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Hyperglycemia and Low Thiamine: Gateways to Modern Disease

Published on April 2, 2026

6.5K views

Thiamine deficiency, hyperglycemia gateway to disease

In Thiamine Deficiency in Modern Medical Practice and Threats to Thiamine Sufficiency in the 21^st 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.

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This article was published originally on May 2, 2024.

Sleep Requires Energy

by Derrick Lonsdale MD, FACN, CNS

Published on March 17, 2026

28.8K views

It is widely believed that almost no calories are used during sleep. That is incorrect: while the body rests during sleep and energy consumption is not high, it is a long way from zero. A convenient way to measure energy use is known as the “metabolic equivalent” (ME). This is defined as the rate of energy used by a person sitting and awake, the “resting metabolic rate”. A person riding a bicycle may be using five MEs; a runner, nine or more. A sleeping person uses about 0.9 MEs, so we burn calories when we are asleep about 90% as fast as while sitting on the couch watching television.

Energy conservation is important in sleep, but it’s expenditure is still required. It has been proposed that sleep is a physiological adaptation to conserve energy but little research has examined this proposed function. In one study, the effects of sleep, sleep deprivation and recovery sleep on the whole-body, total daily energy expenditure was examined in seven healthy participants aged 22+/-5 years. The findings provided support for the hypothesis that sleep conserves energy and that sleep deprivation increases total daily energy expenditure. I read somewhere that an enthusiastic young astronomer decided that sleep was unnecessary and used his telescope for 13 nights without sleeping during the day. He became extremely ill, thus showing the importance of sleep in survival. The recognition that sleep is one of the foundations of athletic performance is vital.

Research in the general population has highlighted the importance of sleep on neurophysiology, cognitive function and mood. In a post on Hormones Matter, we reported several young people who had a post Gardasil vaccination crippling condition that turned out to be due to thiamine deficiency. All of them had been exceptional athletes and students before the vaccination. We concluded that the brain energy requirement for exceptional people put them at greater risk of succumbing to stress if their capacity for MEs was limited, either for genetic or nutritional reasons. We assumed that their thiamine deficiency before vaccination was marginal and either asymptomatic or producing trivial symptoms ascribed to other “medically more acceptable” causes. The stress of the vaccination required an energy dependent adaptive response that precipitated fully symptomatic thiamine deficiency. You might say that they were “weighed in the balance and found wanting” as the proverb says.

The Stages of Sleep

Sleep is a complicated process. The first sensation is known as “sleep latency” and registers the time taken from eye closure to falling asleep. The sleep cycle is then divided into five stages, each cycle lasting approximately 90-120 minutes. Stage one is known as light sleep. In stage 2 the brain is resting the parts used when awake. Stages 3 and 4 are deeply restorative. Stage V is known as rapid eye movement (REM) sleep and may be the most important part. Movement of the eyes behind closed lids is observed. The autonomic nervous system is activated for unknown reasons. It is in this stage when we dream and most sleep disorders occur.

Circadian Rhythm

The word circadian means “about 24 hours”. The circadian clock is a complex, highly specialized network in the brain that regulates its day/night metabolism and is a key for metabolic health. It is modulated by behavioral patterns, physical activity, food intake, sleep loss and sleep disorders. Disruption of this clock is associated with a variety of mental and physical illnesses and an increasing prevalence of obesity, thus illustrating that it is dependent on energy balance (production/consumption). Reduced sleep quality and duration lead to decreased glucose tolerance and insulin sensitivity, thus increasing the risk of developing type 2 diabetes. In other words there is a close link between circadian rhythm and available energy . I have seen patients who were unable to take the night shift at work because they were unable to adapt. The increase in obesity has been paralleled by a decline in sleep duration but the potential mechanisms linking energy balance and the sleep/wake cycle are not well understood. An experiment was reported in 12 healthy normal weight men. Caloric restriction significantly increased the duration of deep (stage 4) sleep, an effect that was entirely reversed upon free feeding.

Sleep Apnea

This condition is fairly common in the United States and is probably generally fairly well-known by most people. The patient stops breathing during sleep and may repeatedly awaken with a start. The disease was discovered because a woman reported that her husband kept waking up with a start because “he was affected by an evil spirit”. Fortunately, the physician took her seriously and it led to the studies that determined its cause. Many patients with, or at risk of, cardiovascular disease have sleep disordered breathing (SDB). These can be either obstructive because of intermittent collapse of the upper airway, or central because of episodic loss of respiratory drive. SDB is associated with sleep disturbance, hypoxemia, hemodynamic changes and sympathetic activation. Brainstem dysfunction combined with heart disease is the hallmark of the thiamine deficiency disease, beriberi.

What that means is that there are two types of sleep apnea. In the obstructive type, the tongue falls back into the pharynx and blocks the airway. In the one where there is loss of respiratory drive, the centers in the brain stem are compromised. It is these centers that completely take over the control of breathing when we are unconscious as in sleep. If their supervisory mechanisms fail, breathing ceases. Carbon dioxide concentration increases and stimulates the brain controls that restart breathing. Occasionally these mechanisms are so sick that breathing does not restart. Hence a form of nocturnal sudden death follows. When we are awake we can override these centers and control our breathing voluntarily. Obesity and obstructive sleep apnea have a reciprocal relationship depending on the regulation of energy balance. When I was in practice I treated several patients with sleep apnea using large doses of thiamine. Because of this I hypothesized that the association of dysautonomia with so many different diagnoses is because of loss of oxidative efficiency and subsequent disorganization of controls that are mediated through the limbic system and brainstem. I came to the conclusion that energy deficiency in the brain was the core issue.

I recently had a letter from the parents of a then five-year-old child who came under my care 35 years ago. She has a genetically determined disorder that affects energy balance and I had treated her by dietary restriction and providing non-caloric nutrients. They informed me that she was doing very well. The condition is known as Prader Willi syndrome, a terminology that indicates that nothing was known about its cause when it was initially described. Today, 10 studies have provided evidence that total energy, resting energy, sleep energy and activity energy expenditure are all lower in individuals with this syndrome. Dietary discipline and nutritional supplementation had paid off.

An Explanatory Analogy

You may think that comparing the human body with an automobile is manifestly absurd, but the principles that I will use in the analogy are simple.

Fuel

First of all, both use fuel: gasoline is the fuel for a car, but it must be calibrated to the design of the engine, giving rise to the gasoline choices at the pump. Although different forms of human food may be compared to gasoline choices, the primary fuel for our cells is glucose and this is particularly true for the brain. Glucose, a carbohydrate, can be synthesized in the body from other components in the diet and different diets are sometimes used therapeutically. Unlike the car, the human body must derive its “spark plug” from the food and is the basic reason why organic, naturally occurring, food is a necessity. The food industry cannot imitate or replace it.

Engine

The engine in a car burns gasoline to create energy. It requires spark plugs to ignite the gasoline and waste gases are eliminated through an exhaust pipe.

Every cell in the human body has an “engine”. Without going into details this is known as the Krebs cycle (named after its discoverer). Its objective is to produce energy and glucose has to be “ignited” (oxidized). The oxidation process, while releasing energy, gives rise to carbon dioxide (the “ash”) that is eliminated in the breath. Energy is stored in an eletrochemical form known as adenosine triphosphate (ATP).The nearest parallel would be a battery. It releases an electrical form of energy that is then used for function. Whether we like to recognize it or not, we are electrochemical machines and the only way that we can preserve or retrieve health is by furnishing the complex of ingredients that enable food to be converted into energy.

To continue the analogy, when you put your car in the garage and turn off the ignition the car is technically “dead”. Obviously, we are unable to do that with the human body, but let us make a simple comparison. Supposing for some reason it was desirable to keep the car “alive” when it was in the garage. The engine would continue to run and it would be consuming fuel. Because the body requires energy to remain alive, the “engines” have to continue running, even when we are asleep. This does make sense for the consumption of energy when we are asleep———it keeps us alive !

Transmission

The energy developed from burning gasoline has to be transmitted to the wheels in order to produce the normal function of the car, which is the ability to move. The transmission is a series of levers that are interconnected.

The same is true in the human body, but it is biochemical in nature. A series of energy consuming enzymes use the protein, fat and carbohydrate to build the diversity of tissues that make up the body. Throughout life, cells are destroyed and replaced, so this is a continuous process of energy consumption and repair. Every physical movement, every thought and emotion, consumes energy. Like the transmission in the car, the energy produced by the citric acid cycle engine is consumed in every movement of the body, every thought occurring in the brain and every emotion.

Chassis

The body of a car is just a container on wheels designed to carry around human beings. Its sole function is to move and until we have driverless cars a human being must be the driver.

In comparison, the body of a human being is merely a chassis that carries the brain around. It might be said that the brain can be compared with the car driver and every function of the body is under the command of the brain. Another analogy that I have used is an orchestra where the brain is the conductor and the organs are banks of instruments in which the cells come under the command of the conductor.

Putting It All Together

The 2019 Nobel prize has just been awarded to three scientists who have discovered how our body cells respond to low concentrations of oxygen (hypoxia). The reaction of medical scientists is very positive since this discovery will certainly be applied to the treatment of many diseases. Apparently scientists are already trying to find drugs that will influence this effect. For example, it has long been known that hypoxia will introduce inflammation. My forecast is that the use of nutrients will often correct the genetics by epigenetic mechanisms and this is already under way.

I found the Nobel prize extremely interesting because of a little-known phenomenon that was described by the early investigators of the vitamin B1 deficiency disease, beriberi. They had found in this disease that the arterial concentration of oxygen was low while the venous concentration was relatively high. Arterial blood carries oxygen from the lung to all the tissues of the body. It has to be unloaded into the cells that then use it to produce energy. The venous blood then returns to the lung to be loaded again with oxygen. A relatively low arterial oxygen reflects an inadequate loading at the lung tissues, while a relatively high venous oxygen indicates poor utilization by the cells to which it is delivered. This means that thiamine (vitamin B1) is an essential catalyst in the delivery of oxygen to the tissues. Its deficiency induces gene expression similar to that observed in hypoxia and has been referred to as a cause of pseudo-hypoxia (false hypoxia).

The heading of this article is that sleep requires energy, but I am making the case that being alive and well simply means that oxygen is being consumed efficiently, as long as the “blueprint” of DNA is healthy. It strongly suggests that hypoxia and/or pseudo -hypoxia are the underlying causes of disease and may explain why thiamine and its derivative are such important therapeutic agents.

We Need Your Help

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

Yes, I would like to support Hormones Matter.

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This article was published originally on October 14, 2019.

Rest in peace Derrick Lonsdale, May 2024.

Energy Loss as a Cause of Disease

by Derrick Lonsdale MD, FACN, CNS

Published on March 4, 2026

17.9K views

I graduated from London University in 1948 and retired at the age of 88 years in 2012, so I have seen some remarkable changes in the practice of medicine. I have entered many reports on this website, detailing what should be a medical revolution. One of the best professional associations that I have ever made has been with Dr. Chandler Marrs, the editor of Hormones Matter. Both of us have tried hard for years now to explain the details of our experience, hoping to reach those many individuals who are being misdiagnosed and treated extremely badly. My recent experience has come from retiring in an excellent retirement home.

I am surrounded by people of my age, many of whom are taking numerous medications to treat their symptoms. The most recent example was in a gentleman who has been in and out of hospital several times with a set of symptoms whose origins are clearly due to cellular energy deficiency. When approaching him as a friend and asking him how he is faring, he told me that his list of symptoms remains as a medical mystery. In addition, two women, with whom I had become acquainted, had symptoms that were similar to his. One of them passed away without a diagnosis and the other one is presently being treated symptomatically. The reader might well ask the obvious question as to what happens if I should state an opinion. The answer is very simple; the offered explanation would fall on deaf ears. Unfortunately, this is eminently predictable and is the major reason why innovation that contradicts the medical standards of the day is regarded as heresy throughout history. Of course, “new” concepts must be backed by evidence to become accepted. We are trying to provide the evidence on this website for defective cellular energy as a major cause of disease.

