thiamine deficiency - Page 6

Treating Sensory Processing Disorder in Children

Published on
15.6K views
sensory processing disorder

On Tuesday, August 16, 2016, I read an article in the Wall Street Journal with this title: Treating Children for Sensory Processing Disorder. Since I have treated hundreds of these children, I am posting here some of the facts that I have learned. First of all let me provide some extracts from this article that is all about a diagnosis of “Sensory Processing Disorder” (SPD). The article says that SPD is believed to affect 5% to 16% of children in the United States.

I want to make it clear what we are talking about. This article describes a three-year-old child who, when accompanying his mother to the grocery store would have meltdowns. His mother was quoted as saying “he would literally bite me throughout the grocery store”. An occupational therapist determined that he had SPD: “a condition in which the body and brain have difficulty processing and responding to sensory stimuli in the environment”. The article goes on to say that “some people with SPD are hypersensitive to loud noises or different textured foods. Others may be agitated by the touch of a clothing tag”. The Director of Occupational Therapy (DOT) research at Cincinnati Children’s Hospital Medical Center was reported as saying

Occupational therapists treat dozens of SPD patients every week. It can affect just one sense, such as hearing, touch or taste, or multiple senses. Sensory processing problems can also affect the body’s vestibular system, creating difficulties with balance, or the proprioceptive system, leading to problems with clumsiness and body positioning.

The DOT “has worked with some children with SPD who are academically gifted and don’t have autism or ADHD. It is clear from the article that the method of treatment, entitled “sensory integration”, looks upon SPD as abnormal psychological behavior. This is  in spite of the fact that a professor of radiology and bioengineering at University of California, San Francisco stated that studies showed that children with SPD had less developed white matter mostly in the back of their brain, compared with typically developing children. This posterior region of the brain is where a lot of sensory processing takes place. This is a major clue as we shall see shortly.

Beyond the Bad Parenting Theory of Sensory Processing Disorder

Now I ask you dear reader, is it common sense to claim that this kind of disorder in 5% to 16% of our children is purely psychological from bad parenting, acceptably normal in a young child, or caused by genetic changes? Since the Wall Street Journal article claims that “adults can have SPD”, it is clearly not confined to children. To believe that any of these facts, or all of them together, can result in so much willful behavioral deviation is a reduction to absurdity. It is absolutely certain that Mother Nature never makes that kind of genetically determined mistake in so many individuals.

The article in the Wall Street Journal reports that “a common treatment at Cincinnati Children’s is called sensory integration, involving three sessions a week for about six weeks”. The founder of the STAR Institute for sensory processing disorder in Denver involves an intensive treatment program of some 31-hour sessions nearly every day for several weeks. The cost is about $175 per session.

When I was a consultant pediatrician at Cleveland Clinic Foundation, I saw many children who were referred because of “emotional problems”. The accepted cause at that time (and still is by many pediatricians) was lack of good parenting. In discussions with parents, I found that bad parenting was rare, but lousy diet was common, particularly because of the enormous overload of sugar, often started in infancy. In fact, sugar was used as an inducement to good behavior, not recognizing the fact that the sugar was the cause of the bad behavior in the first place. By doing a blood test on these children I repeatedly found evidence of thiamine deficiency. To me, the extension of the absurdity is that there is no mention at all in this article about the role of nutrition. I have posted a number of articles on this website concerning vitamins, particularly  vitamin B1 (thiamine). I have pointed out many times that overloading the diet with empty calories, particularly from sugar, automatically induces thiamine deficiency relative to the excessive calories. The scientific evidence for this has been known since 1936. Any attempt to depict thiamine deficiency by measuring its blood level in a person eating “empty calories” will be doomed to failure. The concentration of thiamine in the blood is only normal in relation to a normal calorie content of the diet. It is the calorie/thiamine ratio that counts.

Sugar, Thiamine, and SPD

By pointing out to the parents that they had to get rid of the sugar and providing the child with a supplement of thiamine and magnesium, all the symptoms of “psychological misbehavior”, no matter what pretty name was given to it, quickly resolved. For literally a few dollars and cents, this form of treatment is overwhelmingly simple and effective. The “posterior region of the brain where a lot of sensory processing takes place” is peculiarly sensitive to thiamine deficiency. It will affect balance and in its extreme form, can affect brainstem mechanisms where the control of heart rate and breathing is automatically conducted. This is why an excess of sugar is incredibly dangerous, not because the sugar is a poison in its own right, but because of the secondary effect on energy metabolism in that part of the brain that is essential to life itself.

What seems to be poorly understood is that thiamine deficiency produces the same effect in the brain as lack of oxygen and sensory perception becomes exaggerated. Pain is felt more intensely and may give rise to a phenomenon known as “hyperalgesia”(acute pain perception). Sound and light may be so much more perceived that the sufferer puts hands over his ears or closes his eyes, because the perception is offensive. Touch is grossly exaggerated and may even give rise to screaming by the child when being physically examined by a physician. Because of this poor understanding, the behavior of the child is regarded as “psychological”. Under such circumstances a mild injury to an ankle may give rise to severe pain in the leg. It used to be known as “acute sympathetic dystrophy”. The name has been changed to “acute regional pain syndrome” or “complex regional pain syndrome“. Let it be clearly understood that no matter what kind of injury, obvious inflammatory reaction or source of discomfort occurs in the body, the pain is perceived by the brain. If the mechanism of sensory perception is exaggerated, the pain will be more intense.

Conclusion

It is becoming abundantly clear that a diagnosis of sensory integration, ADD, ADHD, OCD and many other diagnostic refinements are not separate diseases at all. Like variations on a symphonic theme in music, the biochemical changes in the brain are responsible for creating the symptomatic expressions on a completely variable basis. It also explains in practical terms why many of the so-called SPD children in the Wall Street Journal article “were unusually gifted”. Like different models of cars with different horsepower, surely the more intelligent brain requires efficient energy metabolism to meet its “gifted” requirements. For those interested in further details of this concept, turn to the post on “Eosinophilic Esophagitis” on this website. There you will find that the unfortunate patient described with this disease was misdiagnosed for many years as psychosomatic. I will go further than this and say that if the symptoms that are commonly represented by changes in brain processing are neglected, and the malnutrition continues, we can expect damaging changes to take place. I would expect this to lead to a whole series of diseases that also go by different diagnostic nomenclatures, Parkinson’s disease, Alzheimer disease and various forms of dementia that represent the end point damage that has accrued over years. Are we collectively insane?

We Need Your Help

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

Yes, I would like to support Hormones Matter. 

Photo by Alireza Attari on Unsplash.

This article was published originally on August 24, 2016. 

Related posts:

picky eaterFood Aversions in Children with Autism Treating insomnia with thiamineTreating Intractable Insomnia and Cerebellar Ataxia With Thiamine vitamin and multiple sclerosisVitamin D’s Role in Preventing and Treating Multiple Sclerosis treating myopathy myalgiaTreating Myopathy and Myalgia: Lessons from Athletes

You might be interested in

Hyperglycemia and Low Thiamine: Gateways to Modern Disease

Published on
5.9K views
Thiamine deficiency, hyperglycemia gateway to disease

In Thiamine Deficiency in Modern Medical Practice and Threats to Thiamine Sufficiency in the 21st Century, I introduced the concept that thiamine deficiency underlies many common conditions plaguing modern healthcare and identified exposures and mechanisms threatening thiamine stability. In this document, I will tackle the pattern of metabolic changes associated with the modern dietary practices leading to thiamine insufficiency, and resulting in, and sustaining hyperglycemia.

Hyperglycemia Through a Different Lens

Hyperglycemia, and the metabolic dysfunction it initiates, is a worldwide problem that has reached epidemic proportions. Due in part to overconsumption of sugary foods and in part to decrements in mitochondrial capacity that drive cravings for sugars, hyperglycemia fuels the metabolic derangements underlying obesity, type 2 diabetes, cardiovascular disease, and more recently, research suggests Alzheimer’s disease as well. These interconnected disease processes represent the top leading contributors to morbidity and mortality.

Conventional wisdom attributes these disease processes to over-nutrition and the solutions that follow involve the restriction of calories and/or the medical manipulation of the pathways initiated by hyperglycemia. Admittedly, excess caloric intake is a component, but this nomenclature suggests an overly simplified concept of nutrition; one where all that matters is calories consumed relative to calories burned. This view obfuscates the role of micronutrients in the conversion of these calories/foods into adenosine triphosphate (ATP), the energy source for all cells. It ignores the fact that the aberrant cascades so commonly associated with hyperglycemia, are merely adaptive responses to the lack of micronutrient availability and consequent reduction in ATP. Finally, through this lens, the entirety of the blame for overeating is placed upon the individual.

In reality, while the initial choices that precipitated the hyperglycemia may have been the individual’s responsibility, once these patterns become entrenched molecularly, the resulting decline in ATP drives the cravings for high-calorie foods to compensate. In a very real way, these patients are starving despite sufficient or even excessive caloric intake. It is high-calorie malnutrition, but malnutrition nevertheless. Viewed from perspective, hyperglycemia is not a disease of excess, per se, but rather, one of deficiency. As such, the opportunities for treatment are expanded beyond the typical trend to reduce, block, or otherwise override a particular pathway, and shifted towards a rebalancing of metabolic health. Here, the question is not so much which pathways should be blocked to stave off the associated deleterious effects of hyperglycemia, but rather, what does the patient need to more effectively metabolize foods into energy? What is missing from his/her diet that will reduce the body’s drive for sugars as its primary energy source? In other words, what does he or she need to be healthy?

To answer those questions, one has to look more closely towards bioenergetics and ask what micronutrients are needed to convert consumed foods into ATP and whether or not the patient’s diet provides those nutrients. Research suggests that the energy metabolism enzymes from the cytosol through the mitochondria require at least 22 micronutrients to utilize the macronutrients from consumed foods to produce ATP. Many of these micronutrients are in short supply with high carbohydrate diets (see Threats for details). Thiamine is top among them, and because of its gateway role in energy metabolism, thiamine insufficiency is a significant contributor to the disease processes currently attributed to hyperglycemia.

Thiamine, Sugar, and Energy Metabolism

Thiamine is a required and rate-limiting co-factor to five enzymes involved in energy metabolism, including those at the entry points for the glucose, fatty acid, and amino acid pathways (transketolase, pyruvate dehydrogenase complex [PDH], 2-Hydroxyacyl-CoA lyase [HACL], and branched-chain alpha-keto acid dehydrogenase [BCKAD] and alpha ketoglutarate dehydrogenase [a-KDGH]. Insufficient thiamine leads to poor glucose handling resulting in hyperglycemia. It also induces poor protein and fatty acid metabolism resulting in the elevated branch-chain amino acids and dyslipidemias common to patients with hyperglycemic metabolic syndrome.

Conversely, high carbohydrate diets increase the demand for thiamine, which, if left unchecked, ultimately leads to thiamine deficiency, hyperglycemia, disturbed protein, and fatty acid metabolism. In healthy, thiamine-sufficient adults, high carbohydrate consumption results in a significant reduction of mean plasma thiamine concentrations in just over three weeks. Over the longer term, a high carbohydrate diet initiates many changes in thiamine and energy metabolism that ultimately result in reduced thiamine availability, higher circulating glucose, and poor energy metabolism. Thus, whether by cause or consequence, low thiamine and hyperglycemia are inextricably intertwined. One eventually leads to the other.

Altered Metabolism and Mechanisms of Damage

Under normal glycemic conditions and where thiamine is sufficient, excess sugars from glycolysis are shuttled through the pentose phosphate pathway via the thiamine-dependent enzymes transketolase to PDH and onward through the mitochondria. Under conditions of high carbohydrate intake/low thiamine, however, these sugars are diverted away from the primary metabolic pathways used for ATP production, inducing a net decline in ATP, and away from the synthesis of ribonucleotides and NADPH, substrates for RNA/DNA, and fatty acid metabolism and ROS detoxification respectively, to secondary metabolic pathways, specifically, the polyol/sorbitol, hexosamine, diacylglycerol/PKC, advanced glycation end product (AGE) pathways. Research suggests the upregulation of these pathways underlie the macro-and microvascular cell damage attributed to hyperglycemia, related cardiovascular and neural damage, while the decrements in ATP drive the general metabolic dysfunction associated with obesity and a host of other inflammatory conditions.

