of what happened two years earlier. During that week, I was taking 50 mg lipothiamine twice a day, 200 mg magnesium and a potent multivitamin. Personally, I think the antibiotic, surgical procedure and recovery, and resulting diarrhea contributed to the low thiamine despite supplementation. I almost went to the ER in hopes that they’d give me a thiamine injection or IV, but decided to wait until Monday to see my PCP. Her suggestion was that I continue my supplements, then we’d retest in a month. One month later, my thiamine level was low still at 32 ug/L. My PCP said she isn’t comfortable giving intramuscular thiamine injections and suggested I see a gastroenterologist. I mentioned information I found on Hormones Matter, but I don’t believe my PCP was interested in reading the material.  I feel like I’m being bounced around from one doctor to another. I’m going to see the gastroenterologist, whom I’ve seen before but I’m not hopeful that she’ll be able to help. I saw a neurologist recently, who was very kind and listened intently, but could only suggest an MRI and a DO, who “might” be able to help me, but that DO’s office is 1.5 hours away. Next week, I’ll go back to the cardiologist for a check-up because of the ongoing discomfort on the left side of my chest.

For now, I’m sleeping at least 6 hours a night, which feels like a lot to someone who’s experienced severe insomnia. My hypoglycemia is under control. I’m not sure if that’s because of the thiamine supplementation, the gluten free diet or both. The last time I had gluten, I experienced both mild insomnia and hypoglycemia, but again, my thiamine was likely low too. I feel I still have occasional memory issues, but maybe that’s age related. Also, the numbness and tingling in my extremities continues. Migraines occur much less and are less severe, usually. The mild vision problems linger, as well.

The RDN I’m seeing is uncomfortable with me taking more than 100 mg lipothiamine per day. At this time, she is recommending supplements to treat continued GI inflammation too.  Here is my current regimen: 100 mg lipothiamine/day, 200 mg magnesium/day, multivitamin 1/day (RDN wants me to take 2/day), 28 mg iron w/vitamin C, sodium butyrate 600mg 4/day, NAC 600mg 2/day, Ortho-Digestzyme 2 capsules before each meal to help with lipid absorption, and about 4000 IU vit D3.

Unfortunately, I feel I’m just one missed dose of my supplements away from problems all the time now. I’m not sure how to find a physician who can help me solve this ongoing thiamine problem and don’t know where to turn next. Again, I’m going to see a gastroenterologist and cardiologist this month, but feel it may be more of the same. My father died at 45 years old of cardiovascular disease. I know thiamine deficiency can lead to cardiovascular problems too, which is why I’m going back to the cardiologist.

Any suggestions are welcomed!

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Thiamine, Fibromyalgia and Chronic Fatigue

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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.

We need your help.

Hormones Matter needs funding now. Our research funding was cut recently and because of our commitment to independent health research and journalism unbiased by commercial interests, we allow minimal advertising on the site. That means all funding must come from you, our readers.  Don’t let Hormones Matter die.

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

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