Heresy in Medicine

I am pretty sure that I may have recorded the story of Dr. Semmelweiss on this website but it is a story so poignant that it is well worth repeating. It is a story that illustrates the difficulty of introducing innovation in medicine, or indeed anything new. Semmelweiss was a German Hungarian physician who lived before the discovery of microorganisms. He presided over an obstetrics ward in which there were perhaps 10 beds on one side of the room and 10 beds on the other. The physicians of the day would come in and deliver their patients without washing their hands or changing their clothes. It is difficult for some people to comprehend the total lack of any form of hygiene that doctors practiced before microorganisms were discovered. Semmelweiss observed that the physicians would often come into the ward directly from the morgue and concluded that they must be bringing something in on their hands that caused the patient to die from child-bed fever, as it was then called. From this observation, he organized the first controlled experiment in medicine. He directed the physicians on one side of the ward to wash their hands in chlorinated lime before they delivered the patient. The physicians operating on the other side of the ward carried on in the same old way.

The results were dramatic as we would expect today. Child-bed fever was reduced by 85% when the physicians washed their hands. The medical profession, including his colleagues, said that “because Semmelweiss could not explain what was on the hands of the physicians, his explanation was unscientific”. It is important to note that they simply ignored the obvious benefit. He was discharged from his job and excluded from the hospital. He died as a pauper in a mental hospital.

The major point is that the concepts of the medical profession of the day were completely wrong, He had clashed with the current medical model that was then accepted by mainstream medicine as “the truth”. If we apply this lesson to today’s model of medicine, it is impossible not to wonder if the outstanding principle of the use of pharmaceutical drugs in medical practice is fundamentally wrong. Is treating symptoms without addressing their underlying cause scientifically justified? A glance at the Physicians’ Desk Reference that supplies information on the many prescription drugs available might put off the reader’s use of a prescription. For each drug there is a short description of its use, often with an admission that its action is only partly understood. Then follows a page or two describing its side effects. Does this not suggest that the use of pharmaceuticals to treat symptoms causes more problems than it solves? Are we approaching another Semmelweiss moment in medical history?

Envisioning an Alternative Approach

I envision the profession of medicine as like a traveler, hoping that the road leads to the best solution in the treatment of disease. For my analogy the traveler comes upon a fork in the road with a signpost. One sign says “Kill the Enemy“, (referring to the discovery of infecting microorganisms) and our traveler takes that road because the sign for the other fork is blank. “Kill the enemy” became the first paradigm (a model accepted by all) in medicine. We had to find means of killing bacteria, viruses, cancer cells or any other attacking agent and many years were spent in trying to find ways and means of doing this without killing the patient. The information was hard won and a lot of patients suffered untold hardship and even death until the discovery of penicillin. This in itself “proved that the correct fork in the road had been chosen”. As we know, this discovery led to the antibiotic era, but even these drugs are running into new problems.

To continue the analogy, our traveler goes back to the fork in the road and finds that the other sign has now been filled in. It reads “Assist the Defenses” and I believe that it should represent a new paradigm. Louis Pasteur and his colleagues discovered the disease producing microorganisms, but on his deathbed he is purported to have said “I was wrong, it is the terrain that matters”. He meant that the terrain represented the defensive functions of the body that should be assisted. Perhaps he formulated what I believe must be the second paradigm in medicine.

The Second Paradigm

How should we approach the introduction of this concept? It seems to me that the problem is that few people are aware of the basic principles of body function so I must provide another analogy that I have used before in Hormones Matter. The human body can be compared with a symphony orchestra in which part of the brain represents the conductor. The organs represent the banks of instrumentalists that make up the orchestra. Like the instrumentalists who, although they are experts in their own right, still have to obey the conductor, the cooperative function of all our cells must obey the automated signals from the brain to play the symphony of health. Each of us comes with a “blueprint” that is our inheritance and although we are all the same in principle, we are all uniquely different because of accidental or inherited variations in the “blueprint”. The autonomic (automatic) nervous system, controlled by the lower part of the brain, coordinates the function of organs in the body, behaving like a computer. It receives sensory information, enabling it to receive from and send signals to those organs, thus collectively playing the symphony. The endocrine system consists of a group of glands that produce hormones. Their function, also under the command of the brain, is to release the hormones that travel in the bloodstream to the organs and are thus signaling agents.

The voluntary nervous system, controlled by the upper part of the brain, gives us what we call willpower. The voluntary and autonomic systems are completely separate but have many connections, so some of the reflex activity conducted by the autonomic system can be influenced and overridden by an act of will. Perhaps the best example is the fight-or-flight reflex that is activated by a sense of danger but can be modified voluntarily. For example, the reflex response to an insult might result in violence if it is not modified by the voluntary system. Assuming that the blueprint provides all the machinery of survival, all it requires is energy.

The Production and Consumption of Energy

We cannot survive without food and water. There is, however, an overall tendency to ignore the appropriate nature of the food, in spite of the fact that it provides the fuel that gives us energy. Taste is the dominating influence, driving sales for the food industry without an appropriate consideration of calorie/micronutrient balance. It is clear that “vitamin enrichment” has hoodwinked us. Chemical energy is liberated from oxidation of fuel (food), but it must be transduced in the body to an electrical form of energy that enables us to function. The electrocardiogram and the electroencephalogram are both tools that identify the electrical nature of this function. The human body is well equipped with an enormously complex system of defense but its complexity requires energy that has to be increased when a person is under any form of physical (trauma, infection, severe weather etc) or mental (divorce, grief, business deadlines etc) stress. It is very important to think of stress as a “force” to which we have to adapt. The lower part of the brain, acting like a computer must automatically organize the complex defense machinery, including the immune system, so its energy requirement exceeds that required by the rest of the body and must be automatically increased to meet the required response to stress. What we call the “illness” (fever, swollen glands, inflammation, etc.) is evidence that the brain has gone into action to generate a defense. In fact, war is declared and the result is recovery, death, or prolonged chronicity where the attacker has not been completely defeated. A nutritionally deprived individual cannot muster the energy to initiate defensive action and may explain why stalemate or the stress of vaccination can be evidence of failure to adapt.

Of all the aspects of health maintenance, exercise, appropriate rest, socialization and fulfilling job assignment, perhaps nothing is more important than the nature of the food. Genetics, stress and nutrition are visualized as the “three circles of health“. I want to illustrate this relationship by retelling an incident that we reported in “Hormones Matter” a few years ago. The mother of an 18-year-old girl reported by email that her daughter had received the HPV vaccination (to increase immunity against the virus associated with cancer of the cervix) four years previously. Throughout the four years she had been more or less crippled by a condition known as postural orthostatic tachycardia syndrome (POTS). She had been seen by many physicians without any success. Her mother did her own research work and had come to the conclusion that her daughter had the vitamin B1 deficiency disease known as beriberi and she wished to prove it. A blood test clearly showed that she was correct. Because of this, several young people who had also suffered from POTS following the HPV vaccination were also found to be thiamine deficient. One young woman who had not received the vaccination also had POTS and was found to be thiamine deficient. One of the observations that had puzzled the parents of these young people was that, without exception, each of them had been recognized as an exceptionally good athlete and student before they had received the vaccine. We deduced from this that a superior brain was more likely to consume more energy than someone less well endowed, thus increasing the risk of poor nutrition and the ability to adapt to a potentially powerful stressor.

Although proof is not possible, we have accumulated a lot of evidence that has enabled us to hypothesize that the vaccination acted as a nonspecific form of stress in people who were marginally thiamine deficient, but asymptomatic before receiving the vaccine. For the youngster who had not received the vaccine, but who had succumbed to POTS, poor nutrition alone, with or without genetic risk, had to be blamed. Genetics, stress and nutrition are visualized as the “three circles of health“.

The Medical Revolution

We are proposing that energy loss is the major cause of disease and that it results commonly from a less than ideal diet or dysfunctional mitochondria. Failing in the balanced need of the caloric content and the necessary non-caloric vitamins and minerals for efficient oxidation, the result of poor diet is energy deficiency. There is considerable evidence that thiamine plays a vital part in both the production of chemical energy (ATP) and its conversion to electrical energy for bodily function. We have concluded, also from evidence, that genes may or may not usually cause disease on their own. Either nutrition or overwhelming stress may be variable factors that create genetic risk. The prevailing addiction to sugar creates a variable degree of thiamine deficiency by the catatorulin effect. We further hypothesize that a mild to moderate thiamine deficiency leads to a gradual decay in the efficiency of the critical enzyme(s), insufficiently supported by the cofactor(s). Attributing the easily reversible symptoms to other causes and allowing them to continue, leads to chronic disease. This may or may not respond to pharmacological doses of cofactor, used to resuscitate the associated enzyme(s).

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.

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Image by Jonny Lindner from Pixabay.

This article was first published on July 1, 2019.

Rest in peace Derrick Lonsdale, May 2024.

Thiamine Deficiency, Fatigue, and Erectile Dysfunction

by Kash

Published on February 10, 2026

14.9K views

Thiamine deficiency and erectile dysfunction

Hello, I am a 33 year old male who has been experiencing a vast range of symptoms over four years including progressively worsening fatigue, brain fog, muscle weakness, body pain and erectile dysfunction. Only a few months ago, I discovered that there could be a relevance of thiamine in all of my issues. All of my health problems worsened at the age of 29 years old. More context can be found below.

Childhood Problems

I had problems with:

Concentration and focus
Emotionally down
Prone to common cold (infection)
- Unfortunately I was put on antibiotics more often every few months as a kid (amoxicillin)
Brain fog
- My brain is slow at processing things, there is always a latency associated with me to perceive things.

Health Journey

My health journey is complex. In the sections below I have tried my best to capture the sequence of events and diagnostic data we have so far. I began developing fatigue, not feeling refreshed even after sleep in my early 20’s but I continued pushing myself – not knowing how to address this. Irrespective of these limitations, I was an active adult – I was working out regularly, lean and athletic. My food habits were clean i.e., no processed foods, no alcohol, but majority of my calories were from carbs. My macro mix was approximately 50% carbs, 25% fat, 25% protein. Being a South Asian, white rice is part of my staple diet.

Things started to go really bad around 29 years of age when my fatigue, brain fog, muscle weakness, body pain worsened and nocturnal erections started to degrade. I was not able to obtain erection without Viagra. I started my health journey to fix my erectile issues. Because of my appearance (lean and athletic) all the doctors refused to even work with me, saying the issues were psychological. I found an alternative doctor who ordered blood work and we found few biomarkers that were off.

Very low Vitamin-D3 – 12.8
Low Platelets – 60,000 – 80,000 x10E3/uL
Subclinical Hypothyroidism (Elevated TSH – 9.5 uIU/mL and Reverse T3 – 33.8 ng/dl)
Testosterone was low for my age but not below reference range – 525 ng/dl

Unfortunately, this is the first time I had a comprehensive health checkup, so I don’t have any previous data to compare against. Since I was in the Pacific Northwest area where there is not much sun, I was living with low D3 for years. I worked with a hematologist to ensure low platelets were not as a result of any major illness. I started addressing my thyroid using levothyroxine and low vitamin-D3 with a vitamin-D3 supplement.

Subclinical Hypothyroid and Low D3

We developed a plan to address vitamin-D3 deficiency via supplements and also thyroid via levothyroxine. We started with 50 mcg of levothyroxine, which improved some of my symptoms slightly. The fatigue, brain fog and erectile issues improved somewhat. Unfortunately this was short lived and after ~4-6 weeks, my health started deteriorating again. Since I saw initial progress with thyroid, the doctors assumed my health issues were related to thyroid and started treating me with different thyroid formulations, different forms etc., to improve thyroid function.

After looking at my thyroid labs, doctors always mention that my thyroid hormones – FreeT3, FreeT4 were good but my reverseT3 and TSH were always elevated.

