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Thiamine Deficiency Causes Intracellular Potassium Wasting

Published on August 6, 2025

67.5K views

The role of thiamine in potassium deficiency

Whilst I always suspected a direct link between potassium and thiamine deficiency (outside of the context of refeeding syndrome), I had not come across any direct research elucidating the mechanisms – until NOW. In short, thiamine deficiency causes intracellular potassium wasting.

Animal research in rats showed that chronic thiamine deficiency increases sodium tissue content in heart, liver and skeletal muscle by 18-35%, while also decreasing potassium content by 18-25%. Interestingly, although tissue levels were altered, plasma levels of these electrolytes remained unaffected and stayed within the normal-high range (sodium at 141.6 and potassium at 4.8). This means that blood measurements did not reflect tissue content.

The thiamine deficient group also displayed remarkably lower levels of stored liver glycogen (0.3gm/100 vs 2.7gm/100 in controls). This inability to store glycogen is one factor which helps to explain the strong tendency towards hypoglycemia seen in many people with a thiamine deficiency.

Interestingly, the researchers showed a shift towards an increased level of extracellular water and reduced intracellular water. This finding, along with the shift in intracellular electrolyte concentrations, is 100% consistent with Ling’s Association-Induction hypothesis.

In short, the bioenergetic state of the cell governs its ability to retain potassium ions and structure water into a gel-like phase. A cell with plentiful ATP can maintain this ability, independent of the “sodium potassium pump”. On the other hand, cells lacking energy lose their capacity to retain potassium, intracellular water becomes “unstructured” and intracellular concentration of sodium ions increases and the electronic state of the cell is changed. This causes water to “leak” out of the cells into the extracellular space to produce a localised edema of sorts. Thiamine, playing a central role in energy metabolism, is partially responsible for maintaining healthy redox balance and a continuous supply of ATP. Hence, it is no wonder why a deficiency of this essential nutrient produces such drastic changes in the cellular electrolyte balance.

Thiamine, TTFD, Potassium, and Heart Function

The cells of the heart are particularly susceptible to a disturbance in electrolytes. One Japanese study on coronary insufficiency in dogs showed elevated sodium and reduced potassium content in the insufficient left ventricle. Intravenous administration 50mg thiamine, in the form of thiamine tetrahydrofurfuryl disulfide (TTFD), a derivative of thiamine with higher bioavailability and solubility than other formulations, restored electrolyte balance, likely through improving tissue energy metabolism.

Likewise, the same effect was also demonstrated in isolated Guinea pig atria kept in potassium-free medium. TTFD added to cells or administered as a pre-treatment prevented the loss of potassium and increase in sodium, which was shown to occur in controls. Importantly, this effect was not achieved by thiamine HCL or another derivative studied. TTFD also entered the atrial cells much more readily than other forms, demonstrating its superior absorbability and perhaps suggesting that this form would be useful for addressing cardiac thiamine insufficiency.

Low potassium is a known driver of cardiac arrhythmias, and TTFD possesses anti-arrhythmic properties and has historically been used to treat various types of arrhythmia in Japan.

Furthermore, thiamine TTFD was also been shown to be protective against the cardiac toxin Strophanthin-G, preventing the loss of potassium once again to preserve cardiac function. Likewise, atrial cell damage through exposure to the mitochondrial toxin N-ethylmaleimide was also prevented by high concentrations of TTFD in-vitro. This protective action was attributed to the prosthetic group specific to TTFD, and NOT the thiamine molecule itself.

So it would seem that thiamine, probably through its effects on energy metabolism inside cells, and perhaps due to an unknown “kosmotropic” property of TTFD, is extremely important for regulating cell ion concentrations. In thiamine deficiency, an underlying intracellular potassium deficiency may be going unnoticed due to unremarkable blood levels. In cases where potassium deficiency is suggested, thiamine deficiency may be indicated, and TTFD might used to more safely correct the electrolyte balance.

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This article was published originally on May 13, 2020.

Energy Medicine

by Derrick Lonsdale MD, FACN, CNS

Published on July 30, 2025

15.4K views

I have written many posts on Hormones Matter and have tried to answer the questions arising from each post. These questions and my answers have been so repetitive that I decided to try to make it clear what “energy medicine” is all about and why it differs from conventional medicine. It is only natural that the posted questions are all built on our present ideas about health and disease. What I am about to say is that the present medical model has outgrown its use. Therefore it is obvious that I must discuss what this means. First of all, why do we need a “medical model”? In fact, what is the difference between complete health and its lack? The Oxford English dictionary gives the definition of disease as “a serious derangement of health, disordered state of an organism or organ”

The American Model of Medicine

As I have said before, the present American medical model was aimed at making a diagnosis of one of many thousand described diseases. It was devised from the Flexner report of 1910 that was initiated by Rockefeller. Rockefeller wanted to make medical education adhere to a common standard, thus creating the present “medical model”. The Flexner report used the methodology of diagnosis that was current in Germany. This stated that the patient’s report to a physician is called “history”, involving the patient’s description of symptoms and their onset. From this, the physician may or may not have an idea what is wrong. The next part is the physical exam where a hands-on search of the patient’s body is made for evidence of disease. This is extremely complex when put fully into clinical operation and also may or may not provide clues to a diagnosis. The third operation is laboratory testing and it is this constellation of abnormal tests that provide scientific evidence for the nature of the disease. Each test has been researched and aside from one that is either positive or negative, others have a normal range reported in numerical terms. Perhaps, as an example, the test for cholesterol level is the best known. Each test has to be interpreted as to how it contributes to arriving at a diagnosis. Finally, the physician has to try to decide whether medical or surgical treatment must be offered. Please note that the surgical removal of a sick organ may be the signature of medical failure, for example, removing part of the intestine in Crohn’s disease, for it represents a missed opportunity to treat earlier in the disease process.

