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Recovering From Suspected Thiamine Deficiency

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recovering from thiamine deficiency

On and off over the last several years, I have had peripheral neuropathy along with a number of other strange symptoms like air hunger, light and sound sensitivity, and balance and gait issues that I believe are related to an undiagnosed thiamine deficiency.

Peripheral Neuropathy, Air Hunger, Dizziness, Altered Vision and Other Symptoms

I have always taken pretty good care of myself as well as taking supplements. I should note, that for the year prior to my health decline, I was drinking a lot of coffee, approximately 40-60 ounces per day. I have since learned that coffee diminishes thiamine. When I began to develop the neuropathy, I didn’t really know what it was. The strange sensations would come and go, but it became more and more intense in my legs and feet. Last summer, I also started to feel similar vibrations in my rib cage. It was extremely uncomfortable.

In addition to the neuropathy, I would wake up sometimes during the night gasping for air. Toward the end of last summer, I could really feel my energy slowly waning and in November of 2019, I had the flu. After I recovered from the flu, I still felt exhausted and weak. I went back to the doctor in December, 2019 and was found hypothyroid and put on Levothyroxine. I have been diagnosed with Hashimoto’s Thyroiditis. Anyway, I did not feel much better and I went back in January, 2020. I had a chest x-ray which showed lung inflammation and was told it could be COPD or asthma. I was asked if I had been smoking and I said it had been 35 years since I’ve smoked. (I am now 61.)  At this point, I had some serious nervous system disorder signs, which I now think were the signs of both dry and wet Beriberi.

My symptoms had progressed to the point that I was extremely sensitive to light and sound and had extreme lightheadedness/dizziness. My vision plane was tilted to maybe like a 30 degree angle. My gait was weird at times and my balance was terrible. I received a general blood test and was also tested for Lyme disease, Lupus, RA and other autoimmune diseases, with normal results. They also tested my adrenal and parathyroid hormones and that came back normal. My body overall had this continuous buzzing type of sensation. I am normally social but felt so bad that I wanted to withdraw from people.

Was It Thiamine?

I found Drs. Lonsdale and Marrs information about thiamine and started on Allithiamine in mid-March 2020 and continued to see the chiropractor. I started with one, 50mg capsule per day and now am up to three 50 mg capsules a day. I plan on increasing to four capsules per day soon. The dizziness, balance problems, visual disturbances, light and sound sensitivity issues, and gait issues are pretty much gone.

What has worsened is that I have a hiatal hernia that never really bothered me that has begun to bother me a lot over the last 4-6 weeks. When I am having a flare-up, I am short of breath and my abdomen feels extremely tight between my ribs. This happens every few days. I feel that I have been healing but the abdominal discomfort and the effect it is having on my breathing is extremely uncomfortable at times. I am wondering if it is normal for one set of symptoms to resolve and a new set to arise. It is clear that the thiamine is helping with a number of my symptoms, the dizziness, balance and gait and the light and sound sensitivity have all improved, but the hernia and the pressure it causes on my breathing, has worsened. Will Allithiamine possibly help heal my lungs of the damage caused by smoking all those years ago? Will it help with the breathing and hiatal hernia or am I missing something?

I would love to hear your comments about all of this. I am deeply grateful for all of the work and research your site has done shedding light on the importance of thiamine.

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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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Dysautonomia and Hypoxia

Every profession has its jargon that enables its practitioners to communicate relatively easily but is incomprehensible to those outside the

Are Your Mitochondria Stuck in Battleship Mode?

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mitochondrial healing cycles

As part of my work here, I am regularly confronted with desperately ill individuals who have seen dozens of physicians over the course of many years only to have their health continue to decline. Among the more frustrating aspects of this work is the failure of these physicians to assess and address the most basic aspects of health and healing. Namely, they fail to ask what the body needs to be healthy and whether the patient is getting those things. Of course, since evaluating these aspects health comes down to nutrition and exercise it does not align well with the practice of medicine, and if we are honest with ourselves, it is not something many of us want to deal with either. We want to eat what we want to eat and do what we want to do without regard to our health. Conventional medicine has capitalized on those sentiments, arguing persuasively for decades that a disease process is not real if all it requires to resolve is nutrients. Real illness requires medication, we now believe, having forgotten the very real nutrient deficient scourges like beriberi, Wernicke’s, pellagra, rickets, scurvy, and such.

Like most physicians, we have bought into the corresponding notions that fortification of foodstuffs assures that nutrient requirements are met and that in the land of plenty, where obesity reigns, malnutrition is rare. Neither is true of course, but belief in those myths absolves us of looking more closely at the chemistry of health and disease. For when we look at that chemistry, when we follow each of the altered signal transduction pathways, when look at the various patterns of deranged protein expression, and the myriad of genetic and epigenetic markers, we inevitably land at starving, inefficient mitochondria and the simple truth that they require nutrients to function; nutrient requirements that cannot be met by fortification alone and nutrient requirements, that if not met, lead to disease. When we dig a little deeper, we are also faced with a rather inconvenient truth that not only will pharmaceuticals not recover these deficiencies but they damage the mitochondria further. This does not accord well with the practice of conventional medicine and certainly does not fit into our busy, convenience-based lifestyles.

The Capacity to Survive

Among the more remarkable aspects of human physiology, however, is the capacity to survive all manner of illnesses and insults. We are supremely adept at adapting and surviving. We may not be living healthy, but we live. Mitochondria mediate these survival functions. They are responsible for converting the foods we consume and the oxygen we breathe into cellular energy (ATP).  With that energy, they regulate all aspects of basic survival at the molecular level, including survival itself – cellular respiration – but also things like inflammation, immune function, steroid hormone production, cellular life and death cycles, and whole bunch of other stuff. As one might expect, each of these functions is energy dependent.