The high carbohydrate/low thiamine diet disturbs amino acid and fatty acid metabolism as well. Elevated branched-chain amino acids (BCAA) are common with hyperglycemia. Indeed, elevated BCAA may predict impending diabetes. Underlying the elevated BCCA is impaired catabolism due to a genetic or environmentally triggered defect in the BCKAD enzyme. BCKAD is dependent upon thiamine and elevated BCCAs are a manifestation of deranged energy metabolism precipitated by thiamine insufficiency. Genetic aberrations of BKCAD display similarly elevated BCAA, though typically much earlier, and respond favorably to thiamine supplementation.

With chronic hyperglycemia, the increased branched-chain keto acids, a secondary effect of poor BCAA catabolism, lead to excess short and medium-chain acylcarnitines. Surplus acylcarnitines increase the flux of fatty acids through the b-oxidation pathway beyond its capacity. This results in incomplete fatty acid metabolism, the dyslipidemias noted with hyperglycemia, and the formation of the pro-inflammatory diacylglycerol and ceramides that reinforce insulin resistance.

All of this, of course, comes against the backdrop of declining ATP capacity. Under conditions of insufficient thiamine/hyperglycemia, ATP production may be reduced up to 70% depending upon the severity and chronicity of disordered metabolism, the organ or tissue in question, and the model used to test. Decrements in the brain and heart, because of their high energy demands are the most severe, while reductions in the GI system and musculature present most noticeably in the early stages. Fatigue, weakness, and GI disturbances are among the earliest and most common unrecognized symptoms of the initial stages of insufficient thiamine.

Correcting Metabolic Dysfunction With Micronutrients

Ideally, ill-health would precipitate dietary changes, but in the case of hyperglycemia, particularly when it is chronic, the altered metabolic pathways and reduced capacity to synthesize ATP from consumed foods make this prospect difficult to impossible for some. Based upon thiamine’s role in this process, a more amenable approach might be to address thiamine and other micronutrient deficiencies first. Research from multiple disciplines demonstrates the remarkable improvement in metabolic capacity with thiamine repletion suggesting that simply replenishing this and other micronutrients may slow or reverse the progression of disease in these populations. Below are a few of the hundreds of studies published on this topic.

  • Thiamine reduced or reversed hyperglycemia-related activation of the secondary glucose pathways (polyol/sorbitol, hexosamine, diacylglycerol/PKC, AGE) via upregulation of the PDH enzyme. It improved cardiac contractility, reduced cardiac fibrosis and decreased the expression of the mRNA-associated proteins (thrombospondin, fibronectins, plasminogen activator inhibitor 1, and connective tissue growth factor), and prevented obesity in the overfed arm of an experiment using streptozotocin-induced diabetes in rats.
  • In streptozotocin (STZ)-induced diabetic rats, high-dose thiamine and benfotiamine (a synthetic S-acyl derivative of thiamine) therapy increased transketolase and PDH activity increasing ribose-5-phosphate and reduced microalbuminuria and proteinuria by 70-80%. PKC, AGE, and oxidative stress were all reduced significantly.
  • In STZ-induced diabetic/leptin mutant type rats, benfotiamine improved heart function and prevented hyperglycemia-induced, left ventricular end-diastolic pressure increase and chamber dilatation in both models.
  • Benfotiamine administration 150mg thiamine daily thiamine significantly reduced blood glucose within a month, in a randomized, placebo-control trial of 24 drug naïve T2D diabetics.
  • In a three-month randomized placebo controlled trial, 50 T2D patients in the experimental arm were given 3X 100mg thiamine per day. Thiamine therapy significantly improved microalbuminuria, glycated hemoglobin, while decreasing PCK levels. Markers of oxidative stress and fibrinolysis were non-significant.
  • After 45 days of benfotiamine and vitamin B6 supplementation, 19 of the 22 patients enrolled in the study saw statically significant reductions in pain, symptom scores, neurophysiological and biological markers of diabetic neuropathy.
  • A 6 month randomized trial with 60 T2D with medication-controlled blood sugar and 26 age – and BMI-matched controls found that 100mg thiamine daily, significantly corrected lipid profiles and creatinine levels.
  • One time administration of 100mg IV thiamine, improved endothelium-dependent vasodilatation in 10 patients with TD2 during an acute glucose tolerance test.
  • One week of IV thiamine administration at 200mg/day in six patients with heart failure (HF) and who were also receiving diuretics (diuretics deplete thiamine) improved left ventricular ejection fraction (LVEF) in four of those patients from 24% to 37%.
  • A randomized, double-blind, placebo controlled study of HF patients on diuretic treatment found that 300mg/day oral thiamine improved LVEF significantly.

Thiamine Insufficiency Versus Deficiency

Among the more common misperceptions about thiamine is that deficiency is delineated by laboratory testing. While this is true for severe deficiency and when the appropriate laboratory tests are utilized, far too often, the insufficiency syndromes that present months to decades before frank deficiency is detected, are missed completely. This owes in part to the variability of testing methodologies and in part to the very framework from which we determine sufficiency and deficiency. Thiamine testing, like the tests for many micronutrients, carries a high false-negative rate and fails to consider the nature of micronutrient deficiency relative to need. The next paper in this series will addressing testing methods.

As outlined above and in the Threats document, several environmental variables increase the demand for nutrients, a diet high in carbohydrates is top among them. The increased demand will not necessarily or immediately test positive for deficiency. Rather, it will present symptomatically and must be suspected based upon the symptoms of deranged energy metabolism. In these cases, thiamine supplementation is done to support and correct reduced enzyme activity so that consumed foods may be more efficiently metabolized and converted into ATP. This then reduces the use of the less efficient and generally deleterious secondary metabolic cascades linked to the constellation of negative health effects associated with hyperglycemia.

Consider Thiamine

Thiamine is a safe, non-toxic, essential nutrient that has become increasingly difficult to maintain in the face of modern dietary practices and chemical exposures. Thiamine sufficiency is fundamental to energy metabolism, mitochondrial capacity, and thus, health. Consider thiamine in your practice.

We Need Your Help

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

Yes, I would like to support Hormones Matter. 

Image created using Canva AI.

Related posts:

food composition and hyperglycemiaFood Composition and Hyperglycemia thiamine deficiency in modern medical practiceThiamine Deficiency in Modern Medical Practice thiamine and the energy to healThiamine and the Energy To Heal mercury, parkinson's, thiamineMercury, Parkinson’s Disease, and Thiamine

You might be interested in

Vitamin Therapy Paradox: Getting Worse Before Getting Better

Published on
50.2K views
paradoxical reactions with thiamine

Does modern medicine accept the idea of vitamin therapy? The answer is a resounding no!  It has only been a little over 100 years since vitamins were synthesized. Of course, as everybody knows, all of these chemical substances were found to exist in natural food. They were very much part of the mystery of evolution. Essential to all animal life, they were there for the picking. Later, it was also found that a number of essential minerals were required. Both the vitamins and minerals need to be present in minute doses, covered under the eponym of recommended daily allowance (RDA). All we had to do was to obey the rules set out by Mother Nature. Our ancestors were classified as “hunter gatherers”. They hunted animals and gathered the bounty of nature. Yes, we were primitive savages and life was not the ideal by any means, but the food contained all that was necessary for life.

An Evolutionary Imperative To Eat Real Food

To ascertain what kind of food is required by an animal, you simply look at the teeth. We have front teeth called incisors for cutting, the pointed teeth called canine for tearing meat and the back teeth molars, used for grinding. Cows and horses are vegetarian and only have molar grinders. Human beings are omnivores (all foods edible) meaning that we are designed to eat meat, fruit and vegetables. Some of the vitamins are recycled through eating other animals. Others are recycled by being returned to the soil and passing into plants. That is why I have said to many people in answering the question as to what diet they should pursue, eat only nature made food and leave the man made food alone. Well, of course, you know that we didn’t do that.

We now have a food industry and it is quite unbelievable, at least to me, to see some of the stuff that passes as food, based solely on taste and appearance. Sometimes I find a person with these typical symptoms who is very careful with diet and does not practice taste hedonism, but because farming practices have changed in modern times, the produce does not have the same kind of non-caloric nutrient content. It may not be coincidental that such persons are almost invariably intelligent and physically and mentally active. It is reasonable to assume that their nutritional demand exceeds supply and they need non-caloric nutrients.

Sugar and the Vitamin Paradox

Now let me turn to the reason that I used “vitamin paradox” in the title. Anyone that wants to follow my reasoning can look back at previous posts on this website. You will find that there is a significant emphasis on the calamity of sugar ingestion and its association with vitamins, particularly thiamine. I am sure that I will look like a broken record to many people, but here is what happens to your health. Although it is obvious that all the vitamins and essential minerals are required, I am taking the example of thiamine because of its close association with the wide consumption of things called “goodies” or “sweets”.

All simple carbohydrate foods are broken down in the body to glucose. Research has shown that overloading the metabolism with sugar overwhelms the capacity of cellular machinery to burn (oxidize) it by producing a relative deficiency of thiamine, the vital catalyst that ignites (oxidizes) glucose to synthesize cellular energy for function. Recently it has been found that thiamine is required for the oxidation of fats, making the doughnut a perfect example of high calorie malnutrition. This is so important in the brain that I simply cannot overstate it.

High Calorie Malnutrition, Oxygen Deprivation and Brain Function

High calorie malnutrition is exactly equivalent to a mild degree of oxygen deprivation, so it is sometimes referred to as pseudo-hypoxia (false oxygen deprivation). If this is induced by poor diet where the pleasure of taste (hedonism) overrides appropriate nutrition, a curious thing happens! The lower part of the brain that deals automatically with your ability to adapt to a hostile environment becomes much more susceptible in its responsiveness.

I will give you one example: panic attacks, so extraordinarily common in our culture, are simply fight-or-flight reflexes that are triggered by pseudo-hypoxia. Messages go out to the body from this part of the brain, falsely initiated as though you were actually being “chased by a tiger”. Such an affected person will begin to experience the following symptoms as examples: palpitations of the heart, unusual sweating, a sense of anxiety or panic, irritable bowel syndrome, manifestations of allergy, emotional lability (emotions out of control) etc.  He or she will go to the doctor who will do a series of tests. If they are all normal, you will then be told that this is “all in your head” (psychosomatic). On the other hand, the doctor might find evidence for “mitral valve prolapse” (MVP), now known to be an early sign of “wear and tear” damage in the heart and the focus becomes “heart disease”(often used to explain heart palpitations) rather than its original cause, associated with nervous system dysfunction. I have seen MVP disappear in people from correcting their nutrition. It is rare for a patient to be asked about diet and rarer still to question the possibility of a vitamin deficiency.

Vitamin Deficiency: The Walking Sick

This kind of health situation may go one for a long time. The patient has symptoms but is not really a sick person. I refer to people like this as the “walking  sick”. Life continues as usual, but medications have failed to relieve the symptoms, or worse yet have introduced side effects. Over time, the loss of metabolic efficiency gradually leads to damage in cellular machinery (e.g. MVP) because the energy need to drive daily function is not being met. Thiamine activates the most important enzyme in energy synthesis and, in the early stages of nutritional deprivation, a thiamine plus multivitamin supplement would quickly abolish the symptoms. If neglected and the marginal malnutrition continues, it will be gradually more difficult to repair the damage.