Laboratory Tests and A Drug For Every Disease

It is the constellation of symptoms described by the patient and the abnormalities found by the physical examination that constitute a potential diagnosis to formulate what laboratory tests should be initiated. It is the constellation of laboratory tests that may or may not provide the proof. There are problems with this. For instance, there may be test items in the constellation that create confusion, such as “it might be disease A or disease B. We are not sure”. Tests that are “borderline” positive are particularly confusing. The diagnosis finally depends often on who was the first observer of these constellations. For example a person by the name of Parkinson and another person by the name of Alzheimer, each described clinically observed constellations that gave rise to Parkinson’s disease and Alzheimer’s disease. Since they were first described, the pathological effects of each disease have been researched in painstaking detail, without coming to the conclusion of the ultimate cause. Finally, the pharmaceutical industry has indulged in complex research to find the drug that will reverse the pathological findings and produce a cure. Because this concept rides right through the objective, each disease is thought to have a separate underlying cause and a separate underlying cure in the shape of a new “miracle drug”. Witness the recent revival of a drug that was initially found to be useless in the treatment of Alzheimer’s disease. This revival depends on the finding of other pathological effects discovered in the disease, suggesting new clinical trials. When you take all these facts into consideration, it is a surprisingly hit and miss structure. For example, we now have good reason to state that a low cholesterol in the blood is more dangerous than a high one. Why? Because cholesterol is made in the body and is the foundation material for building the vitally important stress hormones. Cholesterol synthesis requires energy and is a reflection on energy metabolism when it is in short supply.

The Physicians Desk Reference, available in many public libraries, contains details concerning available drugs. Each drug is named and what it is used for, but often there is a note saying that its action is poorly understood. Just as often, there may be one or two pages describing side effects. In fact, the only drugs whose action is identified with cause are the antibiotics. The rest of them treat symptoms but do not address cause. Antibiotics affect pathogenic bacteria but we all know that the bacteria are able to become resistant and this is creating a problem for the near future. It is interesting that Louis Pasteur spent his career researching pathogenic microorganisms. However, on his deathbed it is purported that he stated “I was wrong, it is the defenses of the body that count”.

It must be stated that the first paradigm in medicine was the discovery of pathogenic microorganisms and their ability to cause infections. Many years were spent in trying to find ways and means of killing these organisms without killing the patient. It was the dramatic discovery of penicillin that led to the antibiotic era. I like to think that Louis Pasteur may have suggested the next paradigm, “assist the body defenses”.

Energy Medicine: A New Paradigm for Understanding Health and Disease

When a person is seen performing on a trampoline, an observer might say “hasn’t he got a lot of energy!” without thinking that this represents energy consumption. Energy has to be captured in the body and is consumed in the physical action on the trampoline. Many people will drink a cup of coffee on the way to work believing that it “creates” energy. The chemical function of caffeine stimulates action that consumes energy, giving rise to a false impression. Every physical movement, every passing thought, however fleeting in time, requires energy consumption. The person who has to drink coffee to “get to work”, is already energy insufficient. He/she can ill afford this artificial consumption of the available energy.

I am going to suggest that the evidence shows “energy medicine” may indeed be the new paradigm, so we have to make sure that anyone reading this is conversant with the concept of energy. In physics, “energy is the quantitative property that must be transferred to an object in order to perform work on, or heat, the object. Energy is a conserved quantity, meaning that the available energy at the beginning of time is the same quantity today. The law of conservation of energy states that “energy can be converted in form but not created or destroyed”. Furthermore, Einstein showed us that matter and energy are interconvertible. That is why the word “energy” is such a mystery to many people. What kind of energy does the human body require?

We are all aware that the electroencephalogram and the electrocardiogram are tools used by physicians to detect disease in the brain and the heart. If that means that our organs function electrically, then where does that energy come from? We do not carry a battery. We are not plugged into a wall socket and the functional capacity of the human body is endlessly available throughout life. The only components that keep us alive are food and water. Everyone knows that foods need to contain a calorie-delivering and a non-caloric mixture of vitamins and essential minerals. The life sustaining actions of these non-caloric nutrients is because they govern the process of energy capture by enabling oxygen consumption (oxidation). They also govern the use of the energy to provide physical and mental function.

The calorie bearing food, consisting of protein, fat and carbohydrate is used to build body cell structure. This is called anabolic metabolism. If body structure is broken down and destroyed, weight is lost and the patient is sick. This is called catabolic metabolism. In healthy conditions, food is metabolized to form glucose, the primary fuel.

Thiamine (vitamin B1), together with the rest of the B complex, governs oxidation, the products of which go into a cellular “engine” called the citric acid cycle. This energy is used to form adenosine triphosphate (ATP) that might be referred to as a form of “energy currency”. Without thiamine and its vitamin colleagues in the diet, ATP cannot be formed. Research for the next stage of energy production has yielded insufficient information as yet concerning production of electrical energy as the final step. The evidence shows that thiamine may have an integral part in this electrification process, although much mystery remains. Suffice it to say that we are electrochemical “machines” and every physical and mental action requires energy consumption.

Maybe the Chinese Were Right

In the ancient Chinese culture, an energy form called Chi was regarded as the energy of life itself. Whether this really exists or not and whether it is in some way connected to the auras purported to surround each person’s body is still conjectural. It would not be too absurd to suggest that it might be as yet an undiscovered form of energy and that it is truly a reflection of good health. My personal conclusion is that some form of electromagnetic energy is the energy that drives our physical and mental functions and that it is transduced in the body from ATP, the storage form of chemical energy. There is no doubt that acupuncture does work and certainly encourages the conclusion that the meridians described by the ancient Chinese thinkers are an important evidence of electrical circulation. There is burgeoning evidence that energy is the core issue in driving the complex process of the body’s ability to heal itself. The idea that the physician or anyone else that purports to be a “healer” is a myth, because we have the magic of nutrients that are capable of stimulating energy production as already described. The “bedside manner” is valuable because a sense of confidence and trust results in energy conservation. Remember the proverb “worry killed the cat”.