Decrements in cellular energy, thus, elicit those survival mechanisms. If they are not resolved appropriately, when the threat persists, and/or when there is limited energy to face the threat, these normal responses lead to all sorts of tissue and organ dysfunction. It is this mismatch between the energy available and the energy required that leads to the persistence of not only the original illness, but because of the chronically activated survival cascades, leads to new and more complicated illnesses. On the one hand, decrements in ATP lead to things like inflammation and immune system activation – the normal, programmed and encoded survival cascades – but on the other hand, the survival cascades themselves lead to decrements in ATP, which in turn leads to more inflammation and immune reactivity. Without resolution, these cascades can easily become ingrained and ultimately lead to death. This suggests that energy availability is the key to health, or more specifically, that insufficient mitochondrial energy, and thus, impaired mitochondrial function leads to illness.

From Power Plant to Battleship: Mitochondrial Healing Cycles and the Necessity of Sufficient ATP

A recent paper suggests this is true. Just last month, one of the leading experts in mitochondrial function, put forth a compelling synthesis of research delineating what he called the mitochondrial healing cycles. Specifically, he demonstrated by what systems level mechanisms mitochondria maintain health or initiate and maintain disease. Dr. Naviaux argues that chronic illness is initiated by the “biological reaction to an injury and not the initial injury or the agent of injury itself.” He uses melanoma as an example, illustrating how it is not caused by the sun per se, but our biological, or more specifically, our metabolic (mitochondrial) response, to the sun. Chronic illness, he argues, becomes chronic only when there is incomplete healing of the original injury and/or when secondary injuries occur before primary injuries have healed. Illness, he suggests, is a multi-hit proposition.

To Naviaux, illness begins and ends in the mitochondria. Mitochondria are responsible for enacting what he terms the ‘cell danger response’ (CDR), the survival mechanisms that I spoke of earlier. There are three phases of the CDR:

  1. The initial inflammatory/immune response: “activation of innate immunity, intruder and toxin detection and removal, damage control, and containment.” He aptly describes this phase as a shift in mitochondrial energetics and function from power plant to battleship. ATP has to be diverted to fight the threat, initiate and maintain the characteristic inflammatory response. The reduction in ATP results in the characteristic fatigue we all experience at the beginning of an illness.
  2. Once the damage from the initial injury is contained, phase 2 begins. This involves replacing the dead and damaged cells as well as walling off any remaining damaged tissue that was not completely cleared in phase 1. Here stem cells are recruited and enter the cell cycle. Mitochondria in stem cells are critical for this phase, supplying the stem cells with ATP as well as key substrates to help with healing process. An interesting aspect of this phase, is that cell – cell communication ceases. There is no metabolic cooperation between cells as they are continuing grow and migrate. It is only when growth is complete and migration ceases that cell-cell communication reemerges.
  3. In phase 3, we get a return to “cell differentiation, tissue remodeling, adaptive immunity, detoxification, metabolic memory, sensory and pain modulation and sleep tuning”. Once the cells have been fully differentiated and re-educated, cell-cell communication reinstates and healing is complete.

The healing cycles are linear, sequential and ATP intensive. Each must be completed before the next can begin, before a secondary injury takes place, and each requires a continuous supply of ATP. Too many hits and/or too little ATP will derail healing. When we consider mitochondrial metabolism as the root cause of persistent disease, it is difficult not to ask what constrains the availability of energy and thus blocks the body’s ability to progress across each healing cycle.

Recovering Mitochondria: The Role of Nutrition

To answer this question, one has to look at how we produce ATP. Absent outright starvation, to get from food to ATP we need a few things: macronutrients and micronutrients or proteins, fats and carbohydrates along with vitamins and minerals. That’s it. Nothing fancy or complicated, just basic nutrition.

When we look at macronutrient consumption, one of the leading problems in western cultures is the high consumption of junk, carbohydrate-based foods. These foods, though they are often fortified with vitamins and minerals, come with far more sugar and other toxicants than the body can handle. Rather than being a net gain in energy, ultimately, become a net loss, both in macro, but especially, in micronutrients. Without sufficient micronutrients, none of the enzyme machinery, whether in the cytosol of the cell or in the mitochondria themselves, can perform the required functions that moves the macronutrient through the factory and produces ATP. Indeed, even the consumption of molecular oxygen requires the presence of vitamins and minerals. Absent those vitamins and minerals, a sort of cellular hypoxia sets in; one that activates inflammatory pathways, and ultimately, the shift in tale tell shift energy production associated with cancer known as the Warburg effect.

Conversely, because of decades-long advertising campaigns, most folks, but women especially, consume insufficient quantities of protein and fat. This skewed consumption of macronutrients places a high demand on the OXPHOS (oxidative phosphorylation) pathway of the mitochondria to produce ATP, while simultaneously not providing sufficient micronutrients to fuel the enzyme machinery to produce this ATP. It also increases the need for detox, while again, failing to provide adequate substrates to do. Moreover, if the diet is high in the staple sweetener high fructose corn syrup, in addition to everything else that becomes dysregulated at the mitochondrial level, the ability to covert fatty acids into energy, can be shut down entirely, conferring a metabolic inflexibility that is common in western cultures.

Along with issues with macronutrient consumption, large percentages of the population are deficient in one or more of the micronutrients required for healthy mitochondria. Individuals with chronic illness are severely deficient. The mitochondria require 22 vitamins and minerals in varying concentrations to convert the food we eat and the air we breathe into cellular energy or ATP (Figure 1.). Absent sufficient concentrations of one or more of those nutrients, mitochondrial function deteriorates and healing will not progress. Survival mode is all that can maintained.

mitochondrial nutrients
Figure 1. Mitochondrial Vitamins and Minerals

With Naviaux’s framework, it becomes clear that healing is an energy intensive process. The only way to boost energy is via good nutrition. Sure there are compounds that can override certain pathways within the mitochondria and, at least temporarily, provide additional energy, but if the core requirements for optimal mitochondrial health are not met, it is only a matter of time before initial benefits become problematic. (I should note that exercise is also critical for healing the mitochondria. Exercise forces mitochondrial biogenesis among other important processes.) The questions that physicians and individuals with chronic illness should be asking are:

  1. What is required for health?
  2. Is this patient or am I getting those things?

Unless and until those aspects of health are addressed, chronic illness will persist because the mitochondria simply do not have the resources to progress through the healing cycles. There are no short cuts here.