Vitamin Therapy With Chronic Deficiency: Expect a Decline Before Improving

Physicians who practice Alternative Medicine have found that it is possible sometimes to retrieve function at this late stage of development by the use of a course of vitamins given intravenously. They have also learned that the symptoms of the patient actually get worse (paradox) in the initial stages of intravenous treatment but begin to get better following an unpredictable period of worsening. Naturally, the patient concludes that the treatment is bad or that it is causing side effects as in the use of vitamins. That is why I have christened it paradox, meaning that the unexpected happens.

Over the years of administering intravenous vitamin therapy for all kinds of conditions, irrespective of conventional diagnosis, I quickly learned to inform a patient about paradox before instituting treatment. Surprisingly, this paradoxical response usually heralds a good outcome. I do have some ideas about the cause of paradox, but it is so technical that I cannot attempt it here, perhaps in future posts. Intravenous vitamins are tremendously effective in the improvement of most chronic diseases, an effect that is almost impossible to achieve with the standard treatment of drugs as used in modern medicine today.

Related posts:

thiamine paradoxWith Thiamine Paradox Symptoms Patience Is Key Just a vitamin deficiencyJust a Vitamin Deficiency mother daughter B vitamin deficienciesFrom Mother to Daughter: The Legacy of Undiagnosed Vitamin Deficiencies Health requires energyHealth Requires Energy. Energy Requires Nutrients.

You might be interested in

Thiamine Deficiency in Modern Medical Practice

Published on
9.2K views
thiamine deficiency in modern medical practice

Modern medical practices are plagued with patients who present with chronic, complex, and seemingly treatment resistant illness; illnesses that defy most laboratory testing and abound current diagnostic categories. Some data suggest that 25-75% of symptoms experienced by these patients fall under the umbrella of ‘medically unexplained symptoms’.

What if some of those symptoms were not only explainable but treatable and the expression of these illnesses manifested not from some complicated new disease but from a simple but forgotten nutrient deficiency? What if this nutrient was uniquely critical to mitochondrial competence such that its insufficiency would derail energetic capacity, affect cellular function broadly and diversely, and produce many of the symptoms currently ascribed as medically unexplained? Wouldn’t this be worthy of investigation in your patient population?

That nutrient is thiamine or vitamin B1 and it is essential to mitochondrial energetics – the conversion of food into adenosine triphosphate (ATP). This process is the backbone of all health, and absent sufficient thiamine, it grinds to a halt producing many of the diseases processes vexing modern medicine.

Thiamine is a critical and rate-limiting cofactor to five key enzymes involved in this process, including those at the entry points for the glucose, fatty acid, and amino acid pathways. It has a very short half-life (1-12 hours), limited storage capacity, and is susceptible to depletion and degradation by a number of products that epitomize modern life.

When thiamine is insufficient to overcome these variables, oxidative metabolism falters and the ability to generate molecular energy declines. Over time, aerobic respiration turns anaerobic, oxidative stress increases, and cellular, tissue, and organ function dependent upon steady state energetics deteriorates.

Anaerobic glycolysis, the telltale sign of everything from general metabolic dysfunction to cancer, is, at its root, an adaptive response to insufficient micronutrients like thiamine. Replenish thiamine, recover mitochondrial capacity, and aerobic metabolism and health improve.

Critically Ill Versus Walking Sick: Gradations of Insufficient Thiamine

Conventionally, thiamine deficiency syndromes have been described relative to overt, and often later stage illness in the hospital setting. The most common designations include: Wernicke’s encephalopathy marked by nystagmus, ataxia, and cognitive deficits; wet beriberi or high output cardiac failure with edema and dry beriberi, central and peripheral nervous system and cardiovascular disturbances without edema. More recently, sensorimotor polyneuropathy or neuritic beriberi, gastrointestinal dysmotility syndromes, and the dysautonomias have been included in the spectrum, but recognition is lagging.

These designations give the false illusion of a disease process that happens acutely and one that can be categorized by the afflicted organ system. Neither is accurate. While overt thiamine deficiency is certainly a medical emergency and may sometimes develop acutely, the vast majority of cases represent a culmination of years, if not decades, of insufficient thiamine intake relative to need. Until fulminant, these disease processes are marked by low mortality, but high, chronic, and polysymptomatic morbidity. This suggests ample opportunity to treat and prevent more serious illness, improve the patient’s quality of life, and possibly even regain health. Even in overt and emergent cases, where symptomology is obvious, resolution is possible with thiamine repletion.

Thiamine Depleting Factors

Thiamine deficiency is most commonly associated with food insecurity and chronic alcoholism; a narrow view that risks missing early signals of accruing disease across patient populations. Contributors to this deficiency are far more prevalent in first world countries with westernized food production than is recognized. Among the key dietary contributors to insufficient thiamine:

  • Alcohol
  • Tobacco
  • High carbohydrate, highly processed foods
  • Coffee, tea, energy drinks

Additionally, the regular use of common medications and/or exposures to environmental chemicals independently and synergistically provoke thiamine deficiency. Every medication and environmental chemical depletes thiamine directly or indirectly by a number of mechanisms including blocking thiamine uptake, increasing its degradation, preventing synthesis in gut microbiota, increasing excretion and/or by inducing mitochondrial damage by other means that then necessitates a higher thiamine intake to compensate. Some of the most commonly used medications are the biggest offenders:

Sadly, poor dietary habits trigger thiamine insufficiency independently, leading to the prescription of many of these medications, which then further derail thiamine status and mitochondrial capacity. It is an illness spiral that can only be resolved by addressing diet and mitochondrial nutrients like thiamine.

Genetic Contributors to Thiamine Deficiency

While thiamine deficiency diseases are predominantly attributable to diet and lifestyle variables, a number of common genetic polymorphisms in the solute carriers responsible for thiamine uptake, and in enzyme activity involved in thiamine metabolism, increase the demand for thiamine intake. In these cases, disease expression, particularly later in life, represents a latent genetic vulnerability triggered by environmental or lifestyle stressors. Many medication and vaccine reactions fall into this category.

Prevalence Across Patient Groups

Inasmuch as thiamine status is not regularly evaluated in clinical care, it is difficult to know how pervasive thiamine deficiency is within the general population. Moreover, there are no universally accepted cutoffs demarking the progression from suboptimal to frank deficiency. Of the data that do exist, it is likely far more common than recognized across a broad swathe of patient populations.

Strikingly, diabetes confers one of the largest risks for thiamine deficiency across patient populations. This is largely do to metabolic derangements (to be discussed in a subsequent post) initiated by the hyperglycemia. These include the increased excretion of thiamine, and interestingly, the endogenous production of the anti-thiamine molecule oxythiamine.

Thiamine Testing

Laboratory assessment of thiamine status varies in sensitivity and specificity, with some tests carrying a high false negative rate (standard serum and plasma), particularly when thiamine status is marginal and with recent intake of thiamine. The two most sensitive tests are whole blood HPLC and the erythrocyte transketolase activity/thiamine pyrophosphate effect combination, neither of which is readily available. Urinary organic acid tests, while indirect, may provide useful patterns for determining the need for thiamine and other mitochondrial nutrients.

How To Recognize Thiamine Insufficiency

In light of the difficulties associated with laboratory testing, clinical acumen is required. Given its role in energy metabolism, lack of energy, in multiple manifestations, is a cardinal indicator of insufficiency.

  • Chronic fatigue, muscle weakness, or pain
  • Hypersomnia or anorexia
  • Dysautonomic reactions – exaggerated, ill-timed, or inadequate autonomic responses to stressors, most notably in the brain, heart and/or GI system

Office observations to support thiamine insufficiency:

  • Subtle changes in gait, stability, muscle tone, speech, decrements cognitive or affective acuity or stability
  • Asymmetrical pulse pressure, postural hyper- or hypotension, general tachycardia (early stage), bradycardia (later stage)

Standard labs pointing to problems with energy metabolism:

How to Treat

While clinical practice guidelines exist for overt thiamine deficiency in hospital, which include the use of IV thiamine and additional nutrients at a range of doses dependent upon severity, there are no established guidelines for out-patient thiamine deficiency or insufficiency syndromes. This is partly due to its lack of recognition and partly due to the fact that individual need for thiamine, other mitochondrial co-factors, and response to repletion, varies considerably.

There are no known toxicities to high doses, however, there can be negative reactions in the initial phases of thiamine repletion for a subset of patients. These reactions can occur at any dose. In some cases, the reaction involves the specific formulation of thiamine. In other cases, electrolyte disturbances and/or other micronutrient deficiencies unmasked by thiamine are at fault. To mitigate these reactions, thiamine should always be given with magnesium (~50% of the population consumes less than the RDA and magnesium is required to activate thiamine), a clean, lower dose multi-vitamin and a potassium rich diet. It should be noted that additional calcium may also be needed (here, here), especially when dietary calcium has been low for an extended period. Hypophosphatemia may develop as well in patients with recent or extended GI illnesses and/or have a history of low protein consumption and sodium disturbances are also common.

Consider Thiamine

Thiamine is a safe, non-toxic, essential nutrient that has become increasingly difficult to maintain in the face of modern dietary practices and chemical exposures. Thiamine sufficiency is fundamental to energy metabolism, mitochondrial capacity, and thus, health. Consider thiamine in your practice.

We Need Your Help

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

Yes, I would like to support Hormones Matter. 

Related posts:

thiamine testingThiamine Testing in Clinical Practice Thiamine deficiency, hyperglycemia gateway to diseaseHyperglycemia and Low Thiamine: Gateways to Modern Disease The role of thiamine in potassium deficiencyThiamine Deficiency Causes Intracellular Potassium Wasting hyperemesis thiamineQuick Thoughts: Hyperemesis and Early Thiamine Deficiency

You might be interested in

Eosinophilic Esophagitis May Be a Sugar Sensitive Disease

Published on
61.9K views
Eosinophilic Esophagitis

In 2011 a mother called me and asked whether I would be able to help her 14-year old son who had been diagnosed with eosinophilic esophagitis. Because this disease had only been recognized in the past two decades I had to confess that I had never heard of it. Because I used only nutrients in therapy, I confessed my ignorance but that I was willing to have a shot at it. Obviously, the first thing that I did was to see what had been written about this newly recognized condition.

Eosinophilic Esophagitis: Inflammation of the Esophagus

The part of the gastrointestinal tract that is most commonly affected by this inflammatory infiltration is the esophagus (esophagitis), although it has been recorded in other parts of the intestine when it is known as eosinophilic enteritis. Eosinophils are specialized white cells that have a role in inflammation. They have this particular name because they stain with a dye called eosin (the postfix phil is derived from the Latin word for love) making it easy for a pathologist to recognize their presence in tissues.

Eosinophilic esophagitis (EoE) is now by far the most common form of eosinophilically infiltrated gastrointestinal disease. It represents the most recent form of food allergy, and its control by avoiding offending foods has increasingly appeared as a therapeutic approach. It is often poorly responsive to therapy and there is no commonly accepted long-term treatment. The diagnosis has to be made by endoscopy and it is distinguished from other causes of inflammation by finding eosinophils in the inflammatory area.

A Complex Medical History Misdiagnosed As Psychosomatic

The medical history of this 14-year-old boy had begun in infancy with recurrent ear infections and asthma, entailing many doctor visits. But he also had many confusing symptoms throughout childhood other than the chest pain and swallowing difficulties that might be expected from inflammation of the esophagus. In fact, these symptoms had been thought of as psychosomatic until endoscopy was performed when he was 8 years old and the esophagitis was discovered. From that time on, he had been examined repeatedly and had received conventional treatment without success at several prestigious institutions. He came to my attention 6 years after the diagnosis had been made.