Illness and the Lack of Energy

As essentially fragile organisms, we live in a situation of personal stress. We are surrounded by micro-organisms ready to attack us. We have built a culture that is enormously stressful in many different ways, I turn once again to the writings of Hans Selye, who advanced the idea that we are suffering from “the diseases of adaptation”. He recognized that some form of energy was absolutely essential to meet any form of physical or mental stress. One of his students was able to produce the general adaptation syndrome in an animal by making the animal thiamine deficient. Energy metabolism in Selye’s time was poorly understood. Today the role of thiamine is well known. As I have described in other posts and in our book, the lower part of the brain that controls adaptive mechanisms throughout the body is highly sensitive to thiamine deficiency. Alcohol, and sugar in all its forms, both overload the process of oxidation. Although energy metabolism depends on many nutrients, thiamine is vital to the function of mitochondria and its deficiency appears to be critical. Because the brain and heart are the dominant energy consumers it is no surprise to find that beriberi has its major effects in those two organs. Symptoms are just expressions of oxidative inefficiency of varying severity. This is the reason why 696 medical publications have reported varying degrees of success in the treatment of 240 diseases with thiamine. Its ubiquitous use as a drug depends on its overall ability to restore an adequate energy supply by stimulating mitochondrial function. It is also why I propose that energy deficiency is the true root of modern disease.

We Need Your Help

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

Yes, I would like to support Hormones Matter.

Image by Gerd Altmann from Pixabay.

This article was published originally on November 19, 2019.

Rest in peace Derrick Lonsdale, May 2024.

Threats to Thiamine Sufficiency in the 21st Century

by Chandler Marrs, PhD

Published on July 23, 2025

11.9K views

In the first paper, Thiamine Deficiency in Modern Medical Practice , I provided an overview of why health practitioners should consider thiamine in general practice. In this paper, I would like to delve more deeply into how one becomes deficient in the 21^st century.

Thiamine and Its RDA

Thiamine, or vitamin B1, is an essential and rate limiting nutrient required for metabolic health. Like the other B vitamins, it is water-soluble. Unlike some other B vitamins, it has a very short half-life (1-12 hours), and a limited reserve of about 30 milligrams. Absent regular consumption, deficiency arises quickly, manifesting symptoms that range from general fatigue, mood lability, anorexia, and nausea to cardiac irregularities, neuromuscular and neurocognitive deficits. In developed countries, where food enrichment and fortification programs have added thiamine to grain and other products, thiamine deficiency syndromes are considered to be rare and largely confined to specific populations and circumstances where thiamine ingestion, absorption, metabolism, or excretion are impaired such as poverty-based malnutrition, alcoholism, severe gut dysbiosis and/or hyperemesis.

The recommended daily allowance (RDA) put forth by health institutions considers 1.1-1.2mg of thiamine sufficient for most adults to stave off deficiency. This requirement is met easily with any modern diet, even a poor one, suggesting that the suspected low incidence of deficiency is accurate. And yet, across multiple studies that have measured thiamine status in different patient populations, none of whom can be considered malnourished by RDA standards, or alcoholic, the rate of deficiency is found to be between 20-98%; a discordance that suggests both institutional designations of thiamine sufficiency and deficiency are underestimated.

Insofar as thiamine is absolutely requisite for the conversion of food into cellular energy, e.g. ATP, and sufficient ATP is fundamental to metabolic health, something that has become an increasingly rare phenomenon in the Western world, it is possible that our understanding of thiamine sufficiency and deficiency is mismatched to the demands of modern living. If this is the case, then insufficient thiamine may be a key factor in many of the disease processes that plague modern medicine. Indeed, thiamine insufficiency and frank deficiency has been observed with obesity, diabetes, heart disease, gastrointestinal dysbiosis and dysmotility syndromes, post gastric bypass surgery, in cancer, Alzheimer’s, Parkinson’s, and psychiatric patients. Combined, these patient populations represent a far larger percentage of the population than recognized within the current paradigm. From this perspective, it is conceivable that the older designations of sufficiency and deficiency no longer apply and that for the 21^st century patient, thiamine stability is a much more fragile endeavor than recognized.

Micronutrients and Cellular Energy

The most fundamental process to health and survival involves the conversion of consumed nutrients into ATP. Absent adequate ATP, health is impossible. Energy metabolism requires a ready supply of macronutrients (carbohydrate, protein, and fats) and at least 22 micronutrients or vitamins and minerals (see Figure 1.).

In developed countries, macronutrients are readily available, often in excess. Micronutrient intake, however, is inconsistent. A review article from the University of Oregon report found that a large percentage of the population had inadequate micronutrient status (4-65% depending upon the nutrient) despite excessive caloric intake. Moreover, much of the supposed nutrient sufficiency came from enriched or fortified foods. In other words, absent food enrichment or fortification, most children, adolescents, and adults had insufficient micronutrient intake. Inasmuch as most fortified foods come with a high caloric content, which effectively demands a higher micronutrient content to metabolize it; this presents a problem.

mitochondrial nutrients — Figure 1. Mitochondrial Nutrients, from: Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition

Thiamine Dependent Enzymes

From the graphic above, note how many times thiamine (vitamin B1 or TPP) appears. Thiamine is required for the transketolase (TKT), pyruvate dehydrogenase complex of enzymes (PDC), branched chain keto acid dehydrogenase (BCKAD), 2-Hydroxyacyl-CoA lyase (HACL), alpha-ketoglutarate dehydrogenase ([a-KDGH] – also called 2-oxoglutarate dehydrogenase complex [OGDC]) and for lactate recycling as a cofactor for the lactate dehydrogenase complex (LDH). Beyond its coenzyme role, thiamine allosterically regulates the expression and activity other mitochondrial proteins including:

Succinate thiokinase/succinyl-CoA synthetase: together with a-KDGH catalyzes succinyl-CoA to succinate.
Succinate dehydrogenase: oxidizes succinate to fumarate, uses the electrons generated to catalyze reduction of ubiquinone to ubiquinol for complex II (TCA>ETC linkage)
Malate dehydrogenase (MDH): interconversion of malate and oxaloacetate with cofactor NAD+ or NADP+.
Pyridoxal kinase: converts dietary vitamin B6 into the active cofactor form pyridoxal 5′-phosphate (PLP) creating a functional deficiency.

With low or absent thiamine, each of these enzymes downregulates from 10% to almost 30% resulting in a reduction of ATP from 38 to ~13 units (in culture).