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

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This article was published originally on October 17, 2018. 

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Dysautonomia and Hypoxia

Every profession has its jargon that enables its practitioners to communicate relatively easily but is incomprehensible to those outside the

Thiamine Deficiency, Dysautonomia, and High Calorie Malnutrition

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thiamine deficiency book

This book by Lonsdale D, and Marrs C, is available on Amazon books. It is published by Elsevier. Written particularly for physicians who are practicing in the field of Integrative Medicine, it would be of interest to the educated public, particularly those affected by chronic disease.

Beriberi, the classical thiamine deficiency disease, long known to have been caused by consumption of white rice, is thought to have been abolished in developed cultures. It is actually widespread in America due to the colossal ingestion of sugar and is usually diagnosed as psychosomatic disease. Because the standard laboratory studies are negative or nonspecific, it is assumed that no organic disease is responsible.

Beginning with a review of the many symptoms of beriberi, it is described as the “great imitator” of a large number of disease conditions, each of which is thought to have its own etiology. It is relevant in all mitochondrial disease, because thiamine sits astride the vital initiation of energy synthesis. Thiamine deficiency interferes with carbohydrate, fat and protein metabolism, but is particularly important in the etiology of diabetes, types I and II and metabolic syndrome. It also has a place in the etiology of Alzheimer disease and may have an important part to play in cancer.

Evidence is provided to show that the relatively new science of epigenetics is crucial to the understanding of the part played by nutrition and lifestyle in genetic function. If the early symptoms of nutritional deficiency are treated symptomatically and high calorie malnutrition continues, the result is an array of chronic brain diseases. When thiamine deficiency was discovered as the cause of beriberi, the early investigators recognized that therapeutic doses of the vitamin involved the administration of 100-300 mg a day for months. The book reviewed here should be in the library of any Integrative Medicine physician.

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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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Dysautonomia and Hypoxia

Every profession has its jargon that enables its practitioners to communicate relatively easily but is incomprehensible to those outside the

Thiamine and Heart Function

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Since there are many posts on this website about thiamine, it is entirely possible that some readers will regard it as being an obsession of the author’s. I can well imagine a reader believing that an explanation for so many different conditions is the fruit of such an obsession. I will counter this by stating that a paper in a prestigious medical journal reported 696 separate papers in which over 250 human diseases had been treated with this vitamin as long ago as 1962. I think that the explanation for recognizing the place of thiamine in human metabolism is a professional lifetime of clinical observation, resulting in the conclusion that disease is a representation of cellular energy deficiency. To use a simple analogy, spark plugs used in older cars were necessary to ignite the gasoline. Loss of a single plug made the engine run badly and if they were all affected, the car became completely useless. I have used the analogy frequently: thiamine deficiency is like an inefficient spark plug in the engine of a car.

Heart Disease and Beriberi: Case Stories

Heart disease has been central in beriberi, the classic thiamine deficiency disease, for centuries and the painstaking efforts that uncovered thiamine deficiency as the cause is unfortunately a little-known saga of human effort. Modern physicians have been completely convinced that no vitamin deficiencies exist in America, because of vitamin enrichment by the food industry. So is there any evidence that physicians are beginning to wonder whether thiamine plays a part in modern heart disease? This post is designed to show that there is indeed an awakening that could make a big difference to the role of cardiologists in treating heart disease.

Before I go to some medical literature, I want to describe a personal experience that occurred many years ago because it illustrates the incredible psychological resistance of the medical community to a vitamin deficiency. I was a pediatrician at Cleveland Clinic at the time. In the medical hierarchy, a pediatrician is regarded as being largely ignorant concerning disease in adults. A 67 year old anesthesiologist at a Columbus hospital reported to his colleagues with the symptoms of heart failure. He was subjected to heart catheterization and found to be perfectly normal in that respect.

His son was in medical school and studying his father’s case, he came to the conclusion that he had beriberi. For some reason unknown to me, the patient was referred to cardiologists at the Cleveland Clinic. Because my colleagues knew of my particular interest in thiamine, I was asked to see the patient. The story he gave me made the son’s diagnosis virtually a guarantee. Each day, as he went to get into his car in the morning, he would get the “dry heaves” in the garage. He would drive to the hospital where he gave anesthesia to as many as 10 patients. He would then go to the pediatric ward and cut himself a large piece of chocolate cake. When he got home he was too tired to eat dinner and would go to bed. I gave my reading of the case in the patient’s record and had no further contact. He was returned to the Columbus cardiologists and although I believe that he continued to receive thiamine, he died. I never received any information concerning his further care or whether the cardiologists really believed that this was beriberi. One can only conclude that the state of his heart was precarious and the history of thiamine treatment in beriberi had already showed us that there was a “tipping point” beyond which there was no response to thiamine treatment. Whether the cardiologists were aware of this or not is unknown. It is possible that his failure to respond may well have caused them to reject the diagnosis. What really impressed me was the extraordinary resistance to this diagnosis.

I am reminded of another case in my experience. There was a lady pathologist at Cleveland Clinic who was known to be brilliant. I visited her in the Department of Pathology for a reading on one of my patients. She told me that she was so utterly fatigued that a few days previously she had turned around on her way to work and gone home. I found to my amazement that she had a chocolate box in every room in her house and would take a chocolate at random as she went around her house. Without further advice I simply suggested to her to discontinue that practice and to take a supplement of thiamine, whereupon she recovered quickly. Fatigue is a symptom arising in the brain that notifies its owner of energy deficiency and undue fatigue is a logical result in beriberi.