Neuropathy and Disc Herniation

In the end of 2020, I began developing burning pain in my lower back, which eventually started flowing to both my feet. MRI confirmed that disc herniation in my L5-S1 layer impacted S1 nerve root. I also took EMG that confirmed there is mild impact on S1 nerve root. The burning pain coincided with worsening erectile dysfunction. I was no longer responding to Viagra and I was in immense burning pain. After a few months of intense pain, the pain has begun to recede, but I am still experiencing a constant burning sensation, except when I sleep.

Disc herniation or burning pain was not as a result of any incident. It seemed to develop gradually, like everything else. A straight leg test or no movement worsened it immediately. One neurologist had an alternate theory that burning pain was not coming from disc herniation but because my D3 was low for a long time my microbiome was affected. Since gut bacteria synthesize B vitamins, she suspected that I was deficient. Her theory was I was deficient in vitamin-B5, which was resulting in burning pain and sleep issues. It is also possible that burning pain is caused by thiamine deficiency. I talk about this in the thiamine supplementation section below.

Neurological Issues

During this time period when I developed burning pain, I was also struggling with temperature regulation issues. When I moved from outside ~90f to inside ~70f, I would get chills. I was feeling cold most of the time, cold hands and feet, and sweating profusely. I used to get pins and needles randomly when out in the sun or while walking.

Gastrointestinal Issues

When I developed burning pain, I also started experiencing bad constipation. I was not able to empty my bowel at all. I had to take herbal laxatives every day for my bowel movement. I have also been experiencing bloating, seeing undigested foods in stool, chronic bad breath – potentially from SIBO. In the last three years, I have lost more than 20 pounds. I look more lean and weak at this point.

Sleep Issues

It has been years since I woke up feeling refreshed. I rarely dream. I have noticed that I am able to easily fall asleep and stay asleep most of the time but my sleep quality is bad, especially the later half of the sleep where REM sleep occurs.

Erectile Dysfunction

I have no nocturnal erections at this point and have not had any over the last several years. I still rely on Viagra and am now taking more than 100 mg, which is the max dosage of Viagra. On some days I don’t respond to Viagra as well. All other obvious issues associated with erectile dysfunction were ruled out including hypertension, heart issues, and hormonal issues. Essentially, I am a ‘healthy’ individual suffering from erectile dysfunction. With all of the other issues, am I really healthy? I don’t think so, but the doctors do.

Toxins and Micronutrient Deficiencies

One of the theories of a doctor who evaluated me was that I was exposed to some toxins. Testing revealed that I had high levels of ochratoxin A, a mycotoxin, which is usually from aspergillus but may be impacted by glyphosate exposures. Based on my blood and urine markers, they confirmed that my detox pathways were impaired and in need of more B-vitamins. I also did a Spectracell testing, which looks at the vitamins and minerals in the cell level, and it did show a deficiency in vitamin-B5, and borderline deficiencies in few other vitamins, which supplementing with a multi-vitamin didn’t appear help.

Thiamine (Benfotiamine) Supplementation

I began supplementing with Life Extension – 250mg of Benfotiamine and many things happened.

My sleep quality improved and I felt slightly refreshed the next morning.
I started getting partial nocturnal erections.
I started responding to the same dosage of Viagra much better than before taking Benfotiamine.
Better energy and mood.
Burning pain in my feet reduced greatly.

The problem, from second day onwards my sleep quality fell apart. I was easily able to fall asleep but was not able to sleep for more than ~5-6 hours and my REM + Deep sleep was less than 90 minutes.

I increased electrolytes

Potassium
- Add 1 litre of coconut water
- Added 1 teaspoon of cream of tartar
Magnesium
- Increased from 250 mg to 375 mg – I am taking Magnesium Malate

This improved my sleep quality slightly, but I still struggled. I couldn’t sustain taking Benfotiamine at the same dosage for a long time. So I had to stop.

Current State

Supplements I take currently:

Vitamin B12 – 1000 mcg
Vitamin D3 – 10,000 IU
Magnesium Malate – 375 mg
Creatine (~3 grams)
Athletic Greens (Multi Vitamins)

I am still suffering with all the issues mentioned above and struggling to incorporate thiamine. How should I proceed here?

Should I try small dosages of TTFD and proceed from there? What cofactors to incorporate?
Should I work with doctors and take thiamine injections or incorporate IV?
Should I try Myer’s IV – which contains below formula once a week for few weeks to see if I can experience any improvement to validate this theory
- 5 mL of magnesium chloride hexahydrate (20%)
- 3 mL of calcium gluconate (10%)
- 1 mL of hydroxocobalamin (1,000 μ/mL)
- 1 mL of pyridoxine hydrochloride (100 mg/mL)
- 1 mL of dexpanthenol (250 mg/mL)
- 5 mL of vitamin C (500 mg/mL)
- 20 mL of sterile water
- 1 mL of B-complex 100 containing:
  - 100 mg of thiamine HCl
  - 2 mg of riboflavin
  - 2 mg of pyridoxine HCl
  - 2 mg of panthenol
  - 100 mg of niacinamide
  - 2% benzyl alcohol

I have been very determined to get myself out of these conditions. Any help or guidance here will be much appreciated?

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, and like it, please help support it. Contribute now.

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This story was published originally on July 27, 2023.

From Mother to Daughter: The Legacy of Undiagnosed Vitamin Deficiencies

by B. Figueroa

Published on February 5, 2026

20.5K views

This is a story of a mother with undiagnosed vitamin B deficiencies who gave birth to a daughter who was also born with undiagnosed vitamin B deficiencies. In the eyes of conventional doctors and labs, there was not much wrong with us, but we knew that life was harder than it should be. We lived managing debilitating dizziness, daily migraines, fibromyalgia pain, chronic fatigue, allergies, hormonal changes, anxiety, and depression. Until we discovered that we were both hypermobile with histamine issues, hypoglycemic, and had many vitamin B deficiencies. The biggest challenge was for my daughter to start taking thiamine (vitamin B1). Her heart rate was all over the place and she had such a bad paradoxical reaction to thiamine that we believe she had been living with undiagnosed beriberi along with POTS.

Mom’s Health Marked by Asthma, Anxiety, Migraines, and a Difficult Pregnancy

All I remember as a child is being afraid to talk in school even if I knew the answer to a question. I had allergies and could not exercise due to asthma. During college, I had to read over and over the same thing because I could not concentrate. I worked extremely hard because the fear of failure was too much to bear. I started to have hormonal imbalances and missing periods. I successfully finished college and moved away to another state. That is when migraines started. Later, I became pregnant with my first child and started having blood clots. Anxiety and depression would come and go with hormonal changes.

When I was pregnant with my second child, my daughter, I was sick every morning with nausea. After 6 months of pregnancy, I had gained only 6 pounds. Ultrasounds showed that the baby was growing normally, but I was losing weight. At that point, I also could see blood clots on my leg. I was placed on bed rest. By the 8^th month, my water broke and my daughter was born. She was jaundiced and placed under UV light for a week. I also stayed in the hospital for a week dehydrated, with blood clots, and with the “baby blues”. We left the hospital after a week, and she had a “normal” development. However, you could see that she was a baby that would not go with anyone, not even the people close to us, indicating some anxiety.

Daughter’s Early Health Issues: Selective Mutism, Asthma, Concentration Issues

When my daughter turned four years old, we moved out of state and that is when she stopped talking outside the house. I later found out that it is called selective mutism, a form of severe social anxiety. She started seeing a school counselor to try to help with her anxiety and self-esteem issues. I brought a girl scout group to my house so that she could start having friends and talk to others in her area of comfort. She also developed asthma and needed nebulizer/albuterol treatments frequently and daily QVAR for prevention. She was given Singulair, but it made her very depressed. Her grades in all classes were all over, from A to D. She would spend the whole time after school trying to complete homework, but she couldn’t. Her teacher told me that she really did not have that much homework. I would ask her to watch the dog eating and to take her outside as soon as the dog finished but she would be wandering around the kitchen and could not pay attention to the dog. Her neurologist gave her Strattera and that helped a little. Her EGG also showed some abnormal activity. The doctor recommended anti-seizure medicine and said that she was probably having mal-petit seizures. I refused medication based on how she reacted to Singulair and because the doctors were using words like “probably” and “just in case”. I kept an eye on her and noticed when she ate ice cream and got asthma. I had her stop sugars and dairy. Soon after that, a teacher called me, excited to tell me that my daughter was talking at school. She also was able to stop all asthma medication except for 2 weeks every year when seasonal allergies would hit. At this point, it had been already four years since she stopped talking outside our house. She started excelling in all classes and we were able to stop Strattera. However, the continuous anxiety remained.

The Teenage Years: Continuous Migraine, More Medications, and No Answers

At 16 years old, she got a cold that turned into asthma with a continuous headache that just would not go away. She started waking up every day with a migraine, depressed with no energy. We had to wait three months to see a pediatric neurologist. Meanwhile, I would take her to my chiropractor early in the morning, give her an Excedrin, and she would go to school whenever she felt better. She began drinking at least 2 cups of coffee every day to help with the pain. Sometimes she would go to school at 11am, sometimes at 1pm. Even if there was just one class left, she would go to school. At this point, she felt that she wouldn’t have a future.

When we finally went to the neurologist, he recommended amitriptyline. I had been on amitriptyline and woke up one day not knowing which year or season was, but I was told that the issue was the high dose given to me (125mg), after decades of it increasing it every year. I agreed as long as it was a low dose. Amitriptyline lessened the continuous headache, but it was not really gone, and she still needed some Excedrin. She started daily aspirin as well. She was just getting by day to day trying to manage her pain and mood and trying to have a normal teenage life.

Increasing Weakness When Outdoors: Untangling Root Causes

She became very weak whenever we would go to the beach or to a park. We would have to drag her indoors and give her water. On some occasions, she would say that she could not see. Somehow, she successfully managed to graduate from high school. We started seeing functional doctors. We found that she had some variants related to mitochondria dysfunction, but we really didn’t know how to address this. We also found out that she had Hashimoto’s and antibodies against intrinsic factors, which was indicative of pernicious anemia. We knew right there, that she had issues that conventional doctors had missed.

We also did a Dutch test and found that all of her hormones were high. The functional doctors suggested sublingual B12, folinic acid, and a B complex. She said the vitamins made her feel awake for the first time. However, chronic fatigue was still a major struggle for her. Eventually, she had to stop folinic acid because it made her depressed and unmotivated. Meanwhile, she managed her anxiety with herbs, but it was a real struggle. She also continued to have asthma requiring albuterol every fall season. She chose a very challenging career in cell biology with biochemistry. She went through college with many cups of coffee just to control migraines, have energy, and be alert.

Discovering Her POTS Symptoms

The summer of 2019, before her senior year of college, the nurse checked her vitals as part of her new summer internship. The nurse thought the pulse monitor was broken because her heart rate was 120 sitting down. After a few minutes, it went down to 99, so the nurse dismissed it. When she told me that, I started paying attention to her heart rate. We went to her physician and neurologist and in both instances, her heart rate was 100, just sitting down waiting for the doctor. I asked if it was normal, and they said that it was in the upper range but not a concern. I was still concerned and made an appointment with a cardiologist but also bought her an iwatch. She noticed right away how her standing heart rate would be over 100, and by only taking a few steps, her heart rate would go even higher and she would become fatigued and even dizzy. From the heart rate monitor on her iwatch, we could see how quickly her heart rate would climb upon standing and then slow a bit when sitting.

That is when I remember that I have read about POTS and hypermobile people. I remember that when she was a child, the neurologist had said that she was hypermobile, but never said that it could be a problem for her. It just seemed like a fun thing to have. I started asking in health groups and someone mentioned that her medications could also cause high heart rate. I searched and amitriptyline did have that side effect. That is when my daughter showed me that her resting heart rate was in the 90s and it would fluctuate from 29 to 205 without exercising. When we went to the cardiologist and explained all of this, he said that he did not even know how to diagnose POTS because it is rare. He did testing and said that the heart was fine but there was some inefficiency due to some valve leaking but that it usually does not cause symptoms. I asked about amitriptyline and he confirmed that it could raise heart rate. At that point, she stopped amitriptyline and her maximum heart rate was 180 instead of 205.