Thiamine Is Fundamental

Among the 22 micronutrients needed to convert macronutrient ATP, thiamine, along with its cofactor, magnesium, sit at the entry points to this process. That means that thiamine availability controls the rates of carbohydrate, protein, and fat metabolism and their subsequent conversion into ATP. Insufficient thiamine, even marginally so, impedes this process resulting in not only reduced ATP, but also, impaired cellular respiration, and increased oxidative stress and advanced glycation end products (AGEs); the very cascades linked to the preponderance of modern diseases dominating the healthcare landscape.

Cellular respiration, the ability to use molecular oxygen, requires ATP, which requires thiamine. Insufficient thiamine causes cell level hypoxia and upregulates the expression of hypoxia inducible factors (HIFs). HIFs are responsible for oxygen homeostasis, regulating at least 100 other proteins including those involved in angiogenesis, erythropoiesis and iron metabolism, glucose metabolism, growth factors, and apoptosis. HIF stabilization is implicated in a range of illnesses from autoimmune disease, to heart disease and cancer.
Reactive oxygen species (ROS) are a natural byproduct of ATP production and serve as useful mitochondrial signaling agents. Elevated ROS, relative to antioxidant capacity, however, creates oxidative stress, damaging cellular lipids, proteins and DNA. Antioxidant capacity is reduced with thiamine deficiency while ROS are increased.
AGEs, the toxic byproducts of hyperglycemia and oxidative stress, are modulated by thiamine. With sufficient thiamine, AGE precursors are shunted towards energy metabolism via the transketolase and the pentose phosphate pathway rather than accumulating in tissue as reactive carbonyl intermediates common with metabolic disease.

Each of these play a role in the pathophysiology of diabetes, cardiovascular and neurodegenerative diseases. This makes thiamine status, by way of its role in ATP production, cell respiration, ROS management, and AGE metabolism, a critical variable determining health or disease.

Given its position and role in these processes, it is not difficult to imagine how insufficient thiamine intake might derange and diminish energy metabolism and how that, in turn, might impact metabolic health both locally at the cell, tissue and organ level, and systemically. What is difficult to imagine, however, given the miniscule RDA requirement for a little over a single milligram of thiamine, is how anyone in the developed world where food scarcity is rare, where thiamine is readily available in both whole foods and in fortified foods, becomes thiamine deficient. And yet, a growing body of research suggests that is exactly what is happening. Recall from above, that depending upon the population studied, insufficient thiamine to frank deficiency has been found in 20-98% of the patients tested.

Modern Challenges to Thiamine Sufficiency From Consumption to Utilization

As an essential nutrient, thiamine must be consumed from foods, absorbed, activated and transported to where it is needed, and then utilized by its cognate enzymes. At each of these steps there are challenges that diminish thiamine availability, effectively increasing thiamine need well beyond the current RDA values. In fact, many of the products and amenities that make modern living what it is, imperil thiamine status and do so at multiple junctions. The additive effects of these challenges leaves many vulnerable to deficiency.

Dietary Sources of Thiamine

The highest concentrations of thiamine in natural and non-manufactured foods come from pork, fish (salmon, trout, tuna, catfish), many nuts and seeds (macadamia, pistachios, sunflower seeds, flax seed), beans (navy, black, black-eyed peas, lentils), peas, tofu, brown rice, whole wheat, acorn squash, asparagus, and many other foods. A diet rich in organic, whole foods is generally sufficient to meet the daily requirements for the thiamine and other vitamins and minerals. Likewise, though less ideal, a diet of processed foods that has been enriched or fortified with thiamine, will meet the RDA for thiamine quite easily, perhaps even exceed it. Indeed, one serving of breakfast cereal is sufficient to reach the RDA for thiamine.

Despite the ready availability of thiamine in both whole and processed foods, the data suggest that many people find it difficult to maintain thiamine status. This is due to the interactions between the endogenous chemistry of thiamine metabolism and the chemistry of exogenous variables affecting thiamine stability. The most common factors affecting thiamine status, include high calorie, high toxicant load diets, alcohol and/or tobacco use, caffeine products, and pharmaceutical and chemical exposures.

Dietary Impediments to Thiamine Sufficiency

While fortification provides access to thiamine, highly processed foods carry a high calorie and toxicant count making them metabolically deleterious despite any potential gains from vitamin enrichment or fortification. High carbohydrate, highly processed foods diminish thiamine status by multiple mechanisms.

Carbohydrate ingestion requires thiamine for oxidation. When more than 55% of total caloric intake comes from carbohydrates, no matter their source, thiamine status in otherwise healthy and thiamine sufficient individuals declines. In contrast, a lower carbohydrate higher fat diet slows thiamine loss in thiamine-restricted experimental conditions, while protein seems to preserve thiamine degradation in foods.
Diets high in fructose are linked to the endogenous production of oxythiamine, an anti-thiamine molecule.
From farm to plate, every aspect of commercial food production involves the usage of chemical products that are toxic to the mitochondria and to thiamine status, making consumption of these types of foods a net loss metabolically.

Other common dietary contributors to insufficient thiamine.

Alcohol, when ingested with thiamine rich foods, blocks conversion of dietary thiamine into active thiamine, reducing thiamine availability by as much as 54%. If consumed in sufficient quantities with regularity, it damages the intestinal mucosa leading to impaired absorption and dysbiosis.
The nicotine in tobacco products inhibits thiamine transporter mediated uptake in the pancreatic acinar cells by >40%. Deficiency reduces insulin secretion. In combination with alcohol ingestion, smoking is implicated in the development of pancreatitis.
The caffeic acid, chlorogenic acid, and tannic acid in coffee, tea, and energy drinks, oxidize the thiazole ring of the thiamine molecule, impairing its absorption, while the added sugars, flavors and other substances to enhance taste, increase thiamine demand.

Although food scarcity is not as prevalent in developed countries compared to undeveloped regions, poverty still impacts nutrient status. This owes largely to the fact that highly processed foods, high calorie foods are less expensive than whole foods and thus, there is an over-reliance on carbohydrate consumption to meet caloric requirements. Here, obesity and metabolic dysfunction co-occur with micro-nutrient and sometimes macronutrient, e.g. protein, deficiency.