Recognizing Vitamin Deficiencies in Disease

The problem with thiamine deficiency is that a physician has to change his attitude radically towards the cause of disease. This is because the underlying mechanism is derived from cellular lack of energy. If this is not perceived, a physician can be puzzled by a combination of heart and nervous system disease in a single patient. In the present medical model, he believes that he is confronted with two separate conditions.

Because of this resistance, in 1982 I joined a private practice specializing in nutrient-based medicine and began seeing adults as well as children. I joined a group that came to be known as the American College for Advancement in Medicine (ACAM). This relatively small group of physicians had all come to the same conclusion: nutrient-based therapy is, or should be, the methodology of the future. Many of these physicians were practicing alongside their orthodox colleagues in their local hospitals. One of my

ACAM friends told me the following story. He had a patient in the hospital with a pneumonia caused by antibiotic resistant infection. Together with the antibiotic treatment, he had given the patient intravenous vitamin C and she recovered. A patient in the next bed was under another physician with the same pneumonia and my friend approached him, suggesting that he tried the use of the same treatment. He was told to mind his own business and the patient subsequently died. I know of no better example of resistance and rejection of a principle that has yet to reach full acceptance in American medicine. As long as the psychological resistance to vitamin deficiency remains, it is seldom considered. I am happy to say that this resistance is beginning to break down as we shall see by looking at some of the recent medical literature. Not only that, the therapeutic use of vitamins in pharmacological doses it gradually being recognized for its therapeutic value.

Recent Reports of Thiamine’s Role in Clinical Care

Hear what a physician wrote as recently as 2015. The title of the paper is “Thiamine in Clinical Practice” and the author notes that the active form of the vitamin plays a role in nerve structure and function as well as brain and heart metabolism. Unexplained heart and kidney failure, alcoholism, starvation, vomiting in pregnancy or intestinal surgery “may increase the risk for thiamine deficiency”. Understanding the role of thiamine as a potential therapeutic agent for diabetes, some inborn errors of metabolism and neurodegenerative diseases all warrant further research. Surely, this is an indictment of our present approach by merely trying to control symptoms instead of addressing the primary cause.

A group of Canadian physicians stated that “the management of heart failure represents a significant challenge for both patients as well as the health care system in industrialized countries”. The abstract of their paper notes that thiamine is required in the energy-producing reactions that fuel heart contraction. Previous studies have reported a wide range in the prevalence of thiamine deficiency in patients with heart failure and the impact of its supplementation in patients is inconclusive. Of course, Dr. Marrs and I are appalled because such treatment is not only easy, it is completely non-toxic and therefore safe. If there is clinical evidence, why not use a non-toxic agent? However, the psychological restraints of being accused of being a charlatan are very real and can expose a physician to colleague ridicule.

Another paper reported that a total of 20 articles were reviewed and summarized. Recent evidence has indicated that supplementation with thiamine in heart failure patients has the potential to improve heart contractions. These authors recommend that this simple therapy should be tested in large-scale randomized clinical trials to further determine the effects of thiamine in heart failure patients. Diuretic treatment for heart failure may lead to an increased urinary thiamine excretion and in the long-term thiamine deficiency, further compromising heart function. Nine patients with diuretic treatment for chronic heart failure were studied with thiamine supplementation, producing beneficial effects on cardiac function. The authors state that subclinical thiamine deficiency is probably an underestimated issue in heart failure patients. It has even been shown that thiamine pyrophosphate, the active form of the vitamin, prevents the toxic heart injury caused by the cancer treating agent cisplatin. Dietary thiamine that has not been activated by the body did not prevent this.

It has been known for some time that thiamine in the diet has to be absorbed into the body by means of a protein known as a transporter of which there are quite a few. These transporters are under genetic control and absence of one or more of them will make it difficult for a given person to obtain an adequate amount of thiamine from diet into the part of the body where that thiamine transporter is active. A new thiamine transporter has been discovered whose genetic variants have an effect on blood pressure.

Although this post is about heart disease, I want to end by pointing out that vitamin treatment goes well beyond the consideration of just heart disease. Several years ago I received a letter from an aging physician who had specialized in OB/GYN. This letter was so poignant that I am repeating some of this letter:

I am writing to you, because I have found another mortal being who is particularly interested in the biological activities of thiamine. I had previously thought that I was nearly the lone believer in the benevolent effects of thiamine particularly for the treatment and prophylaxis of the toxemias of pregnancy and its many associated problems. I had even written to the chief of the Cleveland Clinic OB-GYN about the “miracles” I was performing and offered to work with him in further development of the concepts.

It was enclosed in a copy of a book by John B Irwin, M.D., the author of the letter.

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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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Dysautonomia and Hypoxia

Every profession has its jargon that enables its practitioners to communicate relatively easily but is incomprehensible to those outside the

Metronidazole Toxicity, Thiamine Deficiency, and Wernicke’s Encephalopathy

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Dr. Marrs and I recently had a book published with the title of “Thiamine Deficiency Disease, Dysautonomia and High Calorie Malnutrition”. I was therefore extremely interested to read one of the book reviews published on Amazon books by a patient who had suffered from what has become recognized as metronidazole toxicity encephalopathy (brain disease). Subsequently, she shared her full story with us. It is published here.