His early history of repeated ear infections and asthma were important because both of these conditions are now known to be related to inefficient oxidative metabolism. Eosinophils are associated with asthma in some cases. The symptoms that had been considered to be psychosomatic included a dramatic response to any physical pain producing stimulus (hyperalgesia), emotional instability, unusual fatigue, headaches, dizziness, panic attacks and increased sensitivity to both sound and light. For example, when I came to the physical examination he would scream when I touched his abdomen and the abdominal muscles would become rigid. Another intriguing symptom was that he coughed in his sleep (an exaggerated cough reflex) without becoming awakened and he also experienced nightmares. He had also been diagnosed by a psychologist with ADHD and OCD. But on physical examination, I also found many intriguing signs that indicated autonomic nervous system dysfunction. The medical history also indicated that he was addicted to sugar, and alcoholism was widespread on both sides of the family, both being related to thiamine metabolism. People who have read some of the posts on this website will be familiar with the association of thiamine deficiency with sugar ingestion and alcohol.

A Family History of Alcoholism and Thiamine Metabolism

Because of this family history of alcoholism, his addiction to sugar, and the known relationship of thiamine deficiency with autonomic dysfunction, I used the blood test known as erythrocyte transketolase and I was not too surprised to find that it was extremely abnormal, proving a severe degree of thiamine deficiency or abnormal thiamine metabolism. He was treated with a series of intravenous infusions of water-soluble vitamins that contained thiamine hydrochloride. Although his symptoms began to improve, the transketolase test became much more abnormal, suggesting that thiamine was not being absorbed into the cells that needed it. Thiamine tetrahydrofurfuryl disulfide (TTFD: Lipothiamine, a derivative of thiamine that is absorbed more easily because it does not require the complex mechanism that is required for the absorption of dietary thiamine) was substituted for the thiamine hydrochloride with the result that the transketolase improved greatly.

Symptoms continued to improve but the most surprising thing that happened was the tremendous growth spurt that occurred throughout a year of treatment. Body weight at the beginning of treatment was 105 pounds, placing him in the 25th percentile. After one year of treatment his weight had increased to 122 pounds (+17#), placing him in the 50th percentile (e.g. male or female members of a school class). His stature increased in the same time period from 64.5 inches to 68.5 inches (+4”), raising it from the 50th to the 75th percentile. Percentiles are used in growth charts to indicate the normal height and weight of an individual as compared with subjects of the same age. For example, the fiftieth percentile would mean that 50% of a given similar group (e.g. a school class) would be taller/heavier and 50% shorter/lighter. For normal height and weight a subject remains in the same percentile throughout growth. A “jump” of this nature is extremely rare. It is unlikely that he would have been considered growth retarded if this dramatic acceleration had not occurred. He would have just been regarded as a “shorty”.

Dysautonomia

As reported in several posts on this website, dysautonomia is used to describe changes in the functional controls of the autonomic (automatic) nervous system. There are two branches to this system known as sympathetic, the action system, and parasympathetic, the “rest and be thankful” system. The first one is activated by any form of stress that includes a mild degree of oxygen lack (hypoxia) in the lower part of the brain or its equivalent from lack of thiamine and known as pseudohypoxia. There is also a genetically determined disease known as Familial Dysautonomia (FD) in which growth retardation is a constant feature. Although FD is a genetically determined disease, it is the resulting dysautonomia that causes growth failure. This suggests that the long-standing dysautonomia in this patient, due to energy inefficiency in brain cells caused by the pseudohypoxia of thiamine deficiency, was responsible for growth failure. Restoration of thiamine concentrations caused improvement in energy metabolism that enabled the growth spurt to take place.

Conclusion: Inflammation Is a Defensive Response

Inflammation is really a defensive response made by the body to some form of attack. In the case of this disease it appears that certain foods act as the attacking agent, hence the term food allergy. The inflammatory reaction is kept under very careful control by the brain acting through a nerve that runs the entire length of the intestinal tract. If this nerve fails in its suppressive action, the inflammation gets out of control. For the normal function of this nerve thiamine is a necessity. But thiamine deficiency, because it results in pseudohypoxia, also activates the sympathetic branch of the autonomic system and was responsible for the many symptoms that had been previously described as psychosomatic. It is very likely that the huge ingestion of sugar in the United States is responsible for thiamine deficiency that results in manifestations of disease that vary in their presentation according to the particular cells affected by the deficiency. Because of the family history I strongly suspect that there was a genetic relationship that created this boy’s sensitivity to foods, particularly sugar, making thiamine deficiency much more likely. It is of course possible that this is but one cause of eosinophilic esophagitis/enteritis. It suggests however that some form of pseudohypoxia (other than thiamine deficiency) is the root cause of the disease and that the inflammatory response gets out of control because of autonomic dysfunction. This case is now “in press”.

Lonsdale D. Is Esosinophilic Esophagitis a Sugar Sensitive Disease? J Gastric Disord Ther 2016;2(1):doihttp://cbcdoi.org/10.16966/2381-8689.114.

We Need Your Help

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

Yes, I would like to support Hormones Matter. 

Photo by Myriam Zilles on Unsplash.

This article was published originally on February 8, 2016.

Related posts:

seizures, EOE, Autism, thiamineASD, Seizures, and Eosinophilic Esophagitis: Could They Be Thiamine Related? Kawasaki Disease Thiamine and sugarSugar Intake and Thiamine Charcot marie tooth disease thiamineCharcot Marie Tooth Disease and Thiamine: A New Genetic Connection

You might be interested in

Diet Induced Pseudo-Hypoxia and Hypertension

Published on
12.4K views
pseudo-hypoxia hypertension

Although hypertension has become almost exclusively used to indicate high blood pressure, it is worth examining the true underlying meaning. The prefix “hyper” is from the Greek, meaning over or above. Tension is defined as “the state of being stretched tight”. Perhaps then it is worth looking at how this applies to blood pressure.

When a blood pressure is measured, there are always two figures represented. The higher number is known as “systolic” and the lower one as “diastolic”. The systolic is when the heart is contracting and indicates the ability of the arterial system to expand enough to accommodate the pressure from an increased volume of blood. The diastolic indicates the pressure in the arterial system when the heart is resting between beats. We are therefore looking at the highest and lowest pressures in a closed tube system that must be capable of expanding and contracting.

Since the system is made from live cells, it does not behave like a rubber tube with elastic recoil. The arteries where blood pressure is measured are lined with muscles. It is the contraction and relaxation of these muscles that control the capacity of the artery to accommodate the amount of blood arriving from the heart. The muscles are controlled by nerves carrying messages from the brain. These muscles are completely different from those that are activated willingly, such as those in the limbs. They are contracted and relaxed automatically by a part of the brain that acts more like a computer. The body muscles are activated by a nervous system known as “voluntary”. The arterial muscles are activated by a completely separate an involuntary nervous system known as autonomic (ANS). We therefore have to examine the control mechanisms.

Understanding the Autonomic Nervous System

I have discussed this nervous system many times in Hormones Matter because, when it goes wrong, it is a potent source of disease. The nerves of this system go to every organ within the body. The control system is in the lower part of the brain. It consists of two channels. One is known as sympathetic: the other is known as parasympathetic. Although they work together, their actions oppose each other and I will try briefly to outline this dichotomy.

Sympathetic. The sympathetic nervous system is designed for both physical and mental action through a reflex mechanism known as the fight-or-flight. It prepares us to meet an enemy or escape from danger. One of its actions is to raise the blood pressure. It does this by contracting the arterial muscles already described.

Parasympathetic. When the action is completed, the brain controls automatically withdraw the activity of the sympathetic and initiate those of the parasympathetic nervous system. When this happens, the body is prepared for resting.

Chronic Activation of the Sympathetic Nervous System

There is a large amount of evidence in the medical literature that this is the primary cause of chronically high blood pressure. If the system is healthy, the blood pressure will go down on completion of the action. If not, the blood pressure remains elevated. From here, I am going to hypothesize why this happens. Please remember as you read it that it is a hypothesis, not a proven fact.

Hypoxia. This word simply means lack of oxygen. Obviously, this is a dangerous state for the brain and it is not surprising that it will activate the sympathetic component described above, including raising the blood pressure.

Pseudo-hypoxia. The prefix “pseudo”, meaning false, or sham (from the Greek, lying, false) has been used in the medical literature to describe a state that is exactly like that of hypoxia when the presence of oxygen is normal. In order to understand this, focus on the fact that oxygen must be introduced to the body but is completely useless unless it is consumed. Therefore we must try to indicate how oxygen consumption occurs.

Oxidation and burning. All forms of burning are derived from oxygen combining with a fuel, liberating heat energy. That is why we are warm blooded, but other forms of energy are produced to drive physical and mental function. Because the burning is incomplete, ash is formed. Our cells derive their energy by the oxygen, delivered in the blood from the lung, combining with glucose. The “ash” is carbon dioxide and water, discarded in the breath. The oxidation of glucose is governed by a set of enzymes that require the vitamin B complex for their action. The leader of this orchestration appears to be vitamin B1 (thiamine). That is why many papers have appeared in the medical literature that describes thiamine deficiency as a cause of pseudo-hypoxia. Its function is to catalyze the enzymes essential for oxidation. Its deficiency results in lack of sufficient energy. It is therefore not surprising that one of the symptoms of thiamine deficiency is fatigue.

Calorie/thiamine ratio. A healthy diet provides us with calorie producing elements that are broken down to glucose and used as fuel. The amount of thiamine provides a normal calorie/thiamine ratio that enables efficient oxidation. If we load the diet with empty calories (calories without essential non-calorie nutrients that include thiamine) the calorie/thiamine ratio becomes abnormal. Measuring the concentration of thiamine in the blood would be normal for a healthy diet but inadequate to meet the demand of the empty calorie load. The laboratory method for identifying thiamine deficiency is by measuring it in the blood. If the result is reported by the laboratory as normal, the relevant symptoms produced by inadequate oxidation may well be ascribed to causes other than thiamine deficiency.

Hypothesis: High Calorie Malnutrition Induces Chronic Sympathetic Overdrive

I suspect that a common cause of hypertension is high calorie malnutrition, inducing a state of chronic sympathetic overdrive. It may be why obesity in children often foretells their rise in blood pressure. Perhaps another cause is the gradual diminution of oxidation associated with aging. There are genetic mechanisms that are turned on by hypoxia and these also may be activated by pseudo-hypoxia, e.g. thiamine deficiency.

Spontaneously Hypertensive Rats

Lipothiamin is a synthetic derivative of thiamine. Its biologic properties enable it to be used as a drug. A rat known as SHR (spontaneously hypertensive rat) is used as the animal model for studying the effect of antihypertensive drugs. Many years ago I took a group of these rats and treated them with Lipothiamin to see if it would prevent the rise in blood pressure that always occurs in these animals. There was a statistically significant difference between the experimental rats and the controls, indicating that this thiamine derivative did indeed prevent the spontaneous rise in blood pressure. This experiment is published in our book (Lonsdale D, Marrs C. Thiamine Deficiency Disease, Dysautonomia and High Calorie Malnutrition). It obviously requires human subjects to research the use of this completely non-toxic, nutrient/drug derivative but nevertheless provides us with solid clues about hypertension.

Conclusion: Diet Matters

It has been said that simplicity must be distilled out of complexity in order to make complex issues usable. The brain/body, whether we like to recognize it or not, is an “electrochemical machine” that must obey all the physical laws designed by Mother Nature. Health is governed by only three factors:

  1. Genetics: the enormous complexity is dictated by a code written in DNA. Passage from generation to generation makes mistakes and represents our inheritance.
  2. Stress: defined as anything that requires physical/mental defensive response. The response, designed for relatively short term action, demands a huge consumption of energy.
  3. Nutrition: this is the only one of the three issues that we can control. It must supply both fuel and the multiple factors that enable the fuel to be turned into energy.

We Need Your Help

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

Yes, I would like to support Hormones Matter. 