She went back to her last year of college when Covid hit. She came back home and we could see the lack of energy and how much doing any little thing or stress would crash her for days. Since I needed glutathione for chemical sensitivities, I decided to see if it would help her. Glutathione with co-factors helped her recover, instead of crashing for days, she would recover the next day. That is when she told me that every time she walked to school, she felt that she would pass out. When she gets up in the morning, she ends up lying on the floor because of dizziness. Despite her dizziness, daily muscle pain, daily migraines, and chronic fatigue, she had big dreams. She just kept pushing through day by day, with coffee, herbs, and whatever it took, but she knew that something had to change. She successfully graduated in May, Magna Cum Laude, and she had a couple of months to deal with her health before she would leave to start her graduate studies and research job. That is when I found people that knew about Dr. Marrs’ work and thiamine, and her life finally changed.

Introducing Thiamine and Other Micronutrients: Navigating the Paradox

A functional doctor recommended magnesium and niacin for her migraines and they significantly helped. This gave the functional doctor the idea to try tocotrienols. High doses of tocotrienols worked better for reducing her migraine pain than amitriptyline and aspirin combined. Then she started taking high doses of B6. This helped her muscle pain and improved her mobility. Despite being hypermobile, easy stretches gave her intense muscle cramps prior to starting B6. Guided by very knowledgeable researchers belonging to Dr. Marrs’ Facebook group, Understanding Mitochondrial Nutrients, we started Allithiamine. The first thing she said was “wait, the sun does not hurt?”. I asked her what she meant. She explained that all her life, being in the sun gave her pain in her eyes and forehead and that she couldn’t understand why people wanted to be outside. No wonder she never wanted to go outside. She also said her migraines were gone. We have waited 4 years to hear that!

After just a couple of days, she started having a lot of nausea and lower-intensity migraines returned. The researchers knew right away that she needed more potassium. She started to eat apricots, coconut water, or orange juice every time she had nausea and it helped. However, it was happening every hour so we decided to try a different Thiamine. We tried half Lipothiamine and Benfotiamine but she didn’t feel as much benefit and still gave her issues. We went back to 1/10 of Allithiamine. Chatting with the researchers, one asked if she also experienced blinding episodes. Yes! Finally, someone that knew about that! They recommended B2 and we started it. That’s when we discovered that her pain in the sun and dizziness were caused by a B2 deficiency. She continued waking up with crashes needing potassium every hour. She did not sleep that week. The researchers suggested taking cofactors including the rest of the B vitamins, phosphate salts, phospholipids, and beef organs. Beef organs and phospholipids helped with energy and bloating, phosphate salts helped with nausea and irritability.

Then researchers suggested that she needed to stabilize sugars and have more meat. That is when we realized that she had some type of hypoglycemia. We had noticed that she would get very tired and got shaky hands if she didn’t eat. Functional doctors had mentioned that she may have reactive hypoglycemia since she had a fasting glucose of 70. She started having more meat to stabilize her sugars and removed all packaged foods, sugars, grains, and starches. She started having just fresh meat, veggies, rice, beans, nuts, and berries. She felt that she was so much better with beef that she started using it for potassium between meals and bedtime.

She was able to increase allithiamine little by little. She would mix a little bit with orange juice since it tasted so awful. Little by little, she started having fewer crashes and feeling better. It took a month for her to be able to tolerate one capsule of Allithiamine. She was sleeping more but not the whole night. That is when our functional doctor suggested supporting adrenals. That really helped but then she began having stomach pain and nausea after eating beef and developed frequent diarrhea. Chicken always increased her hunger and reduced her energy compared to beef and but now she was afraid of having beef. She stopped all sources of beef and phospholipids.

We consulted a very good functional doctor. She did Nutraeval and confirmed that all her B vitamins were low or deficient and recommended TUDCA and Calcium D Glucarate along with trying lamb and bison first. Both helped in reducing bloating/nausea and she was able to start eating lamb and bison along with reintroducing a minimal amount of carbs. Soon after, she was eating beef again with no pain. After starting TUDCA, her bilirubin levels were normal for the first time in her life. We continued to work with the functional doctor to fix other deficiencies.

Recovery from Multiple Nutrient Deficiencies and the Prospect of a Normal Life

After Allithiamine and vitamin B2, we worked with our functional doctor to balance the remaining B vitamins. She is now able to go out in the sun without bothering her eyes and without passing out. She gained weight after starting the B vitamins and began looking healthier, compared to how skinny and underdeveloped she looked before. She also learned how to manage electrolytes. She sometimes needs more sodium, but other times needs more potassium. She feels sick when electrolytes get out of balance. Although she still had some continuous pressure in her head, she no longer needs any amitriptyline, aspirin, or Excedrin for pain. One thing that remained problematic was folate deficiency. She still became depressed with folinic acid, so she tried methylfolate instead. She felt so unmotivated that preferred not to have it, but she realized that it was key to something that she struggled with all her life: anxiety. She figured that she could have methylfolate every other day, so that she could have less anxiety.

Now, for the first time, she began to have a normal life. She can now exercise daily without dizziness and her heart rate skyrocketing. Her heart rate in general is more normal, doesn’t go down to 29 or up to 205. She had not had any asthma requiring albuterol. She started driving without having to deal with anxiety and panic attacks. She was able to walk to her office without fainting. She now can now live alone dealing with the stress of having a full-time job, graduate classes, cooking her food, and exercise every day! She is not cured completely but for a person that once thought she couldn’t have a future, she is doing pretty darned good!

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, and like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter.

This article was published originally on July 22, 2021.

A Life of Low Thiamine Leading to Wernicke’s Encephalopathy

by Mazda Arrx

Published on January 19, 2026

2K views

severe thiamine deficiency Wernicke's Encephalopathy

I am a 40 year old male with recently diagnosed, but chronic, severe thiamine deficiency (plasma thiamine <6 nmol/L September 2025) – Wernicke’s Encephalitis. I have all of the classic symptoms like nystagmus, ataxia, and cognitive issues, along with a long list of other symptoms that have accrued over time. I have had a horrible diet since childhood, consisting mainly of fast food, and in my twenties, I drank a fair amount of alcohol. I have also had several bouts of food poisoning, including a c diff infection in August 2025. Antibiotics have been a mainstay since childhood. Once thiamine deficiency was recognized, I was given IM injections and told to supplement orally. I feel worse. Something is missing and I need help. Below is my case story. If there is anyone out there that can help, please comment.

Childhood Marked By Poor Diet, Infections, and Failure to Gain Weight

My youth was filled with many upper respiratory and ear infections that I was giving antibiotics for. I had a “fast metabolism” and could never manage to gain weight, no matter how much I ate. I never wanted to eat the healthy food that my mother would cook and always wanted candy and junk food. I would eat things like lucky charms, brown sugar and apple cinnamon instant oatmeal. By the time I reached high school, I was consuming fast food quite often, and then when I got into sports and weight lifting, I was consuming sugar-filled meal replacements, and protein supplements, and microwave meals.

At 16, I developed a rash on my hands every winter. It would crack and bleed and my joints became stiff. I later learned that this was eczema or psoriasis. I was given a corticosteroid cream. After high school, the rash continued to get worse, and never healed. When I was about 21 years old my hands were so stiff that I couldn’t bend my fingers. They were completely cracked and bleeding all over.

Along with this, my ears, and all of the cartilage in my body, turned solid. I wasn’t even able to flex my ears or ear lobe and every time breathed in it felt like I was being stabbed in my left lung. The doctor diagnosed me with relapsing polychondritis, pleurisy, and psoriasis. High dose corticosteroids and corticosteroid creams were prescribed.

The Poor Diet Continues: Heart Symptoms Emerge

In my twenties, I lived off of cheesesteak sandwiches, pizza pockets, French fries, and soft drinks. I only at couple meals a day and usually skipped breakfast. I worked, partied and fluctuated being not enough eating too much. I lost a bunch of weight and began losing my hair.

In my late twenties, I got a much better job with a lot more responsibility and a lot of stress but my diet was still horrible. I would skip breakfast and then gorge of double orders of fast food meals for lunch. I began gaining weight but I was going to the gym so I’d managed to build an unhealthy muscular physique.

At some point, I began having episodes where I would have my heart racing, chest pain, and other symptoms that felt like I was having a heart attack. Hospital visits concluded that these episodes were panic attacks, however, they did note that my cholesterol, and triglycerides were high.

A Healthier Diet But More Alcohol and More Unexplained Symptoms

In my thirties, I made some changes to my diet. I began eating a healthy breakfast but was still eating out for lunch and having large portions. I added in raw vegetable powders and multiple organ capsules to diet. I also began drinking more alcohol.

My psoriasis flared. I developed random internal vibration episodes and very subtle full body tremors, as well as being jolted awake in the middle of the night. I decided at this point it was time for a change. I tried to eliminate dairy, grains and gluten, chocolate, sugar with the hope that this would resolve my inflammatory issues. Unfortunately, it made matters worse, likely at least partially due to the alcohol consumption.

Magnesium Oxide, a Benzodiazepine and an SSRI

Within about a year, I had lost a significant amount of weight, ended up with significant sleep issues, increased anxiety, and had the worst brain fog of my life. I could not function properly at work and was losing my hair in significant amounts. I visited my doctor who was very well meaning and spent quite a bit of time trying to help. He found that my magnesium was low (1.6), so he gave me magnesium oxide as a prescription. This caused severe loose bowels and just made things worse.

He also told me that I had a genetic predisposition for high adrenaline, and proceeded to give me propranolol to calm that down, as well as a benzodiazepine and SSRI that would “help with my insomnia”. I was not depressed. I just couldn’t sleep and felt like I was in high gear all the time. Instead of doing research and because I trusted this doctor, I took the medication as he advised.

The SSRI made me want to crawl out of my skin, but the benzo allowed me to sleep 6-7 hours, stopped the tremors and being jolted awake. We went through three different SSRI’s until settling on Lexapro. I was on these for about a year until I actually did some research and learned how they were harming my body. I then decided to ween myself off. That process was brutal, with the feeling of brain zaps, worse tremors than before, and intense insomnia.

Brain Fog and Dizziness Worsen

Around this time, a friend and I started a snow removal company. The job was extremely physically demanding. I was out for 24+ hours at a time in freezing temperatures, not only in the truck, but also out shoveling and carrying around a 50lb buckets of salt to spread. I didn’t eat much while out, and lived off coffee, milk and orange juice. We also started going out on the road for weeks at a time, staying in hotels and working 12-16 hour days in food factories, repairing their equipment, and starving myself. During this time, I experienced some of the worst brain fog I had ever felt. I couldn’t make sense of anything.

In 2016, I discovered the Ray Peat way of living. I eliminated a number of foods from my diet and began consuming a lot of coconut oil, ice cream, milk, orange juice, but at a significant calorie deficit. The diet made me weaker and I wasn’t able to keep up with the business. In 2017, I got a part time job at a grocery store, thinking it would be easier physically but beginning work at 4 am became problematic. The brain fog continued to worsen.

First Bout of Food Poisoning: Cipro and Flagyl Prescribed

Sometime between 2018-2019 I got campylobacter food poisoning from an undercooked burger. I was given Cipro and Flagyl. The Cipro caused joint inflammation and so they advised to discontinue it and finish the Flagyl. After these meds, I had a horrible time concentrating and completing department order at work. I was spaced out while driving, which even led to a couple auto accidents, more frequent tremors that even my girlfriend noticed, and I would randomly wake up with full on shaking, followed by nausea and vomiting. My magnesium still continued at the very bottom of the range, so I started using ReMag in an attempt to move the needle, which mostly just put me in the bathroom. I also started taking taurine, niacinamide, and thiamine HCl. My cholesterol and triglycerides were still elevated.

In 2020, I worked through COVID, as we were essential workers. Luckily, I did not get COVID at this point. I continued taking vitamins, taurine, magnesium, and began desiccated thyroid. I also ate bags of dried organic apricots and mangoes daily. They seemed to help with energy levels.