A Comparison of Flagyl Induced Encephalopathy and Wernicke’s Encephalopathy

This drug, sold as Flagyl, is prescribed to treat infections caused by anaerobic bacteria and protozoa. Uncommonly, it causes central nervous system toxicity that has the same damage configuration in the brain as Wernicke encephalopathy (WE). WE is the condition that occurs in the brain in people with severe thiamine deficiency. A manuscript in the medical literature was entitled “Metronidazole-Induced and Wernicke Encephalopathy: Two Different Entities Sharing the Same Metabolic Pathway?”  There seems to be little or no effort to explain it as a cause and effect relationship rather than seeing the two situations existing with different causes.

Debilitating Symptoms Post Flagyl

The reviewer states that she has, for two years, suffered with what she describes as debilitating symptoms due to a reaction from Flagyl. She states how these symptoms mysteriously wax and wane. On some days she barely notices them, but of extreme importance, she adds that a mild illness or physical exertion will cause the symptoms to reappear, forcing her back to bed for a variable number of days. When she was taking the drug, she lost his ability to walk and speak, but experienced a dozen other symptoms that persisted. These include difficulty in swallowing and breathing, constipation, severe anxiety, insomnia, depression, heart palpitations, chest pressure and several other unspecified problems. She mentions that she has a borderline enlarged heart.

I must point out here that these additional symptoms are surprisingly common in patients attending physicians in America, often classified as psychosomatic. It is the anxiety, insomnia and depression that guides physicians to thinking that the entire list of “inexplicable” symptoms is psychosomatic. Even the use of the word borderline for heart enlargement indicates that the physician could not identify the total symptomology. If thiamine deficiency had been considered as a diagnosis, the “borderline enlargement” would have fit because it is a cardinal sign of this deficiency.

The patient had evidently done some research on her own and had discovered that metronidazole is a thiamine antagonist. She also reported that in the medical literature metronidazole toxicity is constantly being compared with WE. When she came across our book, she had evidently experienced a flare up of symptoms and began to take supplements of thiamine and magnesium. She stated that the flare up calmed down much more rapidly than usual, enabling her to return to work and function in social activities.

She discovered that doctors do not believe in adverse drug reactions and will not treat the condition since they will not acknowledge that it exists. As a result, she has started a support group for people who suffer from this toxicity. Starting with three affected individuals, there are now over 100, all of whom have the same symptoms. Interestingly, they even warn new members how their doctors will react, preparing them for the reality of being dismissed by the medical community.

Thiamine Deficiency and Psychosomatic Disease

As mentioned in our book repeatedly, the multiple symptoms described by this reviewer are common in the offices of American physicians. “Real” diseases, according to the present medical model, are supported “by laboratory confirmation”. Because vitamin deficiency is generally considered to be nonexistent in America, it is only a physician, open to the possibility, who will entertain the laboratory studies required. The cause of many abnormal current laboratory studies performed on behalf of a sick patient is often obscure. None are capable of identifying vitamin deficiency. When positive as a result of the biochemical changes induced in the body by the deficiency, they are ascribed to other conditions that are acceptable to the present medical model. Hence, the diagnosis of psychosomatic disease often rescues the physician from a failure to recognize his own ignorance. It has always seemed to me that blaming the patient for imaginary symptoms without thinking of the brain as an electrochemical machine represents a glaring deficiency in diagnostic perspective. Unfortunately, nutrition has for long been a neglected area of medical teaching and there are extraordinarily few physicians in practice who recognize its vital importance. What is even more important is the recognition that many drugs are capable of precipitating something as bizarre as thiamine deficiency.

Stress and Illness

I mentioned above that it was extraordinarily important for the reviewer to recognize that flare ups of symptoms occur following a mild illness or physical activity. To explain this, I turn to the teachings of Hans Selye, one of the early researchers in the effect of stress as a causative agent in precipitating disease. Stress must be defined as any environmental factor that imposes a necessity for an animal to adapt (resist). Just like a car that climbs a hill, energy requirement must increase to meet the demand. Mental stress is often more energy requiring than physical stress, explaining the breakdown of health that may follow divorce proceedings. Selye had recognized in animal studies that virtually any form of physical or mental stress imposed the requirement of some form of energy in the ability of the animal to adapt. This was pure genius because energy metabolism was largely unknown in Selye’s time. Modern biochemistry has unraveled a lot of its complexities and thiamine stands out as an absolute necessity in the production of energy. Adapting means that the animal being physically stressed in many different ways would be capable of maintaining a state of health. Failure to meet the increased energy demand was marked by many observed performance and biochemical changes commensurate with those seen in sick humans. One of Selye’s students had reproduced in thiamine deficient animals exactly the same manifestations as those caused by physical stressors.

Diseases of Adaptation or Maladaptation?

The conclusion must be obvious. Any form of mental or physical stress induces a complex reaction in the organism that requires a large amount of energy to run the necessary adaptive machinery. In fact, Selye had concluded that illnesses in human beings were what he described as “the diseases of adaptation”. Since it is a failure to furnish the necessary energy, I suggest a refinement by calling them “the diseases of maladaptation”.

A healthy diet is designed to meet the calorie and non calorie nutrients that fully enable the body to synthesize energy. If this capability fails to meet the demand, even under extreme environmental conditions that permit life to continue, disease follows. The weakness may be genetic or nutritional in character or the stress overwhelming. For everyday life, all three factors are in play continuously.

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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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Two New Cases of Beriberi-like Syndromes: Thiamine Deficiency in Modern Medicine

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As a result of my participation in Hormones Matter, I receive quite a few emails that record histories of patients who have often languished with inexplicable symptoms, sometimes for years. I am going to record two histories here without identifying any possibility of the involved patients being recognized.