Related posts:

seizures hypoxiaAre Seizures Due to Hypoxia? dysautonomia thiamine deficiencyDysautonomia and Hypoxia

You might be interested in

Familial Beriberi: Discovering Lifelong, Genetic, Thiamine Deficiency

Published on
19.5K views
Familial Beriberi - genetic thiamine deficiency

In 2017, at the age of 52, I had an unexpected call from my new doctor informing me “I know what’s wrong with you! Come to my office now!” Lifelong increasing chronic fatigue and untreatable Hashimoto’s thyroiditis were my chief complaints.

Past doctors prescribed high dose thyroid medication, which made me feel worse. An autoimmune diet kept me trim but provided no energy. I read adenosine triphosphate (ATP) is required for thyroid production, though ATP isn’t discussed in treatment. Baggage from Effexor and an adverse childhood were also contributors to my health.

Desperate, every relevant supplement and thyroid medication on the market, I tried. Only two were effective. GABA relaxed me, and d-ribose cured my depression 100%. I became bubbly. My personality changed, but after four weeks they both stopped working. Amour thyroid lifted my brain fog for a week. Then, I had side effects. Eventually, I would learn that I, and many members of my family, across several generations, had beriberi or thiamine deficiency. In my case, I had a defect in a key thiamine transporter that made getting sufficient thiamine from diet all but impossible. Unfortunately, I did not learn this crucial information, until I was in my fifties, after years of illness and suffering.

Women’s Issues and Unrelated Problems Begin

While my problems began decades earlier, they seemed to hit a crescendo as I hit menopause. The HRT patch relieved hot flashes, only to fuel a fruit-sized fibroid that split in half with one part covering my rectum. A GP prescribed colon therapy causing severe leg cramps and constipation. A fibroid ablation enabled normal bowel function. Afterward, ozone baths caused my bowel function to stop and I developed air hunger. An ENT said, “you don’t have sleep apnea, there’s another system in your body that is causing air hunger.” He recommends a university clinic over going to different specialists.  I pursued genetics.

Starting to connect my cognitive decline, prediabetes, and depression in my grandparents to myself, I went to the MTHFR expert that wrote the report.  Her extensive 15-page genetic/supplement report offered no results. After failed treatments from endocrinologists, functional doctors, and big-name clinics like Mercola, I took a chance on Orthomolecular Medicine.

Discovering a Familial History of Beriberi

On the day I was diagnosed with thyroid treatment failure, I found a nutrient interaction article and had a light bulb moment, I’m missing a nutrient for thyroid production. I went to the author, the late Dr. Richard Kunin, San Francisco’s legendary go-to doctor for solving mystery illnesses through nutrients. He was a pioneer in antioxidant therapies, utilizing diet, nutrient and genetic testing since the seventies.  His orthomolecular research was the first to verify the use of a mineral therapy in a drug-induced disease.

When his door flung open, I saw wisdom. A rare commodity. Here was this brilliant doctor and a poster of his early collaborator Linus Pauling, staring down at me. Dr. Pauling coined the term orthomolecular meaning “the right molecule in the right amounts.” A doctor like this comes once in a lifetime and I handed him my three-inch binder.

A true scientist, he was able to assess my biochemical individuality, in two sessions.

In the doctor’s intake, the first clue is asking what my parents ate. They ate both Chinese and Western foods, which seemed like no big deal. After lab results, he searches through 300 genes, to find the biggest picture, the gene. Instead of trying to treat multiple gene defects with a supplement. He addresses the root cause first.

He announces, “You’re deficient in thiamine,” and gives me the SNP, called Transporter 2 (SLC19A3) which provides instructions for making a protein called the thiamine transporter, which moves thiamine into cells. Over time, the transporter dissolves.

I had thiamine and asparagine deficiency and riboflavin and glutathione borderline deficiency. The thiamine or vitamin B1 deficiency caused the other deficiencies, but he stays on point and discusses thiamine and only thiamine. He prefaces the session with a history of beriberi and birds fed white rice.  Looking back, it’s rudimentary B1 history, but as a patient stuck in the Hashimoto’s/Adrenal Fatigue paradigm for so long, my mind went blank. I remained silent, I didn’t know if I could die from it.

To make matters more confusing. I had stopped taking thiamine after an OATS showed B1 adequacy.

When he told me I can’t convert energy from food, I thought how absurd. He reminded me “the bottom line is how well you absorb the thiamine; not how much I tell you to take”. A Meyer’s Cocktail IV is an initial part of treatment. The next step is collecting data to prove the relevance of thiamine as an essential nutrient required to make energy.

When I Added Thiamine, My Body Began To Recharge

For the first time, I saw a difference in labs and body function. At 300 mg of HCL, my increasing A1C levels fell below the prediabetes range. I almost took metformin at one point, recommended by an integrative doctor. I felt the effects of B1 utilizing B6, through a lucid dream. Treating methylation since 2006, he says “B1 is the gateway to methylation.”  With before and after data, he points out B1 upregulating the folate cycling. My energy was increasing. Muscular problems resolved, elevated branched chain aminos were absorbing and TMJ and bruxism disappeared. This was just the beginning. familial beriberi - thiamine deficiency

I found the thiamine experts, Dr. Derrick Lonsdale and Dr. Chandler Marrs during my titration period. Nuances of thiamine used as a drug to make ATP are available with a detailed overview of beriberi, throughout Hormones Matter. Post to post, the doctors’ addressed every missing piece to my complex puzzle and more. They prompted me to take a closer look inside my dad’s past, one he rarely spoke of, and connections were made.

While titrating up, I had a short bout of diarrhea in the middle of the night. When I decreased the dose, I developed POTS for the first time, the room would spin 24/7 whenever I stood up. My GP referred me to the ER. I was unaware that I was having a paradox reaction. I just upped the thiamine, POTS, and diarrhea resolved.

Chronic TD is called beriberi means “I can’t, I can’t” in Singhalese. The problem is Chinese typically under 80, have never heard of beriberi, and in the US, beriberi is known but assigned as a disease that does not exist anymore or a condition only seen in alcoholics and bariatric patients. Genetic beriberi is passed through families, causing the inability to absorb thiamine from foods.

Beriberi In Two Families Going Back Three Generations

My family history revealed apparent genetics expressing as neuropsychiatric disorders and other conditions that appeared unrelated. Thiamine deficiency (TD) is not easily identified, due to its polysymptomatic nature. Besides the brain, the heart, muscle skeletal, digestive system, and autonomic nervous systems (ANS) need thiamine to function.

My maternal side lived in prosperity and ate a traditional Chinese diet and tropical delicacies. There were 7 members, including my grandfather that had Alzheimer’s (AD) and one family member had Parkinson’s. My grandmother had TD from kidney dialysis. There was TD in AIDS. Untreated hyperthyroidism resulted in cardiac failure mortality at 58. An alcoholic uncle had deficits, anxiety, cancer, and AD. An anorexic cousin refuses whole meals, develops a damaged digestive tract, severe IBS-C, chemical sensitivities, and major depressive disorder.

My paternal side lived in poverty. White rice was a diet staple. There was an aunt that died from child mortality in China from starvation.

After migrating to the US, food scarcity persisted. My grandfather had obesity and type 2 diabetes. My grandmother had sadness after her husband sold their daughter’s papers in China, never to see them again. At 61, my 4’10” grandmother fell over and died from beriberi.

Her wake was the first time my dad went to a restaurant at age 16. He often licked food and preserved it for later. Falsely accused of stealing, the detention center fed him regular meals. Five siblings had short stature and high IQs. His Chinese brother pictured right, was saved by the U.S. Army from malnutrition and assigned to be the radar instructor. There was bullying, anger, and irritation in the three boys. One, a bar owner exhibited extreme behavior like bringing a gun over a trivial conflict that would leave in-laws aghast.

Ocular diseases, restless leg syndrome, circadian rhythm disorder, cancer, some OCD and hypermobility, and osteoporosis appear. There was TD from chemotherapy. Two aunts left behind in China lived to be centurions and a daughter has fibromyalgia, depression, and other deficits.

Connect the lineage with a pregnancy gone wrong.

Genetics and a Traumatic Pregnancy Sets the Stage for Life

Pregnancy, a hypermetabolic state, requires sufficient thiamine for the development of a healthy child. My mom, a robust woman, was overmedicated and bedridden for a month post-pregnancy. She recovered but my brother was permanently disabled. My brother was born with uncontrollable hyperactivity and oppositional disorder. Our theory was his oxygen supply was cut off to his brain, but it was thiamine deficiency.

Two years later I was born. As a young child, I was hypoactive and didn’t move much. In grade school hearing loss was detected. Early memories included some clumsiness and not having the strength to swing on monkey bars like other children. My first feelings of frustration were over homework, especially math. My overall health waxed and waned and would not draw attention until high school when tiredness, poor memory and learning disabilities appeared. I was bullied by my older brother.

Nine years later my younger brother was born, bruxism as a baby, was his first sign of thiamine deficiency.

The next generation, symptoms of thiamine deficiency show in a gifted child.

Neurological deficits ranging from severe to minor were a sign of impaired methylation since birth.
My mom’s prenatal diet was traditional and American, and we were bottle-fed. This was in the ’60s when women were weaned off breastfeeding.

Now connect the genetics, the pregnancy and untreated thiamine deficiency in a parent and sibling.

A Genius Mind Uses More Energy and Requires More Thiamine

My dad invented the on-line TV guide in the eighties. In a constant state of fight-or-flight, working through the middle of the night on patents, sugary snacks were comfort foods to compensate for early years of food deprivation. The “night owl” term we used was circadian rhythm dysfunction. Thiamine is an overlooked nutrient required for sleep and the breakdown of cortisol.

When my brother’s hyperactivity was unmanageable, breaking things, beating the ADD out of my brother was habitual. A dysfunctional limbic system causes knee-jerk reactions to uncontrollable rage. I just learned that my seemingly nice uncle, an alcoholic, frequently tried to beat the homosexuality out of his young child.

A psychologist thought violence only happens in alcoholics. I think this limited view needs to be updated to include excess processed food intake. I remember “children should be seen and not heard” commercials as a child when hitting and spanking was more accepted.

In 1983, Dr. Kunin cited Dr. Lonsdale’s research that describes the B vitamin link with violence in Mega Nutrition for Women, “patients whose violent behavior was inexplicable by conventional medical diagnosis were found to be deficient in one or more B vitamins, notably B1, B3, and B6”.

During the Covid-19 shutdown, I thought of TD when incidences of abuse spiked, homelessness and random violence spread, and middle-class families now become dependent on food banks.

Poor Health After Antibiotics

As a young teen, I lost my glow, I looked tired, and my skin had a jaundiced yellow-greenish tint. In high school, after a round of tetracycline for transient acne, I was never the same. My metabolism stopped and I gained 40 lbs. I also have leptin deficiency and so I am always hungry. Napping after school was an everyday event. My limited thyroid test given showed normal thyroid-stimulating hormone (TSH). I was also constipated but didn’t know it until middle-aged after I was diagnosed with Hashimoto’s. In my 20’s I took antibiotics for chronic strep throat. Uninterested in nutrient dense foods, I subscribed to carb loading and high-intensity aerobic activity, the trend of the day.

Changes in My 30’s and the Promise of Modern Medicine

When my dad had side effects from sleep medication, he did his research, bought supplements for every system in the body, and stopped going to doctors. He got the family off of rice and put us on B vitamins. Uneducated in vitamins, I gave up on them too soon. I wasn’t taking enough! My mom’s acupuncturist treated my ADD, but I strayed when a well-meaning friend steered me towards pharmacology, and I took Effexor. The damage showed up over the next decade when increased nervous system and mitochondrial dysfunction begin.

Loud bar music in the back of my unit initiated chronic insomnia in my forties. I had open mouth breathing. Elevated cortisol and night sweats woke me at least 8 times a night. If I was mad, I’d have an instant hot flash and sizzle like a red bull. I lost my sex drive. After quitting Effexor, elevated thyroid TBO antibodies appeared. Later diagnosed with sensorineural hearing loss, the psychiatrist prescribed sound therapy but the condition isn’t curable.