First COVID Infection and New Onset Food Allergies

In 2021, I began a new job and got COVID for the first time. At that time, I consuming a daily smoothie with full packs of frozen 365 organic strawberries, mangoes, dark sweet cherries, peaches, a cup of orange juice, and Mt. Capra casein protein. The casein protein exacerbated the brain fog. When I eliminated it, the brain fog wasn’t as bad. Odd because I was able to drink milk in the past, just not consume whey protein.

COVID hit hard and took me out for almost a month. I had fever, low O2, and high heart rate. I took aspirin every 4 hours and this seemed to lessen the symptoms pretty quickly. I spent most of my days in bed, eating scrambled eggs, butternut squash soup, chicken soup, and mozzarella cheese. Toward the end of the COVID infection, I developed excruciating pain in my left thigh. I thought it was a blood clot from lying in bed for too long, but an ultrasound ruled that out. The pain and COVID-related shortness of breath remained for about a month. After that everything was back to normal, except now I had food allergies. I could no longer eat the butternut squash soup nor could I eat mozzarella, or the sweet potatoes or French onion soup I would eat prior to getting sick.

Few Good Years with Thiamax Despite Another COVID Infection

Late 2021, I began taking Thiamax to replace the thiamine HCl I had been taking. When I began, I had a little extra brain fog, but I attributed it to the COVID. I also added methylene blue to the mason jar of orange juice I would take with me to work to sip on, along with great lakes collagen. Things started looking up. The brain fog started subsiding and I was able to function at work.

I continued to have the startle awake reactions and tremors. These mostly would happen if I tried to take a nap during the day. Any time I would start to fall asleep, I would be immediately jolted awake and then experience a full body vibrations sensation. This happened every time I started to nod off. I was thinking maybe it was due to the thyroid, but I was still at the very bottom of the level for magnesium when tested.

2022 Was fairly uneventful year, although I did catch COVID again. This time it was very mild and I was only out of work for less than a week. I had all sorts of allergies to food, but the brain fog seemed much improved. The startle awake and vibrations remained and my magnesium was still low.

In 2023, I was in ER early in the year with odd abdominal and back pain, nausea. I thought it could be food poisoning from daily Uber eats lunch orders. Some blood was found in urine. They said it was gastritis and to take Pepcid. The rest of the year was uneventful. I was still taking Thiamax and desiccated thyroid daily. My energy levels were better. I had less brain fog and my body temperature improved. Magnesium was still borderline low but calcium on many blood tests above 10.

Food Poisoning Again and More Antibiotics

Towards the end of October 2024, I got food poisoning again. This time it was salmonella. I had non-stop vomiting and loose bowels for over a week. I was prescribed Flagyl, but did not take it, and Cipro, which I took for 7 days, with gradually worsening joint pain and inflammation. Cipro was discontinued and replaced with Cefixime. A stool test one month later revealed that salmonella had colonized, and they would not give any additional antibiotics to help clear it up. From this point on into 2025, I never felt the same. I had also stopped the Thiamax and was only taking forefront health b-complex and forefront health desiccated thyroid. I was still borderline low magnesium.

The Downward Spiral

By early 2025, I had much worse brain fog, frequently lost train of thoughts, couldn’t concentrate at work, started getting odd reactions to ice cream, mashed potatoes and other foods. They would cause a full body itching, and internal vibrations when I would eat them. Constipation was the norm, and my doctor told me to take two magnesium oxide tablets a day to help, my gastroenterologist told me to take biscodyl daily to help. I started to have a constant feeling like my throat was inflamed.

In May, I was diagnosed with eosinophilic esophagitis. For the endoscopy, I was given propofol and fentanyl for anesthesia. It took over an hour to wake up from and the entire week following, I felt like I had just woke up from the anesthesia. A few weeks later, I was given high dose Omeprazole to correct the eosinophils. I was also advised to eliminate eggs, dairy, wheat, soy, fish, nuts, and corn from my diet.

In June, I received the results for the buccal swap Mitome profile. It showed 404% citrate synthase, normal Complex I, low-normal Complex II, low-normal Complex II-III, and low (24%) Complex IV.

I tried to start implementing the proposed protocol but it seemed to be causing more symptoms. I started tracking glucose, ketones and lactate daily per Chris Masterjohn’s recommendation. I was going out for daily walks and hitting around 8k steps.

A Tick Bite, More Antibiotics, and a C. Diff Infection

In July, I had a bullseye tick bite and the doctor prescribed doxycycline. The doxycycline causing worsening tremors and severe tinnitus, I stopped taking it, after which both began to subside. I was walking daily.

In early August of 2025, I went to the ER with nausea and vomiting. They sent me on my way after doing a CT with contrast and seeing inflammation of the stomach and intestines. They said it was the stomach flu and to stay hydrated. This persisted and worsened for a week and so I was admitted to the hospital. A stool test it was found that I had an active c.diff infection and was colonized with salmonella from the prior food poisoning. I was given ceftriaxone IV, and vancomycin oral.

In addition to the antibiotics, I was given IV’s with sodium chloride and lactated ringers and initially and I felt better. Then they switched over to D5NS, a saline solution that contains 5% dextrose and I felt worse again. Dextrose depletes thiamine and I was already malnourished and thiamine deficient. Nevertheless, within three days of my hospital admission, I was able to consume food by mouth again, around 2,100 calories per day consisting of burrito bowls for breakfast, lunch and dinner, that contained carnitas, rice, pinto beans. I walked the halls doing lunges and calf raises to stay as active as possible.

The morning I was to be discharged I was advised that my magnesium and potassium were both low and given two pills to correct those levels. Vitamin B1/thiamine was not checked. I was also given a 10 day dose of azithromycin.

Severe Thiamine Deficiency Lurking

At discharge, I felt very weak, had tingling and weakness in the legs and severe brain fog. That night at 6pm I took my dose of vancomycin, and my first dose of azithromycin. The next day, I awoke with severe digestive distress continuous diarrhea throughout the day. I returned to the emergency room feeling like I was dehydrated, but they stated that all of my levels were normal and I was discharged.

The following morning, I awoke again with severe digestive distress, and upon standing my heart rate spiked to over 160 beats per minute. I rushed to the kitchen and grabbed some Pedialyte, thinking it was just dehydration, but this made my heart rate beat faster and caused blurred vision. I thought I would faint and I felt an impending doom sensation like I was going to die.

I called 911, and medics arrived and proceeded to perform an EKG, which merely showed sinus tachycardia. They were unable to get my heart rate down in the ambulance, and upon arriving back to the emergency room, I was left to wait for 6 hours before I was able to get any fluids. When they attempted to draw my blood, my veins were flat and they weren’t able to get blood to flow into the vial. This would later become a trend, with blood vessels in the arms and hands constantly appearing shriveled and misshapen, and my mouth felt dry like sandpaper despite trying to drink water.

Oddly, my electrolytes all came back in normal range. My heart rate stayed around 110 to 120 beats per minute the entire wait even while seated in a wheelchair. When I was finally brought into the ER, I was given one large bag of sodium chloride administered rapidly. This initiated a weird sensation in my chest and uncontrollable coughing.

They took me for a CT scan with contrast, and then for a chest x-ray to check for fluid in my lungs, but found none. I was then given a bag of lactated ringers and my pulse began to normalize. During an orthostatic test, my pulse spiked over 100bpm upon standing. They gave me another bag of sodium chloride, performed another orthostatic test and my pulse remained under 100bpm. I was advised to discontinue the azithromycin, and my diagnosis was listed as severe dehydration.

After discharge, my legs were very weak and I had an odd internal vibration, buzzing sensation. My whole nervous system felt very irritated, worse than I ever experienced before. The nerves in my spine and lower back felt raw and like they were being poked. This and tremors, prevented sleeping. I also developed muffled hearing. I was switched from vancomycin to dificid 3 days later.

From that point on, I had worsening neurological symptoms, odd episodes of confusion while driving. I didn’t know where I was even though I was near home. If I looked in the mirror it felt like the room spun. I finished my round of dificid on September 1st.

Increased Need for Sodium and the Continued Downward Spiral

Since my hospital stay, I the only way to keep my heart rate somewhat normalized was to drink several electrolyte beverages or consume large amounts of salt throughout the day. On September 2nd, I developed severe neurological symptoms and diarrhea after consuming a large fruit smoothie.

I noticed that when I ate pulled pork, I would I had more energy and was in a better mood but developed reactions to the garlic and spices used in it. As a result, I switched to a more bland diet consisting mostly of a plain ground chuck, plain chicken with salt, and applesauce.

In mid-September, I added plain white rice to my bland diet with hope of adding more calories. I had lost over 40lbs at this point. The rice probably made matters worse. I developed episodes fuzzy vison. I saw floaters in my eyes, as if I was staring into a bright light. My hearing would go out and I would just have a loud ringing or buzzing in my ears. My pulse would spike to 150 or higher. I became dizzy and felt completely intoxicated, despite not drinking alcohol. Every muscle in my body twitches including my face muscles, and I’ve been told that my eyes will twitch when trying to look straight forward. This is triggered when exposed to heat, bright light, exercise, strong smells or any sort of stimulating experience.

Polyuria and More Thiamine Deficiency Symptoms

In late September, I was excreting around 2L of urine in a few hours despite normal consumption. I went to the ER for IV fluids and then again two days later after having that feeling of impending again. I had white rice for dinner.

I had an EKG, blood work, and was given a potassium in IV, as my potassium was low. They tried to discharge me, but I argued for admission. Nephrology and endocrinology performed a variety of tests. A 24 hour urine test measured 8 liters of urine despite consuming only 2 liters. After urine began to concentrate again, I was discharged. Upon discharge, when I attempted to stand my legs were so weak they almost collapsed beneath me. I felt numb from the waist down.

We Finally Tested Thiamine: Undetectable

That night, I went to a university hospital emergency room and during my 13 hour wait to get in, I desperately searched for answers. I chanced upon hormonesmatter.com and ordered the kindle version of Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition and began to read. Once a bed was finally ready in the ER, I told them my story and they started running a number of labs.

I was seen by several doctors, neurologists, and a pulmonologist. They ran orthostatic vitals, several blood labs, and upon my doctor’s recommendation they admitted me for observation (he was leaving his practice that day). They did an MRI of my spine, took me for an EMG and nerve conduction tests. In the MRI they noted some slight degeneration in the spine, and red marrow reconversion throughout. EMG and nerve conduction tests were mostly normal, however, they noticed some diminished sensation in my left lower extremities and toes and a mild gait disturbance.

I requested a vitamin B1 plasma test, along with copper, iron, zinc, and others. I was kept for observation for a few days and given IV fluids, which kept pulse fairly normal. The thiamine test had not returned by the time of discharge.

A week later when the result came back, it was <6 nmol/L, which is basically undetectable.

I was extremely excited, finally getting some answers as to why all of these things were happening. The doctor prescribed intramuscular thiamine 500mg in total, to be given daily for a week, followed by 400mg thiamine HCl orally and IM shots every three days for the next two weeks. The first shots were that very night.

Thiamine Repletion Has Been Brutal

After my first dose, I slept well for the first time in months but the next morning when I attempted to stand, my pulse spiked up but my blood pressure tanked to 89/62. I could no longer walk for more than a short distance. I tried to continue my regular 8-10k steps daily, but after a couple hundred steps, my body would completely shut down. My vision became fuzzy, I saw floaters or like flashing lights and my pulse would skyrocket even though it was already high. The Holter monitor recorded sinus tachycardia and some SVT’s. My legs were so weak, they tremor and felt like they were going to give out beneath me and I felt like I could not get enough air in.

This entire time I was getting the thiamine shots, I struggled to consume enough calories on a daily basis. Surely, eating only 900-1000 calories didn’t help my situation, I just couldn’t eat any more. When the shots were stopped in November, my health declined further. At this point that, I began significantly increasing my dose orally and adding other forms of thiamine. This made everything significantly worse.