Pharmaceutical and Environmental Threats to Thiamine Status

After high calorie malnutrition and other dietary habits that limit thiamine availability, the next most common threat to thiamine sufficiency is the use of pharmaceuticals. This variable cannot be stressed enough. Pharmaceutical chemicals deplete thiamine and other nutrients, directly or indirectly by a number of mechanisms. Some of this is by design, such as with antibiotics that target folate and thiamine, some of it represents off-target effects, such as the blockade of thiamine transporters by metformin and the other 146 drugs tested for this action, an increase in demand in order to withstand other mitochondrial damage. Regardless of the intended purpose, however, pharmaceuticals represent chemical stressors to thiamine and nutrient stability. As such, their regular use necessitates a concerted approach to maintain nutrient status. Some of the most commonly used medications are the biggest offenders:

In addition to the ingestion of pharmaceutical chemicals, environmental chemical exposures damage mitochondrial functioning, even at low, and what are considered, non-toxic exposures. These exposures are pervasive, often unavoidable, and tend to accrue over time, with additive and synergistic effects to other stressors. Consider the totality of a patient’s toxic load when addressing the risk of nutrient insufficiency.

Absorption and Metabolism

Assuming sufficient thiamine is ingested from diet and is not blocked or otherwise degraded by food, pharmaceutical or environmental chemicals, it then has to be absorbed in the intestines before it can be activated and transported to organs and tissues for use. Epithelial injury, microbial dysbiosis, and genetic variation, all of which are common, limit the effectiveness of this phase. Epithelial injury and microbial dysbiosis slow passive absorption, while genetic, epigenetic, and environmental variables, slow or block active transport.

At low concentrations, thiamine is absorbed in the small intestine by active transport, while higher concentrations are absorbed by passive diffusion. Active transport is mediated by two primary thiamine transporters, ThTR1 and ThTR2, and a number of additional transporters that fall under the solute carrier family of genes:

SLC19A1: folate transporter, but also, transports thiamine mono- and di- phospho derivatives.
SLC19A2 (ThTr1): systemic thiamine transport, main transporter in pancreatic islet tissue and hematopoietic cells; most abundant, from highest to lowest in the intestine, skeletal muscle, nervous system, eye, placenta, liver, and kidney.
SLC19A3 (ThTr2): primary intestinal thiamine transporter, also located in adipose tissue, breast tissue, liver, lymphocytes, spleen, gallbladder, placenta, pancreas, and brain.
SLC22A1 (OCT1): organic cation transporter 1, primary hepatic thiamine transporter; competitively inhibited with transport of metformin, xenobiotics, and other drugs.
SLC25A19 (MTPP-1): mitochondrial thiamine pyrophosphate carrier.
SLC35F3: endoplasmic reticulum and Golgi thiamine transporter, implicated in hypertension.
SLC44A4 (hTPPT/TPPT-1): absorption of microbiota-generated thiamine pyrophosphate in the large intestine.

Although conventional wisdom suggests that only homozygous mutations affect the performance of these proteins, in reality, there is a gradation of abnormalities that challenge thiamine uptake, particularly when environmental or pharmaceutical variables block or otherwise limit the functioning of the same protein. In some cases, genetic difficulties can be compensated for providing nutrient support at supraphyisiological doses, among the better known examples:

Thiamine responsive megaloblastic anemia (mutations in SLC19A2/ThTr1); megaloblastic anemia, progressive sensorineural hearing loss, and diabetes mellitus.
Biotin-thiamine responsive basal ganglia disease (mutations in SLC19A3/ThTr 2) presents in infancy or childhood with recurrent subacute encephalopathy, confusion, seizures, ataxia, dystonia, supranuclear facial palsy, external ophthalmoplegia, and/or dysphagia or Leigh-like syndrome with infantile spasms. When presenting in adulthood, acute onset seizures, ataxia, nystagmus, diplopia, and ophthalmoplegia.
Thiamine responsive Leigh Syndrome (mutations in in the SLC19A3/ThTr2).
Thiamine metabolism dysfunction syndrome-4 (mutations SLC25A19/MTPP-1); episodic encephalopathy and febrile illness, transient neurologic dysfunction, and a slowly progressive axonal polyneuropathy.
Thiamine Pyrophosphokinase 1 (TPL1) defects cause problems in the activation of free thiamine to thiamine pyrophosphate, rendering much of the thiamine consumed unusable. TPK1 defects have been identified as condition called thiamine metabolism dysfunction syndrome 5 or Leigh-like syndrome because of the similarity in symptoms. More recently, TPK1 defects have been found associated with Huntington’s disease. High dose thiamine appears to overcome the defect in some cases.

Thiamine Activation/Deactivation

Before it can be used, free thiamine has to be phosphorylated into its active form thiamine pyrophosphate (TPP), also called thiamine diphosphate (ThDP/TDP). This is done by the enzyme thiamine pyrophosphokinase (thiamine diphosphokinase), which is magnesium dependent and requires ATP. Magnesium deficiency is common in developed countries. TPP accounts for almost 90% of circulating thiamine.

Additional thiamine metabolites include thiamine monophosphate (TMP) and thiamine triphosphate (TTP) along with the recently discovered adenosine thiamine triphosphate (AThTP) and adenosine thiamine diphosphate (AThDP). AThTP and AThDP are produced by E.coli during periods of nutrient starvation and have been found in most mammalian tissue. This likely represents a salvage pathway common in many pathogenic microbes.

Microbial Thiamine Synthesis

It is important to note, that although the consumption of dietary thiamine provides the main sources of this nutrient systemically, a smaller, but notable (2.3%), percentage of thiamine and other B vitamins is produced endogenously by various commensal bacterial populations in both the small and large intestines. At least 10 species of bacteria synthesize thiamine that is absorbed and utilized by the colonocytes. Endogenous thiamine synthesis is reduced by diets high in simple carbohydrates but increased with complex carbohydrates. Antibiotics and other medications inhibit endogenous synthesis of B vitamins directly by design as in the case trimethoprim and sulfamethoxazole and indirectly via additional that disrupt thiamine availability. Additionally, a number of pathogenic microbes produce enzymes that degrade bacterially produced thiamine suggesting the balance of gut biota is influenced by and influences nutrient availability.