Musculature problems began, I had an unrelenting frozen shoulder from a gym accident, and at one point, I had ataxia and couldn’t walk straight. After a trip, while in Hurricane Ivan, I was unable to walk for a month with ataxia. I once met an advanced multiple sclerosis patient, that experienced the exact same symptom from Ivan. The cause was thiamine deficiency in the cerebellum, the part of the brain that controls movement and walking.

For work, I illustrated 300 skylines from around the world and market them on Etsy. My fine motor skills and artistry remain superior, but my spatial organization was nonexistent. I was very messy. Taking GABA hampered work stress, but I couldn’t cycle it from thiamine deficiency. Managing inventory and college students wore me out. One told me “You can’t retain what I tell you”.  Finding my car in large parking lots was often challenging. The hippocampus circuitry requires thiamine for short-term memory function.

Orthomolecular psychiatry has proven to treat and manage these types of disorders with nutrients and diet, as the first line of defense. There was no need for antidepressants.

After My Diagnosis, I Learned My Parents Were Already Taking Thiamine

When I told my dad about my thiamine deficiency, he pulled out a bottle of thiamine labeled anti-beriberi. He was taking B1 for cardiac support. The heart and brain consume a vast amount of energy and require thiamine to meet the demand. My mom took benfotiamine successfully for shingles, a neuropathic pain.

When I told my original acupuncturist, about my diagnosis he said, “I already know you have beriberi, just take B vitamins and lots of them. You don’t need my herbs.” He had been treating me for dysautonomia, twenty years before I developed POTS. I detested the point because his needling pressure hurt. No questions asked; he needles points by observation and pulse, Western characterization in diseases have no significance.

Part of the treatment for dysautonomia is a needle to the center of the philtrum, this point prevents fainting. Another needle is inserted into the center of the forehead and one on top of the head for balance. Traditional Chinese Medicine (TCM) healers identify liver and lung channels weakness two decades before western medicine.

The New Doctor Damaged My Health In Only Eight Months

Twenty nineteen was a bad year. Dr. Kunin sees Vitamin C deficiency and signs of anemia and then retired. I stopped getting IVs. I would still nap after taking them. My trusted acupuncturist, also a nutritionist moved. I began dry coughing a lot, which later I learned was a sign of TD. Then I met the worst doctor ever.

I showed her, Thiamine Deficiency, Dysautonomia, and High Calorie Malnutrition and she handed it back to me and said “Oh, another patient brought this in the office.” I interviewed another doctor and told him I have TD and he replied with, “what’s your point!” and referred me to a doctor out of state.

I settled on the first doctor, and everything started wrong. She put me on a high-dose thyroid medication without titrating, and Low Dose Naltrexone (LDN), which gave me a stomachache. She wanted me back on LDN after I told her I had side effects. She recommends NAD instead of Meyer’s Cocktails which includes thiamine.

By the time I realized I was in a hyperthyroid state, the damage had begun. A cascade of beriberi symptoms begins. When one symptom would go away, another would begin. The neuropathy was more long-term. I had resting tachycardia, lactic acidosis after five days of yoga stretch that caused feet neuropathy and then trigger finger. All the doctor could say was “I had candida overgrowth”.  The cause of candida was that I had a weakened immune system from TD. I watched videos on lactic acidosis to explain it to her.

When I saw an eleven year old’s homework on glycolysis it made me wonder how much doctors remember from medical school.” I tested the doctor and asked her “What does pyruvate convert to?” She answered incorrectly.

I was developing non-alcoholic Wernicke’s encephalopathy (WE), acute short-term memory loss. I almost walked out of a restaurant thinking I paid the bill. I couldn’t remember putting a credit card back in my wallet and arguing with the clerk after she had handed it back to me. Once I read, “if you think you’re deficient in thiamine, get an IV right away.” After a series of Myers Cocktails with phosphatidylcholine, the progression stopped.

Another doctor got me off the thyroid meds, yet wet and dry beriberi symptoms continued. My left-hand lost circulation and turned hard and purple. The back of my neck hardened and my backside turned into butter. I had unintentional weight loss and my hand reflexes slowed. My minerals were becoming unbalanced. I contacted a refeeding syndrome clinic, for a consult, but was turned away because I wasn’t anorexic. A few months later I traveled to Hawaii and made a mistake.

Orthomolecular Medicine Rescues Me Again

Accidentally packing thiamine HCL instead of TTFD, the HCL initiated my paradox reaction and I had diarrhea several times the first night. Every day I napped from the sun’s UV rays. Excruciating muscle cramps sent me to Dr. Pritam Tapryal, Honolulu’s IV doctor specializing in chronic fatigue syndrome. Thiamine handouts, a stockpile of capsules and vials of B1 were waiting for me.

He calculates that I needed 600 mg of IV thiamine based on the length of time I had been feeling unwell. With an iron load before the second IV, I felt a surge of energy – I got ATP! My vagus nerve stimulated peristalsis and excess fermentation stuck in my body for three months finally released. Elevated liver enzyme activity and low blood pressure normalized.  Afterward, I found a doctor willing to provide high dose thiamine therapy at home.

I went back to the doctor that said “what’s your point” when I told him I had thiamine deficiency and requested 600 mg of parenteral B1 instead of 100 mg. A bit taken back, he shows compassion and custom orders 500 mg of B1 in a Myers Cocktail, after I explained my recent experience. The IV manager thought I was an ICU patient, but I wasn’t. It was the dose I felt best on.

High Dose IV Thiamine Therapy: From  A Patient’s Perspective

A series of high-dose thiamine (HDT) IV treatments, turned into an epigenetic treatment going on two years and two months. I’ve taken 100,000 mg of parental thiamine to this date. Infusions continued to sustain therapeutic effects and increased thyroid production. Unknown cause of malabsorption required ongoing infusions. Resolved through extensive pre-and post-labs.

I self-directed my treatment and gauged myself. I found thiamine articles from all over the world, but high-dose thiamine information was limited to WE treatment only. I received no medical advice on thiamine therapy from allopathic doctors that had clinical nutrition education, or from a young orthomolecular doctor or GP. Familial beriberi - thiamine deficiency

I had two to three IVs per week the first year that included 500 mg of thiamine. The longest time without an IV was three weeks at the beginning of 2020 and eleven days at the end of 2021. Below is a 12-month summary, from a 55-year-old woman with unrecognized lifelong thiamine deficiency from a SLC19A3 gene defect.

Journal From Long Term, IV, High Dose Thiamine Therapy

My high-dose thiamine regimen began 11/21/2019. This is the Meyers Cocktail titration period:

  • 2 infusions of 200 mg of thiamine in 2 weeks in end of Nov. to Dec.
  • 5 infusions 300 mg of thiamine in 2.5 weeks Dec. to Mid Dec
  • 2 infusions 400 mg of thiamine in 2 weeks Mid Dec. to January.
  • 500 mg of thiamine 2 to 3 times a week were taken in the middle of January.

11/2019 Concerned about anaphylaxis. Only a few teeny bumps around lips developed and disappeared after the first day. Visual clarity is the first sign of improvement.

12/2020 – Foot neuropathy and trigger finger for 4 months, resolved with 7 IV’s spread out over 4.5 weeks. The IV thiamine doses were 300 mg or 200 mg. Dexa scan shows osteopenia in lower back and femur and only 3 lbs. of lean muscle mass, muscle wasting, a hallmark symptom of beriberi.

OATS test taken a day after HDT infusion – tested B1 borderline deficient. Borderline and deficient in minerals and vitamins except manganese, doctor thought something was wrong with lab.

1/2020 – Right mucosal lining was demyelinating and slightly bleeding for a month, saw glitter. Zonulin levels over 800, the doctor told me not to be concerned, but I was. Slight rectal bleeding.

An unintentional fast in cold weather caused syncope. Broke out in an intense sweat, became faint and lost appetite. Leaned against buildings every few feet to get home, no thiamine in am. Sitting on bench resolved symptoms. MCV increases to 100, normal range is up to 95.

Tested negative for panel of inborn errors of metabolism. Autoimmune panel negative except – Arthritis – equivocal, Thyroiditis- out of range, Epstein Barr – negative.

2/2020 – New formulation of phosphatidylcholine, with small amount of dextrose without B1 was a mistake.

On three-week break, nighttime driving vision had decreased. Resumed Meyer’s Cocktail after break, fatigued, fell asleep in IV chair after IV. Reduced thyroid medication from I grain a week, increased after break to 3.5 grains a week. A1C 4.8 increased to 5.2 after break.

Right quadrant of my upper teeth dropped down. Oral surgeon said “not pathogenic of disease”.

Last visit with Dr. Kunin. Concerned I looked just as depressed as when we first met. I was happy to see him, unable to express it. Continue a more DIY approach and TCM, “the Chinese have found ways to treat that western medicine has not figured out, and one day technology will be so advanced doctors won’t be necessary”.  He handed me the keys and said, “Figure it out on your own.”

3/2020 – Introduced high fat diet. Lost 3 lbs.in a week. Severe leg cramps from foot to shin. During an IV, felt leg cramping. Normal cholesterol increased from 260 to 400. Stopped diet. No B1 in fat.

4/2020 – Lowered stress from semi-retirement and resting. IBS starts to resolve for the first time at 55. Felt extreme chill one day.  Took injectables at another doctor’s office due to shut down. I took 100 mg B1 in a B complex in intramuscular (IM) with B12 to ease B1 ‘pinch’, plus IM biotin for a month.  Not as effective as HDT infusions.  Combination of B1 with complex and biotin had best results.

5/2020 – Meyer’s Cocktail and 350 mg of NAD back-to-back infusions lifted brain fog profoundly.  Able to do tasks I couldn’t perform prior. I cried with joy, my cells were not permanently damaged from past use of Effexor and antibiotics. Unable to replicate treatment. Oral Inositol reduced elevated triglycerides dramatically, then stopped working. IBS came back off and on.

6/2020 – Tested borderline low on calcium, choline, magnesium, B5, B12, Vit C, K2, zinc on a three month average. GI lab shows mal-digestion, metabolic imbalance, and dysbiosis. Stomach pain from psyllium and flax, phytobezoar build up, rash on neck since 2019 getting worse, insomnia resolved.

7/2020 – Severe anemia showing and severe muscle weakness. I couldn’t lift a 5 lb. weight. Acute memory loss, almost walked out of lab before taking the lab.  Waking up early in am in summer at 8:00.  Hemoglobin normal and then drops frequently, IV doctor sees bleeding. Ophthalmologist finds arcus build up from high cholesterol, strong arteries, and recommends latanoprost for glaucoma after field test.

8/2020 – Decreased parenteral 500 mg B1 to 300 mg to test if high dose thiamine is depleting B12. Began coughing after 7 days. Post NAD IV lab tested  B12 deficiency, causing hemoglobin and T3 deficiency.  Acupuncture treatment creates switch sensations throughout body allowing oxygen flow, heart channel under arm point pulsated – oxygen and lung channels communicate. Leg bruising – Vitamin C deficiency.  Insomnia came back when B1 parental dose decreased, never resolved fully after increasing B1.

9/2020 – ANS dysfunction – uncontrollable body flipping in bed two nights in a row, movements like a fish out of water.  Resumed 500 mg of prenatal B1 after two weeks at 300 mg. Ophthalmologist said “you look more alert”, compared to two months ago. Started IM Mic-B and hydroxocobalamin, 5 days a week. IBS-C decreased with B12 IM. Coughing on Lipothiamine, switched permanently to Allithiamine, cough resolved. Normal zonulin levels return, reduced gut inflammation. GI didn’t order endoscopy after I told him something hit my stomach when walking and had rectal bleeding. He wrote IBS on notes. Stopped EDTA IVs for cadmium after a few treatments, when urine began foaming.