By mid-November, at this time I was getting around 300mg of magnesium malate per day, taking a daily multivitamin (Seeking Health One Chewable), as well as Forefront health thyroid B-complex), and only able to eat boiled chicken and applesauce. Anything else made my GI symptoms unbearable and caused worsening tremors and internal vibrations. Per my records, here is the dosing I followed.

Week 1 (first 5 days): 500mg IM thiamine HCl shots, once per day.
Days 6 & 7 picking up with 200mg of thiamine HCl by mouth twice per day for 400mg.
Week 2: 200mg thiamine HCl by mouth twice per day for 400mg, with one 400mg IM shot on Thursday.
Week 3: 300mg thiamine HCl, plus 150mg benfotiamine by mouth twice per day, with one 400mg intramuscular thiamine HCl shot on Monday and 400mg IM thiamine HCl shot on Thursday.
Week 4: 300mg thiamine HCl plus 300mg benfotiamine by mouth twice per day, with one 400mg IM thiamine shot on Thursday.
Week 5: 300mg thiamine HCl, plus 300mg benfotiamine by mouth twice per day, no intramuscular shots.
Week 6: 300mg thiamine HCl, plus 300mg benfotiamine by mouth twice per day, no IM shots. Wednesday and Thursday attempted to add morning and afternoon dose of Thiamega and cut benfotiamine back to 150mg and thiamine HCl back to 100mg. This led to extreme anxiety, significant increase in pulse and panic attacks.
Week 7: same as above but have begun having random panic attacks, adrenaline surges, pulse spiking to 160bpm randomly. I can’t sleep at all (last week and the weeks before I was getting 7 to 8 hours per night typically). Now I wake up at 2am and feel air hunger and have random surges in pulse, spasms and closing of my esophagus. I went to the ER yesterday and they found nothing wrong. All electrolytes were on the lower end of normal. I have tremors, dysautonomia and POTS symptoms again and I am losing weight again.”

The Hell Continues: Confusion and Food Intolerances

Thinking I was taking too much thiamine, I reduced intake to just 150mg benfotiamine and 350mg thiamine HCl for a couple days. This was right before Thanksgiving. My neurological symptoms were getting worse, and now I was experiencing dizziness, cognitive decline and new vision problems, but the shortness of breath had begun to subside.

I had an appointment to see a nutritionist. I showed up at the appointment and had this new surge of confusion, as well as a significant increase in pulse while walking in, my body felt ice cold even inside the building.

After going over all of the foods that I was having issues with and what my allergist told me to avoid, we were left with almost nothing. She said, at this point you’re going to just have to try to start eating anything you possibly can to add more calories, because you’re lucky if you’re getting 600 calories per day.

As I walked out of the building from this appointment, I experienced the worst brain fog that I had experienced to date. I walked around the entire parking lot but I could not remember where I parked my car. My pulse extremely high and I was dizzy. I felt like I was in a dream and I could not make sense of anything that was going on around me. I eventually found my car about 20 minutes later.

Since I was struggling to come up with ideas of what I could eat and unable to tolerate most of the things that I tried at home, I decided to go back to trying Chipotle. It turns out, I can tolerate Chipotle carnitas. So now, I eat two chipotle bowls with double meat, double brown rice and light beans. It’s nowhere near an ideal healthy meal but at least I can eat – sort of. I now get migraines a few hours after eating and internal vibrations and tremors.

I started taking Zyrtec daily, because I tested positive for a rice allergy on both blood and skin tests. I continue to eat Chipotle and use Zyrtec to manage the allergic reactions. I also take quercetin, a mast cell stabilizing supplement, and butyrate supplement.

Another Medical Procedure With Anesthesia

Mid December, I had a recommended colonoscopy and endoscopy. Given my problems with anesthesia, I was worried. The prep process was very rough on my body and caused even more palpitations and higher heart rate. I don’t think the thiamine I was taking was absorbed and not eating made things worse. Surprisingly, coming out anesthesia was okay, but the first time I tried to drive, I had a major energy crash. I felt like everything was moving in slow motion and my brain was running out of energy would shut down. My vision was fuzzy, my hearing went out and I just had a loud ringing as my pulse spiked up. I felt like I was completely intoxicated. Every muscle in my body started twitching, tremoring and then lost strength. I messaged my neurologist and they responded that it sounds like a panic attack, and I should take some Tylenol for my intense migraine headaches. I was not a panic attack.

I have been unable to drive since. Every time I am in the car with someone going to an appointment, all of the visual stimulation from trying to process cars and what’s going on the road and around me, causes what feels like a mental shutdown. I also feel like I’m intoxicated constantly, especially when in the car, or looking into a mirror. It has gotten to the point where it is hard for me to focus on things mentally, or make sense of things I read or watch. I’m not sure if this is all due to the B1 deficiency or if it’s partially due to the c diff infection and all of the antibiotics.

My Health Is Failing and I Don’t Know What to Do

I am struggling daily to maintain a proper electrolyte balance. If I sip a 33oz coconut water throughout the day and add a little salt here and there, in addition to the sodium I’m getting from food, I end up feeling dizzier, like my blood pressure is too low. If I take 450 mg of sucrosomial magnesium, I still have full body tremors, muscle twitching and a migraine. If I increase the magnesium the twitching subsides, but dizziness increases and I feel faint. I’ve even tried using 350mg sucrosomial magnesium with 144mg of magnesium l-threonate (hoping this would help with brain symptoms.

I’ve tried to introduce healthier foods, such as the farm eggs that I used to eat every morning, ground lamb, fresh-squeezed orange juice, but my body just seems to reject these. So I am left with the Chipotle, with double carnitas, double brown rice, and light pinto beans. I realize these meals are not the healthiest options and probably not doing me any favors with the brain fog, migraines and other symptoms but I don’t know what else to do. Are my continuing symptoms all related to the thiamine deficiency, my diet or something else?

Adding More Supplements

On December 19^th, I began taking Lipothiamine. I began with 12.5 mg once at breakfast, along with 150mg benfotiamine, and 250mg thiamine HCl. For lunch, 150mg benfotiamine and 100mg thiamine HCl. That day I had much more severe dizziness, my head felt like it was in a vice, and I was experiencing lapses in time. I went to the ER thinking maybe it was an electrolyte issue. They said electrolytes looked fine. Potassium and sodium were at the very low end of normal, but they were not concerned. They did a CT of my brain (again) and did not find any irregularities. I was offered a migraine cocktail consisting of antihistamines and morphine or something like that, and they offered to keep me for 24 hour observation. Since there was nothing else they could do for me, so I declined. I was given a bag of sodium chloride and discharged.

On the 20^th, I increased to 12.5 mg with breakfast (plus 150mg before/250mg HCl), and then 12.5 mg with lunch (plus 150mg benfo/100mg HCL. I held that dose until December 23rd, when I was able to resume the intramuscular shots.

After the intramuscular shots, I felt like I had more energy, I was much more social, and felt like symptoms had improved slightly. The next day, I increased my Lipothiamine dose to 25mg with breakfast, keeping the same benfo and HCl doses as the prior days. All of the symptoms got much worse. I felt a significant increase in the dizziness, heart rate picked up, it felt like I was walking through a dream.

On December 25th I added another 25mg of Lipothiamine with lunch and kept the bento and thiamine HCl the same (so 25mg lipothiamine with breakfast and 25mg with lunch). Symptoms continued to worsen. I also began taking CoQ10 ubiquinol (50mg with breakfast and 50mg with lunch), mitosynergy copper (split .5mg with breakfast and .5mg with lunch), black seed oil/curcumin (one capsule with breakfast, one with lunch). Lactoferrin (one capsule with breakfast, one with lunch), Jarrow reduced glutathione (one capsule before breakfast, one before bed), liposomal vitamin C (twice a day), creatine (4 split doses 3g total per day),

Elite IgG ImmunoLin blend for gut healing (one scoop before breakfast), ProButyrate (2 capsules before breakfast, two before dinner), and Hesperidin capsules (one capsule with breakfast to help with neuroinflammation).

From December 25th on I have been following the same protocol, with everything listed above, with the exception of adding Thiavite to my morning doses which adds all cofactors and increases TTFD by 15mg in the morning dose.

Reasoning Behind the Recent Supplements

I added the lactoferrin and black seed oil/curcumin as part of my Mitome protocol. When I did the Mitome test back in May 2025, it showed complex IV was at 24% and noted that I should be supplementing with heme iron, or if my ferritin levels were high that I should utilize whey protein/lactoferrin, with black seed oil and curcumin to lower inflammation so that trapped iron was released from ferritin. It also noted that I should be using copper to support complex IV cytochrome C oxidase enzyme. For the low complex II and II-III it noted coq10. I’ve added all of these in, and hope that if what I’m also dealing with an addition to a thiamine deficiency, is also mitochondrial dysfunction, that this will help to support my mitochondria and correct all of the issues that I’m having. In recent lab tests my copper was on the low end of normal, but so was ceruloplasmin, with a free copper over 15. In my iron labs, my iron was at the low end of normal, with transferrin below the normal range, and ferritin at the top of the normal range, with saturation at around 30%.

On December 31^st, I did another 400mg of thiamine HCl intramuscular shots, and again the first day I felt more social and talkative, but since the 3rd I’ve been feeling very off. Migraines are back even worse, a sensation of extreme nervous system irritation and randomly losing hearing in my right ear. I feel like I still cannot get my electrolytes managed properly, and I’m left feeling like I’m never going to get back to my old self. My pulse was somewhat normalized in the morning before eating breakfast and at night, now it’s elevated again.

Where I Am Now

The last few days I’ve also had a lot of digestive upset. I’m getting more hives like reactions to all foods. Overall, I am very fatigued and feel like I’m walking through a dream. I don’t know how to continue supporting my body without causing more inflammation. I don’t know if this is all related to the B1 deficiency or if this is a much larger issue that I need to be working on.

I’m trying to walk around as much as possible so that my body will stimulate more mitochondrial biogenesis. I would to get to the point where I can drive again but my legs feel weak and I have very low energy levels. My doctors are pushing for me to do a stress test in one week, and if all goes well, they would like me to start physical therapy and occupational therapy. At this point, I feel like that is just going to make things worse, because every time I try to do anything physically or mentally taxing, I crash and then the next few days are miserable.

My time is also running out for being able to return to work. If I’m not able to return in the next 4 weeks, my position will be opened up. I’ve even tried to spend time with family, and simply holding a conversation causes the over stimulation reaction where I start to feel faint, my pulse rises, and my vision gets fuzzy, etc.

Please help me get my life back. I want nothing more than to return to work, spend time with family, and friends and help others who are in similar situations.

Post Script: I just learned that the IM thiamine shots I was prescribed contain 400 mcg/mL of aluminum each. I have been injected with a neurotoxin for months now. I have not been able to find a clean IM. If anyone knows of an IM thiamine without aluminum, please let me know.

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Mitochondrial Capacity and Thiamine: Notes from a Presentation

by Chandler Marrs, PhD

Published on January 15, 2026

2.5K views

Mid December, I gave a talk on mitochondrial capacity and thiamine’s role therein (included below). My argument was that mitochondrial capacity e.g. their capacity to produce ATP efficiently from the foods we consume, and to meet the demands of living, drives health or illness. I also argued that thiamine drives mitochondrial capacity, and thus, is implicated in modern illness.

It is an argument I have made for years now, and of course, I wrote a book about it, together with the late Dr. Derrick Lonsdale. It is not something readily considered by western medicine, however. Even as our understanding of the molecular mechanisms and pathways connected to mitochondrial functioning has expanded over the last century, the fundamental nature of mitochondrial energetics remains underappreciated. We look to everything else the mitochondria do as somehow more important to health and disease than simple energetic capacity, forgetting that these other processes do not happen without sufficient energy.

Energy is the most basic unit of life. It is the capacity to transform something into something else. Absent this, we are nothing more than rocks.