Patient number 1: Cyclic Vomiting, Hyper-salivation, Sensory and Neurological Issues

This is the story of a boy who had what was described as “chronic cyclic vomiting from 11 months until 24 months of age, sometimes 3 to 4 times a day”. Food refusal with chronic vomiting and severe weight loss (failure to gain) was described. His diet was recorded as consisting basically of chicken/beef and vegetables. Frequent use of Paracetamol for ear infections with fever was described. As an infant he experienced hyper-salivation, bad enough for wearing a bib 24/7. Extreme sensory issues were mentioned but were not specified. Dilated pupils from a very young age***, neurological issues with confusion, memory problems, speech difficulty and heart racing/palpitations were mentioned together with eye tracking difficulties. A high concentration of arsenic had been found, presumably in urine, although this was not specified. Candida, a form of yeast, had evidently been a frequent infection. He was reported to have Hashimoto (a thyroid dysfunction) and a high blood glucose ***. He exhibited complete lack of coordination, always “appearing drunk”, talking gibberish and repetitive behavior.

Discussion of Symptoms: Patient 1

Cyclic Vomiting

Sometimes known as winter vomiting, the cause of this relatively common condition is said to be unknown. Recurrent vomiting is one of the symptoms recognized for centuries in the thiamine ( vitamin B1) deficiency disease, beriberi. I had several patients with cyclic vomiting, described in our book (Thiamine Deficiency Disease, Dysautonomia and High Calorie Malnutrition) that responded to thiamine treatment.

Food Refusal

Appetite is governed in the lower brain by several hormones, explaining why a voracious appetite and food refusal could both be a signature of thiamine deficiency, depending on severity and chronicity of the deficiency.

Weight Loss

Severe weight and stature increase (failure to thrive), is a signature finding in familial dysautonomia, a genetically determined disease. Thiamine deficiency also causes dysautonomia. I reported a patient with eosinophilic esophagitis whose dysautonomia resulted in failure to thrive. With thiamine treatment his weight and height increased dramatically (see: Eosinophilic Esophagitis May Be a Sugar Sensitive Disease).

Ear Infections

Extremely common in children, this and jaundice of the newborn are both now known to be the result of inefficient oxygen utilization. Thiamine deficiency is an outstanding cause.

Excessive Salivation

The salivary glands are under the control of the lower brain and this fits with thiamine deficiency.

Extreme Sensory Issues

This is the result of inefficient oxidative metabolism in brain and has been a well known problem in thiamine deficiency beriberi. It is interesting that diabetics are sometimes pulled over and accused of drinking because of erratic driving and subsequent “drunken” behavior. I strongly suspect that this is a thiamine deficiency affect, because thiamine metabolism has recently been found to be closely related to metabolism in diabetes.

Permanently Dilated Pupils ***

This is a cardinal sign of sympathetic nervous system overdrive, fitting in with the diagnosis of dysautonomia.

Neurological Issues: Confusion, Memory, Speech, and Eye Tracking Problems

All of this is the result of inefficient oxidative metabolism in brain.

Tachycardia

This is the term for a fast heart rhythm and is a cardinal sign of dysautonomic sympathetic nervous system overdrive.

Urinary Arsenic

Pressure-treated wood in the United States contains a significant amount of arsenic and is generally touted as being the source for children using playgrounds. This is much more significant than arsenic in drinking water. Arsenic damages oxidative metabolism and could be contributive to the effects of thiamine deficiency.

Candida Infections

Candida is a common form of yeast that infects humans. It dislikes oxygen: consequently this infection is much more likely to occur in people whose oxygen metabolism is inefficient.

High Blood Glucose***

Of course, this means that the patient has some form of diabetes. Both type I and type II diabetes are now known to have thiamine deficiency as part of the syndrome. Alzheimer’s disease may be diabetes type III. Thiamine is absolutely vital in glucose metabolism.

Pattern Suggests Pyruvate Dehydrogenase Complex Disease

Pyruvate dehydrogenase is an enzyme that demands thiamine and magnesium in order to function properly. I would be willing to bet that this boy would be responsive to high doses of Lipothiamine and should be studied in detail by a physician who understands the possibility of inborn errors of metabolism. Note the two starred items above. The observation of permanently dilated pupils indicates excessive activity of the sympathetic branch of the autonomic nervous system. The high blood glucose is a sure indicator that thiamine metabolism is involved, even if there is insulin deficiency.

Patient number 2: ROHHAD

This is a little girl, age not specified. She was described as a patient with ROHHAD. This stands for “rapid onset weight gain, hypothalamic dysfunction and autonomic dysregulation”. The parent described this as “a very rare syndrome and only 150 cases have been recorded worldwide”. Children with this diagnosis are said to have similar symptoms. Most of them have central and obstructive sleep apnea. Many depend on CPAP. This child requires it only during sleeping but many other kids have tracheostomy and all are living on CPAP day and night.

Symptoms of patient 2: Sweaty Palms, Cold Intolerance, Tachycardia and More

At my request, the parent observed that there was no family history of alcoholism or smoking. The mother had been thinking of thiamine deficiency because of the child’s autonomic dysfunction. I have noticed that alcoholism and sugar sensitivity appear to be closely related genetically.

She has palm sweating. Father has blepharospasm (spasm of the eyelids) frequently, lasting for weeks at a time. She also has tachycardia (fast heart rate), excessive vomiting, cold intolerance with persistent cold extremities, peripheral neuropathy, binocular diplopia, double vision, gastrointestinal dysmotility, mood swings, and low pain perception are all symptoms of dysautonomia, the commonest cause being thiamine deficiency. Fortunately the family is working with a physician who had started thiamine treatment for this child. The parent closed with the remarks that “since she started TTFD she is having a fast heart rate at 140 beats a minute and low oxygen saturation with restless sleep. I decreased TTFD from 250 mg to 50 mg but my opinion is that she became more stable with oxygen saturation and pulse rate”.

Discussion of Symptoms: Patient 2

ROHHAD

Rapid weight gain, hypothalamic dysfunction, dysautonomia and sleep apnea are all included in this syndrome. I must point out that the word “syndrome” is always used for a collection of symptoms whose cause is unknown. In fact, all can be caused by thiamine deficiency.