In the large intestine, bacterially synthesized TPP is absorbed directly into the colon via a population of TTP transporters (TPPT-1) in the apical membrane and then transported directly into the mitochondria via the MTPP-1 for ATP production. The reduction of colonocyte thiamine and thus ATP, would force a shift towards the more pathogenic microbial populations that thrive in nutrient deficient environments and dysregulate bowel motility. This local thiamine deficiency may be a contributing factor in large bowel microbial virulence and the dysmotility syndromes so common in modern medical practice.

Enzyme Activation

The final step in attaining thiamine sufficiency is utilization. Returning to Figure 1., the key enzymes involved in this process include: TKT, PDC, HACL, BCKAD, a-KGDH and LDH. This is an addition to the enzymes involved in the phosphorylation of free thiamine and the remaining enzymes in the Krebs cycle whose gene expression depends upon thiamine status. As with the variances and mutations in the transporters, supraphyisiological doses of thiamine may compensate for decrements in enzyme function. This has been observed in thiamine responsive PDC deficiency, characterized by excessive lactic acid; and in maple syrup urine disease, where mutations in the thiamine dependent BCKAD enzyme responsible for amino acid metabolism is impaired; also in Leigh-like syndrome, where mutations in TPK1 enzyme, which converts free thiamine to active TPP, is affected.

Is the Thiamine RDA Sufficient?

Both the chemistry and the data suggest that the current RDA of just a single milligram of thiamine is insufficient to meet the challenges presented by modern diets and chemical exposures. Owing to its role in energy metabolism, thiamine insufficiency may underlie many of the disease processes associated with metabolic dysfunction, where cellular hypoxia, increased ROS and AGEs are present. These disease processes develop long before, and sometimes absent, frank deficiency suggesting there may be gradations of insufficiency relative to the individual’s metabolic needs. Whether thiamine is a causative variable in these disease processes or simply a consequence of a complicated history of negative interactions between genetics, diet, and exposures is unclear. What is clear, however, is that thiamine insufficiency is likely far more prevalent than recognized and given its role in energy metabolism, ought to be addressed more consistently in clinical care.

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The Perils of Diagnostic Overshadowing

by Erica Peirson, NMD, FMAPS

Published on July 21, 2025

5.5K views

Diagnostic overshadowing is a phrase used to describe a cognitive bias employed by many practitioners. It assumes that all of a patient’s symptoms can be ascribed to a particular pre-existing or chronic condition. This is common in pediatrics, where health issues in children with complex needs, such as Down syndrome, are misattributed to the Down syndrome and not investigated or addressed independently. This leads to delayed diagnoses and treatment, and in many cases, poorer outcomes. It is also common when the root of the ill-health emerges from vitamin deficiencies. By way of example and with the parent’s permission, below is the case of a two-year old boy who developed both wet and dry beriberi due to thiamine deficiency. His condition was worsened by medical treatments and missed because of diagnostic overshadowing.

When Real Treatable Conditions Are Missed

Lev is a bright-eyed, curious two-year-old with Down syndrome. His eyes light up when he hears familiar voices, and he delights in interacting with his parents and siblings. Behind his bright smile, however, lies a complicated medical journey. Like many children with complex medical needs, his early years have been filled with specialist visits, medications, and hospitalizations. For much of his short life, he has been profoundly weak, struggling to gain weight, battling constant vomiting and diarrhea, and falling far behind in gross motor development. What Lev’s story illustrates most powerfully is the danger of diagnostic overshadowing: when real, treatable conditions are missed simply because a child has a known genetic diagnosis.

Lev’s story is complex. Born at 39 weeks with congenital heart defects (a large VSD and ASD), intrauterine growth restriction, and early respiratory distress, he spent his first 13 months in the hospital. By three months old he developed seizures, and by six months he was diagnosed with pulmonary hypertension. He required a GJ-feeding tube, a tracheostomy tube, and was given multiple cardiovascular medications, including high-dose Lasix (furosemide), a loop diuretic known to deplete thiamine (vitamin B1).^[1]^,[2],[3],[4] Despite the intensity of his medical care and frequent hospitalizations, his worsening weakness and developmental regression were never investigated beyond his genetic diagnosis. His inability to lift his head or bear weight was simply attributed to “Down syndrome,” and his declining function was accepted as inevitable. No one on his conventional medical team ever evaluated him for B1 deficiency.

At two years old, Lev has not yet undergone the life-saving surgery to repair his VSD and ASD, an intervention that many children with Down syndrome receive in infancy, because his profound weakness, frequent infections, and uncontrolled pulmonary hypertension have made him too medically fragile to tolerate the procedure.

His mother, worried about his persistent vomiting, diarrhea, poor tone, and developmental delays, began researching on her own. When she came across the symptoms of pediatric beriberi, the severe form of thiamine deficiency, she brought it to the attention of his doctors. They dismissed her concerns.

Fortunately, she persisted.

Profound Mitochondrial Dysfunction

She brought Lev to me after watching my online lecture “Thiamine Deficiency in Children with Special Needs”. At our first visit, it was clear that Lev was experiencing profound mitochondrial dysfunction. He was being fed via GJ-tube with a formula that didn’t provide adequate thiamine to meet his needs. He had been exposed to more than 10 rounds of antibiotics for pneumonia, which likely disrupted his gut flora and impaired his nutrient absorption. He was still taking Lasix, a medication known to deplete thiamine, yet no one had evaluated his thiamine status.

My initial recommendations without any testing included:

TTFD (thiamine tetrahydrofurfuryl disulfide) – 50 mg daily in the morning
Riboflavin 5-phosphate – 25 mg daily in the morning
Magnesium glycinate – 60 mg daily throughout the day
Polyenylphosphatidylcholine – 900 mg daily in the morning
Vitamin D – 800 IU daily anytime of day
Iron bisglycinate – 12 mg daily, preferably on an empty stomach

Lev’s story is not unique in my practice. I’ve identified thiamine deficiency in many children with Down syndrome, often after months or even years of unexplained symptoms that were overlooked or misattributed. Children with Down syndrome are especially vulnerable to thiamine deficiency due to slower gastrointestinal motility, which increases the risk of small intestinal bacterial overgrowth (SIBO) and subsequent nutrient malabsorption.^[5] Unfortunately, these underlying contributors are rarely acknowledged in conventional care. Nearly all of my patients have experienced some form of diagnostic overshadowing, where serious but treatable issues are dismissed as “just part of Down syndrome.” This pattern is far too common and far too harmful.