10/2020 – Latent deficiencies appear: B12, CoQ10 malabsorption. B1 not absorbing. Vitamin C deficiency appears, lifelong subclinical scurvy, bleeding gums, gingivitis, pilaris keratosis, bruising, poor iron absorption, rectal bleeding, low tyrosine.  Sick people are low in B vitamins and Vitamin C.  Repeated thiamine depletions cause heavy Vitamin C deficiency in lung, kidney, thymus, and liver.

Tested positive for Intrinsic Factor AB, Pernicious Anemia (PA).  Hematologist defensive when I asked him if TD can cause anemia, cancelled next appt., told me to see a GI. Doctors booked from Covid-19 delays.

Oral surgeon cleared teeth shifting. Orthodontist ordered aligners, short teeth roots in scan.

Trialed compounded thiamine cream from Lee Silsby pharmacy and replaced TTFD.

11/2020 – Stomach pain increasing after meal. Twelve days in, I thought I was going blind. The thiamine cream wasn’t absorbing. Indoor and night vision blurry. Back to TTFD and Myers Cocktail together. My vision came back, but not as clear before getting blurry. Mild paradox reaction, a bowel movement in the middle of the night.

12/2020 – Endoscopy shows chronic gastritis, h. pylori and peptic ulcers. A combination of a lack of nutrients cause ulcers, including B1.  Refused triple therapy (antibiotics and PPI). Treated with cabbage, herbals, mastic gum.  ION Panel indicated GSH and potassium deficiency, lactic acidosis (TD), ketosis, oxidative stress, transmitter deficiencies and metabolic syndrome.

Elliot Overton of EO Nutrition interprets mitochondria in battleship mode, suspects mold toxicity. Unseen mold or water damage. Incontinence and frequent urination. Second ophthalmologist told me don’t take latanoprost. MCV high still high with regular IM B12, since 10/20. With small veins and bursting arteries, it’s difficult to maintain IV’s.

In 2020, my health was like my dad’s. My hearing and vision deteriorated, I was unable to hear people speak with masks on and had difficulties focusing on conversation in noisy rooms. Gingivitis developed into periodontal disease; teeth aligners require lifetime use. My dad is deaf in one ear, and now going blind in the second eye and had the periodontal disease the same year and wears dentures.

Observations at 43,500 mg IV Thiamine After 13 Months

Intravenous therapy can target issues in ways oral thiamine cannot reach.

Improved thyroid production, A1C, insomnia, IBS and CFS, overall energy level partially improved.  Foot neuropathy and trigger finger resolved.  Cocktails with phosphatidylcholine, iron, and NAD, had increased effects, latent deficiencies appear, no nutrient depletions from high-dose thiamine.

Infection, gastritis, ulcers during treatment caused malabsorption. Reducing thiamine caused insomnia to reoccur and acute vision reduction, increased ANS dysfunction caused temporary uncontrollable body movements.  Increased dose of 300 mg to 500 mg of B1 resolved uncontrollable body movements and regained vision.

I saw one patient vomit, and a patient have nausea during 300 mg B1 Meyers Cocktail.

ROS from unknown cause extends treatment into 2021.

High Dose Thiamine IV Therapy, Toxins, Diet, Labs, and Gigong

In 2021, I tapered to two IVs a week and increased the 500 mg to 600 mg mid-year. Hot flashes returned after 5 years of remission causing a three-month setback. Insomnia made me delirious and had to take naps. PEMF bio-mat calms the nervous system to assist in sleep, without it I’ll wake up a few times during the night. For over 10 years, I wake up and urinate once a night. My eyes became blurry and I walked slowly like an old lady for a short period. Daily clear phlegm wants to come out since 2020 when I eat.

In spring my bloodwork showed Stachybotrys and Aspergillus mold. I found growth on papers in a storage box against a wall with the laundry room on another side. Condensation went through the wall.

With my gut healing and IV therapy, my TBO antibodies levels reduced significantly. The increased T3 raised my steroid hormones. Reducing thyroid medication again was a real possibility. IBS-C was resolved by mega-dosing powder magnesium with fiber, B1 and B12. I once had an offer to see the world authority on IBS-C, though all I needed was a good form of high-dose magnesium. I was feeling better until I experienced unexpected setbacks.

Everything Changed With Two Major Endocrine Disruptors

Microscopic brick debris during construction flew under my windows. Debris flew inside over 50 ft. and landed everywhere, never thought my eyes and lungs could clear it. Due to an HLA-DQB1 gene defect, I’m unable to break down mycotoxins (mold).  Mold is an anti-thiamine factor and it oxidizes B1 and B12.

When inflammation started to calm down, my hallway went under remodeling, and material debris and paint fumes went under my door. The chemicals shut down my thyroid. Antibodies rose from 180 to 535. Inflammatory markers that were improving became elevated and deficient. My killer cell function, HNK1 (CD57) level was 50 and now 18.  The doctor thinks I have Lyme. I’m testing for MARCoNS, a staph infection that resides deep in the nasal passage, due to sinus inflammation from the biotoxins.

After trialing Cholestyramine for mold binding, it made me constipated. My acupuncturist gave me a two-hour treatment to undo the damage. To detox, I use an FIR infrared sauna on the mat. I’m getting an ERMI test kit to test other rooms, an air test hardly detected mold.

HDT Isn’t a Standalone Treatment

With the amount of IVs I took, I tested questionable foods. A few small gluten-free snacks put me into a comatose within 20 minutes. Less than two ounces of coffee initiated leg/foot cramping. I never had this problem a few years ago.  Removal of processed carbs is the only way I can maintain my thiamine storage.

Staying in mild ketosis, on a paleo diet is optimal for me. When I tried high-fat and vegan diets, they caused deficiencies. I have a nonfunctional gene cluster FADS1/FADS2, that requires the consumption of EPA and DHA found in seafood. Drinking concoctions of vegetables and minerals activate B vitamins throughout the day.  TD causes nitric oxide deficiency and I replete myself with nitric oxide greens.  My one kryptonite food is liver, it elevates my copper.  Using food as medicine supports my overall immune function as I recover from Chronic Inflammatory Response Syndrome.

My hydrochloric acid is deficient from TD, and I have low gastrin. I’ve taken 13,000 mg of Pepsin Betaine and feel no sensation. Apple cider vinegar doesn’t seem to work. My amino supplements aren’t absorbing.  I also have oxalates, Elliot recommends more B6 and I’ve increased molybdenum to meet my sulfur intake.

I take a blend of B1 that includes: 900 mg Allithiamine, 300 mg benfotiamine and 500 mg thiamine HCL. Over 900 mg Allithiamine and sulfur come up. Before a Meyers Cocktail, I’ll soak in magnesium salts. I’ve increased all the B’s and take them with other essential nutrients throughout the day in moderate to high doses. I require biotin intramuscularly every few weeks, otherwise my nails chip, this started last year. My transporter may be dissolving.

Utilizing Biomarkers and Managing Nutrients

Every six weeks I rotate biochem panels and adjust diet and supplements. My weaknesses this year have been lipids, omegas, aminos, and inflammatory markers. My B12 continues to pool due to suboptimal thiamine levels unable to utilize B12, so I stopped testing. I inject 35 mg of hydroxocobalamin a week, plus sublingual, and hemoglobin is always on the lowest end of normal after I had pernicious anemia. Mold is the suspect cause. I may also have scar tissue from ulcers and scurvy of the colon. The GI doctor recommends an endoscopy once every three years when there’s been a problem.

I’ve found nutrient panels reliable when B1 is extremely deficient. On two occasions my lactate tested normal. Then I had beriberi symptoms after I took the labs on the same day. This was from eating beans and walking in sun, which forced me to sleep. My citric acid markers were normal on an ION panel and I was in ketosis, but the clinician didn’t know I had POTS on the morning of the lab. This was from a three-day fast suggested by a doctor. Thiamine deficiency can worsen on a dime.

Diagnosed with TD on a SpectraCell micronutrient panel, I had long-term B1 deficiency. Normal B1 levels are misleading on my labs once there’s been intake. The Vibrant America panel showed B1 malabsorption at 35,000 mg of parenteral B1.  I’ll continue with this panel and monitor nutrients connected to B1.

My doctor’s friend offered me the two-part transketolase lab for research, but my doctor forgot to arrange the sampling. I was upset at the time, but it doesn’t matter now. I manage myself by how I feel. With Excel journaling, the more elements I add, the more clarity I receive. Observing physical changes are equally valuable to the labs.

A Revisit to Energy Medicine That Compliments Nutritional Balancing

I recently discovered group Primordial Qigong. I haven’t found any other modality that has the same restorative benefits that give energy instead of using energy. Movements connect the body, mind, and soul with the focus on living in the present. Gentle stimulation of systems and body parts creates rejuvenation from within. Who doesn’t want that?

Dysautonomia, the fainting prevention point, is taught in practice. The bank of hands faced together inverted pushed downwards from the forehead over the philtrum encourages balance. Made for masses with no resources, it only requires continuity. This is a welcoming alternative compared to the nutrient-depleting therapies, recommended by for-profit western doctors that made my health worse when they didn’t know what they were dealing with.

At 100,000 mg Of IV Thiamine – It Feels Like I’m on a Train I Can’t Get Off

Overall, the quality of my life has improved. I no longer need to lie down and sleep during the day, even if I feel tired. I’m more active in mind and body. I can sit up and read, wake up earlier, and exercise. My processing speed and speech are faster. The left side of my brain is strengthened. I did audits on my condo association to trace missing dues and one over BlueCross when many claims were unpaid. My brain fog had been too severe to do this previously.

Neuropsychiatric issues appear in less frequency. I still experience forgetfulness and minor learning impairments. Irritation is manageable. I believe some brain function is permanently damaged along with hearing loss. Considering my long-standing history, I’m pleased with the results even though it is only a partial recovery.

Since my body called out for a high dose, there’s a chance I can regress. At 11 days off the IVs, I was deficient in Co2. I don’t know if the thiamine coenzymes can function without high-dose therapy because of my genetic liability. I’m patiently waiting to see how my body changes after the toxins are eliminated and figure out how to taper down from the IVs.

Final Thoughts

Thanks to Dr. Marrs and writers on HM for elucidating thiamine awareness, I learned how to use thiamine as a drug at a time when I needed it most.

Through luck, I found nutritional clinicians that made a significant difference in my health. Educated in Dr. Lonsdale’s thiamine research, they applied his nutrient-based knowledge into their practices. Understanding that beriberi still exists today and is not an ancient scourge from yesterday, is critical.

By assimilating the genetic impact of beriberi and orthomolecular dosing, I’m regaining health in my late fifties. However, no patient should have to spend a lifetime finding a treatment based on luck. There’s no reason to it’s all here: Thiamine Deficiency, Dysautonomia and High Calorie Malnutrition, Derrick Lonsdale and Chandler Marrs; www.orthomolecularmedicine.org

We Need Your Help

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

Yes, I would like to support Hormones Matter.

This article was published originally on February 14, 2022. 

Related posts:

thiamine deficiency - dry beriberi legsDiet and Medication Induced Thiamine Deficiency – Dry Beriberi Modern thiamine deficiency - foot dropGenetic Thiamine Deficiency Ravaged My Family Charcot marie tooth disease thiamineCharcot Marie Tooth Disease and Thiamine: A New Genetic Connection new thiamine bookThiamine Deficiency Gaining Recognition: New Book

You might be interested in

Beriberi is Alive and Well in America

Published on
20.2K views
beriberi thiamine deficiency

Readers of this website must surely be aware that the American medical profession completely resists the possibility of vitamin deficiency as a cause of any disease in America. This is so deeply ingrained that anybody claiming such a diagnosis is considered a fool. This seems to be particularly addressed to the classic vitamin B1 deficiency disease, long known as beriberi. It is unfortunate that we use a Chinese word that, translated to English means: I can’t. I can’t. It is the expression of the profound associated fatigue. There is good reason for denial of its modern existence. It has always been common in countries where rice has been the dietary staple. It existed unrecognized for centuries. In fact, the incredible intricacies of this complex disease took many years to unravel, much of which was performed in China and Japan where there was an obvious interest. It was a series of important historical events that led to its final solution and the history is fascinating. I really think that it is an example of the proverb “those that forget history are condemned to repeat it”. For example, groups of factory workers developed their first symptoms of the disease together after an exposure to sunlight. “Epidemics” of the disease occurred in the summer months. It was only natural that the investigators at that time had concluded that beriberi was an infectious disease. Their search for the responsible micro-organism was a futile endeavor.