Palm Sweating

Sweating is a result of sympathetic nervous system overdrive. She also has tachycardia, excessive vomiting, cold intolerance, peripheral neuropathy and double vision. Various forms of peripheral neuropathy are cardinal symptom in thiamine deficiency.

Gastrointestinal Dysmotility

The intestine is innervated by the vagus nerve which originates in the brain. This nerve uses a neurotransmitter known as acetylcholine, highly dependent on energy metabolism and therefore also dependent on thiamine. Japanese physicians have used thiamine derivatives for years to treat postoperative intestinal paralysis.

Mood Swings

I learned the hard way about mood swings in children when I found that the dominant cause was poor diet resulting in thiamine deficiency.

Low Pain Perception

Decreases in pain perception are described in familial dysautonomia, a genetically determined condition. Thiamine deficiency results in dysautonomia and may well be responsible for low pain perception.

Points of Consideration: Polysymptomatic Disease and Thiamine Deficiency

Both these children have fallen into diagnostic cracks. It seems only to be the persistence of struggling parents that do their own research and persist in trying to find an adequate explanation that addresses the plight of these children. To me, the problem is obvious. Polysymptomatic disease that affects so many body systems can only be explained by some form of energy deficiency, dependent on oxidative metabolism. Thiamine deficiency, arising from both genetic and nutritional abnormalities is a common cause. It could be a simple thiamine deficiency from diet but this is unlikely in the case of these two children who may have a genetically determined condition that is responsive to megadose thiamine.

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Cognitive Testing Post Adverse Reaction: A Lost Opportunity

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In the not too distant past, before sophisticated brain imaging tests became available, it was the job of the neuropsychologist to assess brain function and brain damage based upon an array of cognitive and behavioral tests. These tests measured the functional capacity of different brain regions. They were entirely behavioral and performance based and could, with a fair degree of accuracy, identify whether and where a brain injury was located and the extent of the damage. Results from these tests could then indicate a need for surgical intervention and/or suggest a prognosis and therapeutic options; options that generally involved a cognitive therapy of sorts to retrain or regain lost capacities.

And then, technology caught up; brain imaging became possible and physicians no longer needed the neurocognitive assessment as a diagnostic, but only for rehabilitation purposes once the brain damage was identified. Non-invasive brain imaging was a remarkable technological advancement. How much better and more accurate diagnoses and interventions could be if physicians were able to see the damage in advance, and indeed, at every phase of treatment. No need to delineate the subtle behavioral signs linked to brain injury in order to diagnose, just scan the brain to rule in or rule out trauma and deal with the deficits after the fact.

Functional Cognitive Testing – A Missed Opportunity

I can’t help but wondering though, if we’ve lost something important by switching so completely to visually based diagnoses. For example, what if the damage is at the molecular level and unable to be detected via imaging, or even via current laboratory markers? How do we even know which lab markers to look for if we don’t ascertain that there are in fact decrements in functioning? Do we even recognize brain injuries as extant if they are not visible by current imaging or laboratory techniques?  I have a sense that we don’t. Cognitive deficits, especially those occurring in previously healthy individuals, following an illness, medication, vaccine or even post pregnancy, may be disregarded along with further diagnostic and therapeutic possibilities when the indices of injury exclude assessing functional capacity.

I was reminded of this recently from a patient story. She, and others like her, experienced a loss of reading comprehension post-fluoroquinolone reaction. Medication and vaccine induced cognitive disruptions are not uncommon. In elderly populations they are quite well documented. In the younger adult populations, however, the research is sketchy at best. In the case I mentioned, the patient was a previously healthy, active young woman. After taking a course of fluoroquinolone antibiotics, and in addition to a myriad of other side effects, she reports losing her ability to comprehend text; something that would be quite disabling in our current text-based world.

I lost a lot of my reading comprehension while I was floxed. I could still officially read – if you gave me a short memo that said, “buy milk,” or something like that, I could read it. But reading a novel or complex materials for work became really difficult. I lost track of the content of the beginning of a paragraph by the time I reached the end of the paragraph. I struggled to understand things that I used to be able to read with ease.

Another fluoroquinolone patient describes her deficit:

I remember going into a restaurant a few months after being floxed. I sat down, looked at the menu, and couldn’t understand a single thing. I couldn’t make sense of anything. It was as though trying to read a foreign language. I put it down, and wanted to stand up and start screaming, and breaking glasses and dishes.

Read any of the fluoroquinolone social media and these observations are not uncommon. Similarly, decrements in cognitive function have been reported in our research on the side effects of the HPV vaccine, during and after Lupron treatments, and even with oral contraceptives.

What I find both most interesting and most troubling is that the loss of attentional capacity, loss of short term memory and loss of language comprehension following the administration of a medication or vaccine may be indicative of a broader health issue; one that should be investigated further. No doubt in many patients these deficits were not explored, at least not functionally, as imaging tests are often negative. That is a shame. Functional cognitive assessments, like those common in clinical practice in the past, and yet still in academic research, would more finely delineate the patterns of medication induced cognitive disorders. These tests could tell us the brain regions susceptible to the medication-induced events in the absence imaging or lab markers. In fact, these tests might help us design more appropriate lab markers. More importantly, functional neurocognitive testing could provide clues about the patient’s overall health. Let me explain.

Linking Cognitive Performance to Overall Health

Each of the medications I mentioned above have distinctly different pharmacological mechanisms of action; so different, one might wonder why I would even consider looking for commonalities in their adverse reaction patterns. Initially, I didn’t. But then the data from our research began flowing in, and along with the data, patient stories began arriving. Slowly, pattern similarities began emerging; similarities that I could not explain by solely looking at the drug’s specific mechanisms of action. There had to be an underlying factor or factors that somehow connected these medications and vaccine reactions. What were they? And per the current topic at hand, how might have functional neurocognitive assessments inspired or expedited our understanding? Not all of the pieces to the puzzle are clear, but here are the clues thus far.