We proceeded with further testing, including an organic acid test and microbial stool analysis, to better understand the underlying contributors to his complex symptoms.

A Two Year Old With Wet and Dry Beriberi

When Lev’s lab results returned, they were staggering. His organic acid test showed:

Severely elevated pyruvic acid, lactic acid, and alpha-keto acids – textbook markers of pyruvate dehydrogenase dysfunction, a hallmark of B1 deficiency
Broad mitochondrial failure, with elevated markers across the entire Krebs cycle
Elevated tartaric acid and D-arabinitol, suggesting significant Candida overgrowth
Functional markers of B12, folate, B6, CoQ10, and magnesium deficiencies
Elevated quinolinic acid, indicating neuroinflammation
Oxidative stress with high lipid peroxides and 8-OHdG

His stool test revealed a severely imbalanced microbiome:

Overgrowth of Enterobacter cloacae and Candida albicans
Absence of Lactobacillus and E. coli, both important for nutrient absorption and gut health
Overgrowth of Clostridium species, which may contribute to inflammation and further disrupt digestion

The conclusion was clear: Lev was suffering from wet and dry beriberi, driven by severe thiamine deficiency, worsened by chronic diuretic use and malabsorption. His seizures, vomiting, poor tone, delayed gross motor skills, and even pulmonary hypertension could all be traced back to a lack of essential B vitamins, especially thiamine. ^[6]^{,[7], [8]}

By the time he came to my clinic, Lev could not even lift his head when placed on his belly, a basic milestone typically achieved in the first months of life. His early seizures (including infantile spasms) had resolved with medication, but their cause had never been identified. In hindsight, these seizures were likely driven by energy failure in the brain, a known consequence of B1 and other B vitamin deficiencies that impair mitochondrial function and neurotransmitter balance.^[9]

Within days of starting thiamine and other supports, his mother noticed small but encouraging changes: Lev became more alert, more interactive, and began reaching for toys for the first time, as well as holding his head up when prone (on his belly). His vomiting and reflux diminished. His digestion improved. His body, for the first time in a long time, was beginning to catch up.

My recommendations after reviewing his lab results and discussing them thoroughly with his parents included:

Nystatin 500,000 unit tablets – ½ tablet 4 times per day
Biocidin – 2 drops twice a day, increasing dose slowly over one week
Lactobacillus rhamnosus GG – 15 billion per day, given away from Biocidin
TTFD – 200 mg per day in the morning
Liposomal CoQ10 – 125 mg per day
L-carnitine – 635 mg per day
Active B Complex – 1 capsule per day
- Thiamin (hydrochloride, benfotiamine): 30 mg
- Riboflavin (riboflavin-5-phosphate): 10 mg
- Niacin (inositol hexaniacinate): 100 mg
- Vitamin B6 (pyridoxal-5-phosphate): 25 mg
- Folate (from (6S)-5-methyltetrahydrofolic acid [MTHF], glucosamine salt, Quatrefolic®): 680 mcg DFE
- Vitamin B12 (methylcobalamin): 500 mcg
- Biotin: 250 mcg
- Pantothenic Acid (calcium D-pantothenate): 100 mg
- Choline (dihydrogen citrate): 50 mg
- Inositol: 25 mg
R-alpha lipoic acid – 50 mg per day
Potassium citrate – 224 mg per day
Continue:
- Riboflavin 25 mg per day
- Magnesium glycinate 60 mg per day
- Polyenylphosphatidylcholine 900 mg daily in the morning
- Vitamin D 800 IU daily anytime of day
- Iron bisglycinate 12 mg daily, preferably on an empty stomach

The Bigger Picture: Diagnostic Overshadowing in Down Syndrome

Lev’s story is a powerful and heartbreaking example of diagnostic overshadowing, a common but often unspoken problem in the care of children with Down syndrome. This occurs when medical professionals attribute new, worsening, or unexplained symptoms to the child’s known diagnosis rather than investigating further. In Lev’s case, his profound weakness, inability to lift his head, chronic vomiting, diarrhea, and history of seizures were all seen as “typical for Down syndrome.” But they weren’t. They were red flags for severe nutrient deficiencies, particularly thiamine (vitamin B1).

It is imperative for physicians, especially specialists working in critical care units, to recognize the profound impact that vitamins and vitamin deficiencies can have on the physiology of their pediatric patients. In children with complex medical conditions, underlying micronutrient imbalances often go undetected, yet they can significantly impair mitochondrial function, immune regulation, neurological development, and cardiovascular stability. Medications commonly used in hospital settings, such as diuretics, antiepileptics, and proton pump inhibitors, can further deplete essential nutrients like thiamine, magnesium, and B12, compounding the medical vulnerability of these children. A deeper understanding of nutritional biochemistry is essential for preventing avoidable deterioration, improving outcomes, and delivering truly comprehensive pediatric care.

In children with Down syndrome, symptoms like poor muscle tone, delayed milestones, constipation or diarrhea, fatigue, and even seizures are frequently dismissed as part of the condition. This mindset can be deeply harmful. When clinicians stop asking why a symptom is happening, especially when that symptom is new or worsening, they miss opportunities to identify treatable, reversible causes that can dramatically change the trajectory of a child’s health and development.

Lev’s case is sadly not unique. Thiamine deficiency is well-documented in children who are on diuretics like Lasix, who have gut dysfunction, high metabolic demands, or malabsorption – all common features in children with Down syndrome. Yet this critical nutrient is rarely tested, and even less frequently treated. In functional medicine, we are trained to look beneath the surface, to question assumptions, and to search for root causes. For Lev, the cause was clear: his thiamine was being depleted faster than it could be replenished, and no one had been monitoring this vital nutrient, until it was nearly too late.