That said, I did learn a few things when preparing for this talk. Namely, I learned how many discrete disease there are. Did you know that we now have over 26,000 separate disease entities recognized by the medical profession and over 18,000 ‘global’ or ‘systemic’ disease entities? I did not and was shocked. Before I looked this up, I thought we had maybe a few thousand, ten thousand if I were being generous. Never once did I contemplate 26,000. That is absolutely insane. Worse yet, apparently there are over 20,000 pharmaceutical products currently on the market. A pill for every ill – almost.

With all of this knowledge, one might think we have advanced in our capacity for health and healing. One would be wrong. According to the latest research, 76% of the population deals with at least one chronic condition. And quite unironically, despite the endless discrimination of discrete diseases, most symptoms, from 25-75% according to one report, remain medically unexplained. We are drowning in distinctions where perhaps there should be none, or at least far fewer, and we are none the wiser or healthier for it.

From my perspective, I cannot help but wonder how many of these discrete diseases are not simply expressions of poor mitochondrial capacity? Sure, there are potentially millions of combinations of interactions between genetics and the lived environment that are likely to affect disease presentation, but is each set of symptoms really representative of a separate disease? From a mitochondrial perspective, probably not.

Moreover, if mitochondrial capacity is the key to health, then instead of searching for and naming each permutation of disease expression and creating new drugs for each, we could go back to the basics and ask ourselves – what do I need to be healthy and am I getting it? If I am ill, chances are I am missing something, probably lots of somethings and those missing components to health, along with the long list of environmental toxicants and genetic interactions that lessen mitochondrial capacity, are what is driving illness. Perhaps if we support the mitochondria and view health from that perspective, we can reduce the burden of disease while culling the impossible and growing list of supposedly discrete diseases.

Alas, none of that will happen, at least not on a scale that would make a difference. That said, perhaps my lectures and articles might help a few people reclaim their health and their family’s health. For me, that is a win.

Here is the latest.

Mitochondrial Capacity, Thiamine, and Dysautonomia

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

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Is TTFD Toxic?

by Elliot Overton, DipCNM CFMP

Published on January 6, 2026

21.4K views

I regularly receive correspondence from people asking whether thiamine tetrahydrofurfuryl disulfide (abbreviated TTFD), a thiamine (vitamin B1) derivative, is toxic or not. Most people following this line of inquiry base the assumptions of “toxicity” on statements previously made by the famous (and now deceased) Andrew Cutler, PhD. Cutler is most well-known for his work on mercury chelation and detoxification protocols and has amassed thousands of followers over the years. He was strongly opposed to the application of TTFD therapeutically and explicitly advised people against using this molecule as a nutritional supplement for thiamine repletion or heavy metal detoxification. Much of what he said on this topic was documented in the archives of the Onibasu website which can be found here. Cutler’s statements were speculative in nature, based on anecdotes, and to my knowledge, were never backed by any scientific evidence. In this article, I would like to address his claim that TTFD is toxic. I should note, based upon all of the available research, which is substantial, TTFD is not toxic, even at supra-physiological dosages. A version of this article was published on my website.

Is TTFD Toxic?

To understand whether TTFD or any compound may be considered toxic, it is important to recognize how toxicity is determined in pharmacology. Here toxicity is represented by something called a therapeutic index (TI). In animals, where much of the research is conducted initially, the TI is determined between by ratio of the lethal dose 50 (LD50), a dose at which 50% of the animals die, and the effective dose 50 (ED50), the dose at which a therapeutic response is noticed in 50% of the animals. This is represented as TI = LD50/ED50. In humans, instead of lethal dose, toxic dose is used (TD50). Here, the TD50 represents negative or adverse reactions in 50% of the population tested. The equation is basically the same, TI = TD50/ED50.

In both cases, higher therapeutic dosing windows relative to efficacy confers greater drug safety. Compounds where there is little wiggle room between the TD50 and LD50 – a small TI – are considered the most toxic. See Figure 1.

Therapeutic Index — Figure 1. Therapeutic index.

By way of example, alcohol/ethanol has a TI of 10, whereas LSD and cannabis have TI’s of greater than 1000. This means that one has to consume far less alcohol to achieve toxicity and lethality than either LSD or cannabis. Indeed, it is virtually impossible to overdose (OD) with LSD or marijuana compared to the ease at which one can OD on alcohol. Figure 2.

Lethal doses for common drugs — Figure 2. Lethal dose of common drugs.

Similarly, the TI for many common drugs is quite low. Figure 3. from a pharmacology lecture on SlideShare, shows the TI of common medications.

Figure 3. Therapeutic index of medications.

What Does Any of This Mean for TTFD?

In mice studies, the LD50 for TTFD has been calculated at 450mg/kg when given intravenously (IV) while the LD50 for an oral dose is 2200mg/kg. Since the conversion from mice to human dosage is not calculated directly based upon on weight, but accounts for interspecies differences in metabolism, an equivalent LD50 for a 70 kg (154 lb) human would be 2.5 grams of TTFD when administered via IV and 12.5 grams if taken orally. Whilst 2.5 (IV)-12.5 (oral) grams may seem low, no one realistically takes that amount of TTFD per day for therapeutic reasons. The highest oral doses I have observed are around ~1-2 grams per day. These are individuals with chronic thiamine deficiency, usually accompanied by underlying genetic issues. More commonly, observation and clinical research suggest between 100-300 mg/day is used for most treatment/research protocols (see the ‘What about Research in Humans’ section below).

Back to the math, the RDA for thiamine, not TTFD, but thiamine consumed from food naturally, from food fortification and/or via supplementation using the most common formulations of thiamine mononitrate or hydrochloride (HCL) is 1.1 and 1.2 mg per day for adult females and males respectively. Assuming that the RDA values represent an effective dose (there are no actual data on the ED50 for thiamine), and for simplicity, that TTFD is as effective as the other two formulations, when we calculate the TI for humans (TI= ED50/TD50) for humans, we get a huge range between effective dose and toxic or lethal dose. For IV administered TTFD the ratio would be ~2,500:1, while oral dosing, it would be ~12,500: 1. If we assume, based upon its bioactivity that TTFD is more potent than the other two formulations, the TI would increase even more.

Based just upon standard toxicology parameters, it is clear that TTFD is not toxic. An individual would have to take ~12,000 times the effective dose to approximate lethality. I say approximate, because there are no documented cases of TTFD overdose. Lethality, however, is just one component of toxicology. Adverse reactions are an important consideration. That is why, in human research, instead of LD50, TD50 is used. Here though, the work becomes a little murky, partly because animals are used and partly because the chemistry of TTFD metabolism is complicated.

Toxicity Studies Using High Dose TTFD

Consistently, the animal data show that excessive doses for extended periods of time, even during pregnancy and across multiple generations, TTFD is not toxic.

Research performed on the reproductive effects of TTFD in monkeys showed that massive doses of 500mg/kg, close to supposed LD50 for that species, found no deaths. To put this in context, it would be the human equivalent of taking 10-11 grams per day for MONTHS.
That same study also looked at massive doses in rabbits and found no significant increase in incidence of fetal malformations in either group was observed, even in groups treated with high doses and no significant teratogenic effects or developmental abnormalities in pregnancy occurred.
As referenced in this document, Takeda’s research by Mizutani demonstrated that administration of 100, 300 and 500mg/kg in rats for two generations from the time of maturation to the time of reproduction showed no abnormalities. The average human equivalent (70Kg) of these doses would be 570mg, 1.7 grams and 2.8 grams per day for life.
The results of another study showed that long-term oral administration of 30-300mg/kg to pregnant animals failed to produce any significant developmental abnormality. Intraperitoneal administration of 1000mg/kg also showed no sign of chromosome aberration, damage to sex organs or spermatogenesis.

TTFD Metabolism

If TTFD is not toxic via the traditional measures, is there something about the molecule itself that may be problematic and cause unwanted effects? Cutler speculated that the mercaptan part of TTFD was responsible for toxicity, and that this primarily affected the liver. The word “mercaptan” refers to the thiol group that breaks away from thiamine after its absorption into the cell. This mercaptan group essentially accounts for the “TFD” of the abbreviation TTFD. After TTFD is absorbed, it gets “broken apart” (the disulfide bond is chemically reduced) by glutathione, cysteine, or hemoglobin to release the free thiamine molecule, which will become trapped inside the cell and ultimately used by the body.

mercaptan metabolism — Figure 4. Mercaptan metabolism phase 1.

In more technical terms, the prosthetic mercaptan is released and then rapidly metabolized by the liver through methylation and later sulfoxidation by liver mono-oxygenase enzymes into breakdown products which are then excreted in urine. Is mercaptan toxic as Cutler suggested? The original series of studies on the enzymatic breakdown of TTFD and mercaptan show that it is not toxic and is rapidly excreted from urine.

If mercaptan itself is not toxic, perhaps it metabolizes into something else and one of its by-products are problematic. From Figure 5., we see that mercaptan is metabolized into a sulfate that is then eliminated via urinary excretion and a few other compounds that are processed by the liver first before being eliminated via urinary excretion as well. The breakdown products are shown below in Figure 5.

TTFD - mercaptan metabolism — Figure 5. TTFD – Mercaptan metabolism.

A study titled “Pharmacological study of S-alkyl side chain metabolites of thiamine alkyl disulfides” sought to determine the acute and sub-acute toxicity levels of each metabolite. They concluded that toxicity of these breakdown products was low. Remember the LD50, the dose that causes death in 50% of the study animals, research shows that the LD50 each of these breakdown products is enormous, far more than would be clinical relevant in humans. The results of this study showed:

Inorganic sulfate: non-toxic
Delta-methylsulfonyl-gamma-valerolactone: also non-toxic.
- Intravenously, the LD50 in mice was in excess of 5 grams/kg body weight. For comparison, the LD50 estimate for a 70KG human: 5 grams intravenously.
- Orally the LD50 in mice was 6 grams/kg body weight, which, for a 70 kg human would translate to approximately.
4-Hydroxy-5-(methylsulfonyl) valeric acid
- Intravenous LD50 in mice: 1.5 grams/kg body weight
- LD50 estimate for a 70KG human: 3 grams intravenously

Once again, it appears that none of these compounds is toxic. In humans, approximately 82-90% of these metabolites are excreted within 24hrs and 100% are excreted within 48hrs. What this tells us is that by themselves, these metabolites are not toxic except in supra-physiologic doses, which are not relevant from a clinical perspective.

What About Liver Damage?

Cutler speculated that metabolism of TTFD resulted in liver damage. To quote Cutler:

My guess is the tetrahydrofurfuryl mercaptan part kills your liver.

Here too, however, the data suggest otherwise. In animals with artificially induced liver damage by carbon tetrachloride and/or hepatic dysfunction due to choline deficiency, the breakdown products of TTFD were assessed. They showed that the quantity of excreted metabolites in the hepatotoxic group were equal to the control, and in choline deficiency the quantity of excreted metabolites was only slightly reduced. In the hepatotoxic group, a qualitative difference was found with a lower proportion of methyl metabolites (MTHFSO, MTHFS02). This suggests, even in with pre-existing or induced hepatotoxicity, TTFD can be excreted albeit slightly differently.

A peer-reviewed study published in 2018 entitled “The Effects of Thiamine Tetrahydrofurfuryl Disulfide on Physiological Adaption and Exercise Performance Improvement” studied the effects of different doses of TTFD in 30 animals for a period of 6 weeks. The highest oral dose used was 500mg/kg in 10 test subjects, which is the human equivalent to 40mg/kg which, in a 70KG human, is 2.8 GRAMS per day for 6 weeks. Remarkably, they showed that this highest dose produced significant improvement in endurance capacity and lactate homeostasis.