The explanation can only be provided from modern knowledge. We now know that ultraviolet light imposes a stress on the human body, requiring mobilization of energy in order to meet it. For example, a car requires more energy to climb a hill. The hill is an analogy for “stress”. The groups of workers described above were in a state of mild deficiency of the vitamin and the stress of the sunlight precipitated full-blown disease, simply because of lack of extra energy required to adapt to the stress. Thus, any form of stress has to be considered in relationship to genetic risk and nutrition if and when the symptoms of beriberi are precipitated.

With this preamble, let me describe some of the clinical experiences that I have been exposed to. First of all, I was lucky enough to be able to think about health and disease in my position in a multi-specialty clinic. I came to the realization that the human body is a wonderful “machine” where the coordination of 70 to 100 trillion live units called cells, depends on chemical energy that has to be transduced to electric energy in order to carry out cellular function. Not only that, I had recognized something that is taken for granted today, that brain cells have an extravagant use of energy. The case that precipitated my lifelong interest in thiamine (vitamin B1) was a six-year-old child who had intermittent brain disease that had confounded all the studies and tests applied in the search for a solution. To put it simply, it was a biochemical approach that showed that he and his brother had a genetically determined condition that, for the most part, allowed them to pursue a relatively normal childhood life. However, each episode of spontaneously resolving brain disease left a little bit more permanent damage. The disease was invariably precipitated by an exposure to a form of stress, represented by a simple viral infection, on one occasion by a mild head injury, and even after an inoculation.

With the help of John Blass M.D. who was working at the National Institutes of Health, we were able to prove that these boys represented the first example of what came to be known as vitamin dependency. In order to prevent brain disease, both of these children required enormous doses of thiamine, but if they were affected by any form of stress such as a viral infection, the daily dose of the vitamin would have to be doubled or tripled in order to prevent a brain disease episode. I came to understand that under these circumstances I was using thiamine as a drug and that it was not a matter of simple vitamin replacement. It was an early example of epigenetics, the relatively new science concerning the way nutrition and lifestyle affect our genes.

You have to understand a very simple idea: thiamine and magnesium are known as “cofactors” to a series of enzymes that represent the machinery of energy production. Both the cofactors are derived from nutrition and have to be bound to their enzymes by a genetically determined mechanism. Not only that: thiamine has to bind to a protein known as a thiamine transporter. The transporter is also genetically determined and conveys thiamine into the cell. All of this takes place in thousands of minute organelles called mitochondria. I refer to these organelles as the “engines” of our cells. That is why glucose can be compared with gasoline in a car engine. Like an excess of gasoline chokes the engine, an excess of glucose chokes mitochondria. Thiamine and magnesium can be compared to a spark plug that ignites the gasoline. Perhaps the reader can begin to understand that this vitamin deficiency disease can literally develop any symptom anywhere in the body according to the distribution of the deficiency and its degree. The brain, heart and nervous system are the most oxygen demanding organs so it is not surprising that they are the first to be involved in thiamine deficiency.

Additional Cases of Thiamine Deficiency

My colleagues knew of my interest and although I was a pediatrician I was asked to comment on the following case. A 67-year-old anesthesiologist at a hospital in Columbus, Ohio came down one day with “a heart attack”. He was subjected to catheterization of the heart that was found to be completely normal. Meanwhile, his son was a medical student and having researched his father’s symptoms, he claimed that the disease was beriberi. The patient was referred to Cleveland Clinic and I was asked to comment on the situation. I found that when he went to his garage to drive to the hospital he would be afflicted by a series of dry heaves. This alone would immediately call to question the possibility of thiamine deficiency. He would give the anesthetic for a series of cases, after which he would go to the pediatric ward and cut himself a large piece of chocolate cake. On returning home, he was too tired to eat dinner and would go to bed, only to repeat the performance the next day. He returned to Columbus with the advice that the patient’s son was correct. I never received a follow-up and don’t know how he was treated but I later heard that he had died. I suspect that he was, in fact, given thiamine in too large a dose that overwhelmed his fragile metabolism.

My next experience was with a brilliant pathologist who was well known in the specialty. She told me that she had extreme fatigue. In fact, a few days previously she had been driving to work but felt so ill that she had turned round and gone home. I discovered that she had a chocolate box in every room in the house. As she went around from room to room she would consume one of the chocolates in each box. I advised her to stop doing this and take a supplement of thiamine, whereupon she rapidly recovered. Note that this was purely a hedonistic urge and had nothing to do with her three meals a day routine.

Ondine’s Curse

A mythological character was a water nymph who supposedly lived in a puddle. She fell in love with a mortal who jilted her and she cursed him with the loss of automatic breathing when he was asleep. There is a disease known as “Ondine’Curse” where this form of breathing ceases, usually at night and the patient dies. So one day I was having lunch with one of the Ear Nose Throat surgeons who knew of my interest. He had seen a woman in the intensive care unit who had stopped breathing and he was called to put in a tracheostomy. He suggested that I should view the case. She was under the care of a rheumatologist and she had had a history of periods of unconsciousness as well as joint pain. In using my knowledge of chemistry, I was able to show that she had thiamine deficiency and began treatment with thiamine.

During her clinical recovery she developed a profound anemia which proved to be due to a deficiency of folate. The importance of this is that her brain was affected by thiamine deficiency but when she was treated with the vitamin, her energy dependent metabolism increased. This exposed a previously adequate sufficiency of folate related to her slow metabolism. The increasingly efficient metabolism stimulated by thiamine required more folate to meet the new demand. She was a chronic smoker that had contributed to the metabolic changes in brain function that precipitated a disease that had gone unrecognized for years. I remember visiting the rheumatologist to ask her whether we could conference the patient to expose this information. She obviously thought that it was an absurd idea and refused to consider a meeting of physicians for further discussion. I learned something else from this patient. She was discharged from the hospital taking supplements of thiamine and folate. When she returned for review, the paralysis in her legs was worse and she had developed a rash on her arms that may occur occasionally in association with deficiency of vitamin B12. It has long been known that B12 and/or folate deficiency could individually be responsible for pernicious anemia (PA). However it had also been known that folate supplementation could not be given on its own for folate deficient PA. It had to be given with vitamin B12 and I had forgotten this. I gave her an injection of vitamin B12 and over the next few days she had some fever and muscle pain but the rash disappeared and she felt better.

The Complexity of Treating Vitamin Deficiencies

I provide these details to show that an understanding of vitamin deficiency disease introduces complexities that require study. When she began receiving thiamine and became clinically worse, it would be easy to blame it as a “side effect” that required administration of the vitamin to be stopped. A physician must first of all have enough knowledge to suspect the possibility and then apply the necessary tests. Obviously, if the collective psychology refuses to accept that possibility, the complaints of the patient, together with the clinical observations of the physician, will be treated symptomatically without a full recognition of the underlying cause. My exposure to a case for which I had no medical responsibility provides an example, for I was merely a visitor. I heard from her that she had been diagnosed with heart disease. She went on to say that her heart rate had dropped to 30 beats a minute, an extraordinarily dangerous situation for which she had received the drug atropine. Atropine blocks the nerve mechanism into the heart, thus controlling the danger symptomatically. She had then been given a diuretic drug and she went through an agonizing 24 hours of almost continual urination. It was clear to me that this was a dramatic exposure of thiamine deficiency heart and nerve disease. She had in fact “wet beriberi”. It has been referred to as “wet” because of the profound collection of fluid in the body and that had been treated symptomatically with the diuretic. The point that I am trying to make is that although the patient had been treated successfully with drugs, the underlying cause had not been recognized. These are uncommon cases, but I am claiming that they are the end-point of years of nutritional and medical neglect and yes, medical ignorance.

Because thiamine deficiency has its major effect in the lower part of the brain, the earliest effects are those of a deregulated autonomic nervous system (ANS). The reader will remember that the ANS conducts the traffic of body organs under the command of the brain. It consists of two basic systems, one of which stimulates action and is called sympathetic. The other one stimulates rest and is known as the parasympathetic. An early symptom of thiamine deficiency is an overdrive in the parasympathetic system, whereas at a later stage of the disease there is usually an overdrive of the sympathetic system. Accepting this factor, it can easily be seen that the patient described above, whose heart rate was drastically slowed, had been endangered because one of the nerves to the heart had carried an overdrive of parasympathetic activity. This, accompanied by a huge collection of fluid in the body, was characteristic enough to look further for the ultimate diagnosis.

Common Presentations of Thiamine Deficiency: The Walking Sick

Looking back at the history of finding the solution to this disease, it is known to have a long morbidity and a low mortality but with a long life of chronic illness gradually leading to some form of mental or physical crippling. In the elderly patient it is often attributed solely to aging. In the 1940s an experiment was carried out in a group of human subjects who were provided with a moderately deficient thiamine diet. Their symptoms were characteristic of those that are presently regarded by most physicians today as psychosomatic. They were irritable, quarrelsome and experienced heart palpitations, headaches, loss of appetite, insomnia, diarrhea or constipation, chronic fatigue and/or intolerance to heat and cold. The vast majority of patients that I treated when I was in practice had a polysymptomatic presentation of this nature, many of whom had been doctor shopping without relief. I was dealing with what I call the “walking sick”, a large group of patients that are haunting the offices of physicians throughout America. Sometimes they had been given a named diagnosis but had not benefited from drug treatment.

The behavioral characteristics of children, particularly those with ADD or ADHD, are dietary in origin, often coupled with some form of genetic risk, not the least of which is superior intelligence. They are being treated symptomatically, but I offer the possibility that failing to recognize these symptoms as nutritional in character may be a failure to recognize them as the forerunner of chronic neurological or heart disease. It is a reflection of high calorie food ingestion overwhelming the action of non-caloric nutrients that enable the necessary synthesis of cellular energy for function, particularly in the brain. In our book “Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition”, we note that our present culture is cursed with a hedonistic ingestion of high calorie malnutrition, responsible for much loss of health. In fact, I have suggested that it is the equivalent of what happened to the ancient Romans whose wine tasted sweet because of lead infiltration from the glaze used in their wine containing jars. They did not know that they were suffering lead poisoning. We don’t seem to grasp the danger of sugar. Each symptom, as it appears, is treated symptomatically with a medication. Rarely is there an interest by the physician concerning diet, particularly the ingestion of empty calories consumed socially. Given the challenge of hedonism, it seems to be part of life joy, particularly in the elderly, to indulge in all the dietary aspects of sweet, sweeter and sweetest. However, it is inappropriate to fail in recognizing the symptoms that might or might not develop as a result. If one or more of the many symptoms is recognized and the patient informed, it is then his/her choice to make the necessary changes.

We Need Your Help

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

Yes, I would like to support Hormones Matter. 

Photo: Seated Youth by Wilhelm Lehmbruck 1917. Edited. Wilhelm Lehmbruck, PDM-owner, via Wikimedia Commons.

This article was published originally on April 11, 2019.

Related posts:

thiamine deficiency beriberi in americaA Case of Classic Beriberi in America thiamine deficiency - dry beriberi legsDiet and Medication Induced Thiamine Deficiency – Dry Beriberi beriberi great imitatorBeriberi: The Great Imitator beriberi Chinese historyFrom the Legs to the Heart: Historical Descriptions of Beriberi

You might be interested in

1 … 4 5 6 7 8 … 14