Clue 1. Three of the medications we study negatively affect the thyroid (Lupron, Fluoroquinolones and Gardasil). Thyroid influence on central nervous system functioning, cognitive and behavioral performance is well known.

Clue 2. Thyroid damage is linked to cerebellar ataxia, acute and chronic, via white matter demyelination. Cerebellar ataxia has been noted post fluoroquinolone, post Gardasil and post Lupron.

Clue 3. Thyroid damage is linked to peripheral demyelination. Again, all three medications include demyelination syndromes as part of their reaction profiles.

Thyroid dysfunction alone, without any other intervening variables could explain the cognitive and many of the neurological symptoms we were seeing, but was it sufficient to explain all of them? Probably not, there must something else at play. What could it be?

Clue 4. Each of these drugs are linked to mitochondrial damage (mitochondria are an unrecognized target for many pharmaceuticals and environmental agents). These drugs increase the production of reactive oxygen species (ROS) and decrease cellular energetics via changes in mitochondrial functioning. Mitochondrial damage evokes multi-system, seemingly disparate illnesses, much like what we are seeing. Cerebral mitochondrial dysfunction can cause serious cognitive and behavioral symptoms.

Clue 5. Thyroid and mitochondrial health are reciprocally connected. Damage the thyroid and mitochondrial functioning diminishes. Damage the mitochondria and thyroid functioning diminishes. We have two factors that are inherently related.

Thyroid and Mitochondrial Functioning

What factor could initiate a thyroid – mitochondrial cascade and connect completely dissimilar drugs to these reactions; reactions which are often complex, affect multiple physiological systems, but are also integrally dependent upon proper thyroid and/or mitochondrial function (because of their reciprocal relationship)?  Could there be such a connection?  A few more clues.

Clue 6. A heartwrenching patient story: A Long and Complicated History Topped by Levaquin, highlights a particular set of neurological symptoms that every neuropsych student should immediately recognize.

Clue 7.   Patients from the post fluoroquinolone and the Gardasil groups have been identified clinically with thiamine deficiency. I suspect post Lupron patients may also have thiamine deficiencies, but none have been tested yet.

Clue 8. Both the fluoroquinolones and Gardasil increase thiaminase, an enzyme that blocks thiamine. Higher thiaminase means lower thiamine. Oral contraceptives are believed to increase thiaminase and so women using oral contraceptives in combination with a fluoroquinolone and/or the HPV vaccine Gardasil or Cervarix would be at higher risk for thiamine deficiencies.

Drug Induced Thiamine Deficiency, Cognitive Deficits – The Mechanism

It turns out, thiamine deficiency, or more specifically, a medication induced blockade of thiamine may be at the root of these adverse reactions. Thiamine is a co-factor in mitochondrial and cellular energy, the currency of which is adenosine triphosphate (ATP).  Without thiamine, the mitochondria become defunct, as do the cells in which they reside, and they eventually die. High energy organs like the brain, the heart and the GI tract are often affected dramatically. Similarly, given the reciprocal relationship between the thyroid and mitochondrial functioning and their combined influence on cerebral, cardiac and metabolic homeostasis, diminished drugs that attack the thyroid and diminish thiamine may be doubly dangerous.

In most recent work, thiamine deficient syndromes have been expanded to include five conditions, with fair degree of overlap between them.

  1. Gastrointestinal beriberi: abdominal pain, lactic acidosis, vomiting.
  2. Neuritic beriberi: sensorimotor polyneuropathy, peripheral neuropathy (likely multiple B vitamins involved).
  3. Dry beriberi: high output cardiac disruption without edema
  4. Wet beriberi: high output cardiac disruption with edema (dysautonomias, including POTS)
  5. Wernicke’s encephalopathy: mental status changes, ocular abnormalities, gait ataxia

Given the current nutritional trends with high intake of sugar, fats and processed foods, it is likely that when these medications directly block thiamine production, they do so against the backdrop of already suboptimal thiamine intake. When we consider that oral contraceptives block also block thiamine and that women are more likely to already suffer from low thyroid function, the effects of either the fluoroquinolones or Gardasil on the mitochondrial thiamine could be devastating. How many other medications or vaccines affect mitochondrial functioning and/or thyroid health? How many other medications or vaccines contain anti-thiamine components and diminish this critical mitochondrial co-factor?

Loss of Reading Comprehension and Other Missed Opportunities

Thiamine deficient cognitive decline is well characterized and includes the loss of language comprehension, in more severe cases, deficits in language production, cerebellar ataxia, tremors and as it progresses, seizures, coma, and death. All reversible with thiamine replacement. The cognitive deficits reported by patients, post medication or vaccine reaction, when observed alone but especially when taken in combination with the other tell tale signs of incipient thiamine deficiency, could have lead researchers or clinicians to these diagnoses. At the very least, it should have lead clinicians to thyroid dysfunction, but more often than not, this was not the case.

Cognitive deficits in previously high functioning individuals are reported regularly after medication or vaccine reactions. Almost to a tee, most are ignored once imaging tests rule out blatant injury, but they shouldn’t be. These deficits, when functionally assessed, would provide valuable clues regarding the regions of the brain most susceptible to medication or vaccine induced injuries; clues that could identify damage and disease processes well before detected by imaging tests. By dismissing patient complaints of cognitive deficits we lose valuable research, diagnostic, and therapeutic opportunities. And perhaps, even more importantly, when we segregate symptoms by organ or body part and fail to see the inherent connections among symptoms and physiological systems, we miss the opportunity to help patients heal.

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This post was published originally on Hormones Matter on May 21, 2014.

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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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Dysautonomia and Hypoxia

Every profession has its jargon that enables its practitioners to communicate relatively easily but is incomprehensible to those outside the

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