More importantly, this study also performed comprehensive measures of sub-acute toxicity with the aim of evaluating the safety of high doses in humans. Even at the highest dose taken for 6 whole weeks, no changes in behavior, diet, growth curve, or organ weight (liver, kidney, muscle, heart, lung etc.) was observed. Furthermore, to assess liver function, they performed comprehensive metabolic analysis including liver enzymes (ALT, AST), creatine, uric acid, total cholesterol, triglycerides, albumin, total protein, ammonia, creatine kinase, and total protein. The only significant changes were a slight reduction in total cholesterol and significant reduction in lactate, creatine kinase and blood urea nitrogen (all of which are considered positive changes). Every other liver marker was perfectly in range. To gain further insight into the liver function and the health of other tissues, they performed histopathological analysis of the tissue under microscope and showed that massive doses caused no pathological changes in any tissue whatsoever. The authors conclude:

In the current study, we proposed that the higher thiamine derivative, TTFD, could significantly improve physical activities and physiological adaption with evidence-based safety validation. For practical application, we recommend that athletes should consume a daily intake of 40 mg/kg TTFD (equivalently converted from mouse 500 mg/kg dose based on body surface area between mice and humans by formula from the US Food and Drug Administration [36]) to improve energy regulation for higher performance in a combined nutritional strategy, including carbohydrate loading for efficient energy demand during extended exercise.

They were so convinced of the supplement’s safety that they recommended athletes take the equivalent of 2.8 GRAMS per day LONG-TERM to improve athletic performance.

What About Research in Humans?

To those who complain that these are “animal studies”, the comparative metabolic studies have found that the metabolism of TTFD is essentially the same in animals and humans. This means that humans are likely to respond similarly. As one of the first medical doctors to use TTFD as a clinical intervention in the Western world, Dr. Derrick Lonsdale obtained a special license from the FDA to import this molecule and studied its effects in his pediatric patients. In his own words:

I was able to study the value of this incredible substance in literally hundreds, if not thousands of patients. Far from being toxic, as this person claims, I never saw a single item that suggested toxicity.

Some reports published by Lonsdale and other authors include:

22 children with Down’s Syndrome, 12 of which were administered TTFD for 12 months and 12 of which were administered TTFD for 6 months. No serious adverse events noted.
Brainstem dysfunction – three infants saw symptomatic improvement with thiamine disulfide treatment.
Abnormal brainstem auditory evoked potentials, one infant was administered intravenous TTFD and displayed normalization of brainstem function
21 patients subacute necrotizing encephalomyelopathy treated with thiamine derivatives TPD/TTFD 10 Children – no serious adverse events – 1 experienced worsening of behavior/symptoms, 2 with rash
44 polyneuropathy patients treated with 50mg TTFD injection, no adverse effects reported.
Prosultiamine (TPD) at 300mg per day for 12 weeks (TPD, a very similar molecule to TTFD) used to treat spinal cord injury in human T lymphotropic virus type I-associated myelopathy/tropical spastic paraparesis (2013). Significant improvement in motor functions and bladder control, as well as reducing viral numbers in blood. Only adverse symptom was mild epigastric discomfort. No safety concerns.

For a comprehensive look at thiamine research, refer to Drs. Lonsdale and Marrs’ book: Thiamine Deficiency Disease, Dysautonomia and High Calorie Malnutrition

TTFD Used in Other Countries

It is worth noting that TTFD is not well known in Western medicine. The regions of the world in which it is used extensively include Japan, China, and other countries in the Far East.

Japanese Cases

Unfortunately, much of the Japanese literature is not published in English, so it can be difficult to find. I use a translator application called DeepL to read these articles. Furthermore, TTFD is so regularly prescribed for treating thiamine deficiency that much of the literature refers to TTFD simply as “thiamine” or “vitamin B1”, using the terms interchangeably. This means that finding research papers without TTFD in the actual title is very difficult. Below are 33 case reports from the Japanese literature, including some in children, which document the benefits of TTFD clinically. In all of the papers I have read, I have not once seen mention of safety concerns using this. In several reports, hundreds of milligrams are maintained indefinitely with no apparent issues.

267 cases of sudden-onset deafness was treated with 150mg TTFD orally, with most therapeutic effect seen after 2-3 months of treatment
20 cases of perceptive deafness, 20 cases of laryngeal disease, 7 cases of facial nerve palsy and 3 cases of anosmia injected with TTFD 50mg once per day for 5-20 days. 60% effective and no side effects.
24 subjects without nutritional deficiency, 20 cases of alcoholism, and 48 cases of alcoholism with signs of deficiency and/or liver disease were given either TTFD, Thiamine propyldisulfide (a similar disulfide derivative), or thiamine HCL. They showed no toxic effects at 3-6 months in any group, and demonstrated that oral TTFD/TPD increased whole blood, erythrocyte, and cerebrospinal fluid thiamine levels at an equivalent level to intravenous thiamine HCL.
Beriberi treated with 150mg IV one week, followed by 100mg oral long-term (2014)
Cardiac failure 100mg IV (1987)
Heart and circulatory failure (2008)
TTFD administered to 15 year old boy to treat beriberi, remained on the therapy long-term
18 patients with non-diabetic peripheral neuropathy 1-3 months, no serious side effects
Wernicke encephalopathy in hemodialysis – 100mg/iv, later oral continued for 2 months until improvement (2009)
Diabetic lactic acidosis – 100mg/day IV for 7 days resolution in symptoms, followed by 75mg indefinitely (2008)
Beriberi w/ pulmonary hypotension – 50mg long-term (2019)
E/beriberi after intestinal resection – 150mg IV three days, 75mg long-term (2018):
E/Shoshin beriberi – 150mg/IV, 75mg oral long-term (2013)
A case of Wernicke’s encephalopathy with severe cardiac sympathetic dysfunction – 100mg (2012)
Marked anasarca with impaired consciousness, which was thought to be caused by shoshin beriberi due to impaired vitamin B1 utilization. – TTFD 40mg +400mg HCL, followed by 2 months+ TTFD 100mg (2015)
Beriberi neuropathy and shoshin beriberi that developed 6 years after gastrectomy on the cardia side – 100mg TTFD long term (2013)
Chemotherapy induced W.E – IV thiamine HCL followed by TTFD 75mg long-term (2008)
Postoperative W.E treated with 100mg IV TTFD (1998)
Cardiomyopathy associated with mitochondrial disease that developed heart failure, treated with 100mg long-term (2017)
Mitochondria rescue formula recommended for acute encephalopathy: including TTFD 100mg (2019)
Pediatric acute encephalopathy neuroprotection protocol – cocktail including 200mg TTFD in 15 children (2013)
200mg TTFD x 31 children childhood acute encephalopathy (part of protocol) (2014)
Lactic acidosis caused by low-dose metformin: Thiamine HCL 100mg followed by 75mg TTFD long-term, normalization of all liver values (2014)
Beriberi mimicking Guillain-Barré syndrome – IV TTFD 100mg resolved this
Shoshin beriberi – IV TTFD 150mg for 11 days, indefinite oral dose 150mg TTFD long-term
6 infants (0-1 yrs old) treated with TTFD for childhood congenital lactic acidosis. Doses included 35mg/KG – 50mg/KG. Some cases were unresponsive to thiamine HCL, where TTFD ONLY could reduce lactate significantly “Fursulthiamine hydrochloride was significantly superior to thiamine hydrochloride in reducing lactate.” Only the cases which used TTFD survived. Children were kept on high doses permanently with no adverse effects.
75mg TTFD improved cerebral blood flow in deficiency
75mg TTFD used in mitochondrial myopathy long-term
50mg TTFD used to treat edema and weight gain and marginal thiamine deficiency – authors recommend TTFD instead of thiamine HCL (2021)
Biguanide-induced lactic acidosis treated with 100mg, then 300mg TTFD (2017)
100mg used to treat encephalopathy w/ hyperammonemia (2003)
Subacute spinal degeneration caused by B12 deficiency treated with B12 and 75mg TTFD long-term (2020)
Statement by a Japanese physician: recommendation to use TTFD instead of thiamine HCL due to superior qualities.

Chinese Cases

Like the Japanese research, most (if not all) of the Chinese studies using TTFD are not published in English. However, it is clear that the Chinese medical system uses TTFD frequently and has done so for several decades. Most of the studies below were reported within the last 20-30 years. Once again, I could not find any concern regarding the safety of this molecule and it was demonstrated as remarkably effective for a variety of conditions. Interestingly, the Chinese not only use it for deficiency, but also for non-deficient conditions where it is often injected directly into acupoints (acupuncture meridians) either alone, or in combination with other nutrients/medications. They still use these methods to this day. Here are 32 more articles regarding the safety and efficacy of TTFD from the Chinese literature.

194 cases of infantile beriberi cured with IM/IV thiamine and TTFD (1987)
50 infants treated with TTFD for cardiac beriberi (1997)
70 children with infantile beriberi cured with intravenous TTFD (1990)
48 cases of infantile cerebral beriberi (0-3 years old) treated with TTFD (1997)
35 cases of infantile beriberi cured TTFD (2010)
10 cases of infantile cerebral beriberi cured with B1 HCL and TTFD
10 cases of cerebral beriberi and basal ganglia damage treated with TTFD injections (2003)
125 children with pneumonia treated using TTFD as primary treatment (10mg IM <3 months old, 20mg IM <6 months, 20mg twice per day >6 months old)
283 out of 285 children with rectal prolapse cured by TTFD injection into “changqiang” acupoint (1988)
89 cases of rectal prolapse also treated with TTFD acupoint injection (1998)
50 cases of cerebral hypoplasia improved with acupoint injection of acetyl glutamine and TTFD (1983)
35 patients treated for hyperthyroidism with TTFD as adjunctive treatment (1999)
50 cases of costochondritis cured with Analgin + TTFD injection (1993)
13 children with ocular nerve palsy cured with TTFD (2010)
50 cases of urinary incontinence treated with acupoint injection of combination of acetyl glutamine, TTFD and/or r-aminobutyric acid (1990)
26 cases of delayed peripheral neuropathy due to organophosphate poisoning treated with acupuncture and TTFD injection (2001)
47 cases of lumbar disc protrusion treated with acupoint injection, B12 and TTFD (1994)
38 cases of facial neuritis treated with acupuncture and vitamins including TTFD injection (1999)
60 cases of migraine treated with Chinese medicine, flunarizine, and TTFD (2004)
24 cases of migraine treated with TTFD acupoint injection (1990)
40 patients with cerebrovascular disease addressed using acetyl glutamine and TTFD scalp acupoint injections (2001)
30 cases diabetic neuropathy, 75mg TTFD used as a control in– 60% effective (2002)
69 cases of Bell’s Palsy, TTFD used with acyclovir (1999)
120 cases of Bell’s Palsy treated with oral TTFD, methylb12, and/or electroacupuncture and facial muscle exercise (2019)
65 cases of Meniere’s Diseases treated with TCM, vitamins including TTFD injections
118 cases of herpes zoster treated with TTFD in conjunction with acyclovir and traditional Chinese medicine (2013).
100 cases of senile deafness treated with cocktail including TTFD (2000)
36 cases of cervical spondylotic radiculopathy treated with control of TTFD and naproxen – 75% effective (2009)
60 cases of postherpetic neuralgia treated with cocktail including TTFD
1 case of polerarteritis nodosa w/peripheral neuritis treated with cocktail including TTFD
1 case of central paralytic dysphagia (tuberculosis meningitis) unresponsive to conventional treatment cured by injection of TTFD at meridian acupoint (1974)
1 case of drug-induced diplopia treated with methyl B12 and TTFD

TTFD Is Not Toxic

At this point, it should be clear that TTFD is not toxic at either therapeutic or even supraphyisiological doses. This is supported by in vitro, animal, and human studies. One would have to use ~12,000 times the therapeutic dose to approximate toxicity and even then it is not clear that there would be the problems that Cutler suggested. That is not to say that everyone who takes this supplement responds favorably. Clinically, there are individuals for whom other formulations of thiamine work better. This is generally related to a lack of the necessary nutrient cofactors involved with the detox enzyme glutathione. I have written about that previously here. That perceived intolerance, however, is not the same as toxicity. The toxicity data are clear. TTFD is safe. The clinical data are also clear. TTFD is effective. The molecule has been in use for over half a century and is used extensively in medical practice in Eastern countries. No safety concerns or claims of toxicity have been raised, apart from those made by Cutler.

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This articles was published originally in February 2022.

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