When diagnostic overshadowing leads to inaction, children suffer unnecessarily. Lev’s story is a call to parents, caregivers, and clinicians to keep asking questions and to never assume that something is “just part of the diagnosis” without first considering what else might be going on.

Lev’s journey is not over, but he is now on a path of healing. His mother continues to advocate fiercely for his care. His treatment plan includes thiamine, mitochondrial support, targeted antimicrobial therapy, and continued nutritional repletion. His case may be complex, but it is not hopeless. He will be monitored closely under my care using functional testing to guide next steps and track progress. I hope his conventional medical team takes the time to carefully review the detailed letter I sent, which outlines the root causes we are addressing and the importance of collaborative support.

Parents – Trust Your Instincts

If you’re a parent of a child with Down syndrome, or any child with complex medical needs, trust your instincts. If something feels off, don’t stop asking questions. If you’ve ever been told, “It’s just part of the condition,” I urge you to ask again. Ask why. Ask what else could be going on. Don’t be afraid to bring up what you’ve read or researched. You know your child best, and your intuition is often the first and most reliable clue that something important is being missed.

Lev’s story is proof of that. His mother recognized something deeper was going on when his professional medical team didn’t. Her persistence is what led her to me and our discovery of a severe, life-altering thiamine deficiency, a diagnosis that had been overlooked despite months of symptoms, hospitalizations, and medications. Her advocacy quite literally changed the course of his life.

If you’re a medical provider, please remember this: Down syndrome is not a catch-all explanation. It is not a reason to stop investigating. Children with Down syndrome deserve the same level of curiosity, biochemical inquiry, and individualized care as every other child. In fact, they often need it more. Micronutrient deficiencies like thiamine (B1) are easy to miss, but they are crucial to mitochondrial function, GI motility, neurodevelopment, and vascular tone. These are not minor contributors; they are foundational to a child’s health and development.

Lev’s weakness, seizures, vomiting, and severe delays were not “just part of Down syndrome.” They were symptoms of a preventable, diagnosable, and treatable condition, and tragically, they were ignored for far too long.

Let’s do better. Let’s listen closer. Let’s not miss it again.

References

^[1] Rieck J, Halkin H, Almog S, Seligman H, Lubetsky A, Olchovsky D, Ezra D. Urinary loss of thiamine is increased by low doses of furosemide in healthy volunteers. J Lab Clin Med. 1999 Sep;134(3):238-43. doi: 10.1016/s0022-2143(99)90203-2.

^[2] Sica DA. Loop diuretic therapy, thiamine balance, and heart failure. Congest Heart Fail. 2007 Jul-Aug;13(4):244-7. doi: 10.1111/j.1527-5299.2007.06260.x.

^[3] Ritorto G, Ussia S, Mollace R, Serra M, Tavernese A, Palma E, Muscoli C, Mollace V, Macrì R. The Pivotal Role of Thiamine Supplementation in Counteracting Cardiometabolic Dysfunctions Associated with Thiamine Deficiency. Int J Mol Sci. 2025 Mar 27;26(7):3090. doi: 10.3390/ijms26073090.

^[4] Ryan MP. Diuretics and potassium/magnesium depletion. Directions for treatment. Am J Med. 1987 Mar 20;82(3A):38-47. doi: 10.1016/0002-9343(87)90131-8.

^[5] DiBaise JK. Nutritional consequences of small intestinal bacterial overgrowth. Pract Gastroenterol. 2008;32(12):15–28 (https://www.peirsoncenter.com/uploads/6/0/5/5/6055321/sibo_artikel.pdf)

^[6] Pache-Wannaz L, Voicu C, Boillat L, Sekarski N. Case Report: severe pulmonary hypertension in a child with micronutrient deficiency. Front Pediatr. 2025 Jan 31;13:1478889. doi: 10.3389/fped.2025.1478889.

^[7] C S, Kundana PK, Reddy N, Reddy B S, Poddutoor P, Rizwan A, Konanki R. Thiamine-responsive, life-threatening, pulmonary hypertensive crisis with encephalopathy in young infants: A case series. Eur J Paediatr Neurol. 2022 Jan;36:93-98. doi: 10.1016/j.ejpn.2021.12.010.

^[8] Rabinowitz SS. Pediatric beriberi clinical presentation: history, physical, causes. Medscape. Updated March 17, 2014. (https://www.peirsoncenter.com/uploads/6/0/5/5/6055321/pediatric_beriberi_clinical_presentation__history_physical_causes.pdf)

^[9] Lanska DJ, Fatal-Valevski A. Epilepsy in children with infantile thiamine deficiency. Neurology. 2010 Feb 23;74(8):702-3; author reply 703. doi: 10.1212/WNL.0b013e3181d2b857.

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With Thiamine Paradox Symptoms Patience Is Key

by Jeff Mitchell

Published on July 17, 2025

50.2K views

I wanted to share my experience going through thiamine paradox so that others may find hope as they navigate the process. In November of 2019, my life was completely flipped upside down. My full story is here, but briefly, I had taken an antibiotic called Tinidazole, the less popular but almost identical sister drug to Metronidazole. Within days of taking the antibiotic I began to experience frightening symptoms like loss of mobility in my hands, heart palpitations and intense feelings of depression and doom. Less than two weeks later, I went into surgery to get my wisdom teeth removed and was put on a course of penicillin for two weeks.

Within weeks, my health was in a total spiral. I began to experience constant bouts of tachycardia and panic, low blood sugar, dizziness, blurry vision and the inability to sleep. I went from somebody who sleeps 8 hours a night to sleeping for less than an hour on various nights. When sleep did come, I was jolted awake in a panic attack. At times, I was feeling symptoms that mimicked asthma…it was like I couldn’t breathe.

I had no idea what was going on. Multiple trips to the ER did nothing. I continued to get worse. It wasn’t until I traced back what drugs I had taken that I made my way to a Facebook group called “Metronidazole Toxicity Support Group.” It was in that group that I discovered that thousands of others were dealing with the same set of symptoms caused by this horrendously neurotoxic antibiotic. I had known for years that one should avoid fluoroquinolone antibiotics, but research has shown that metronidazole and others in its class present some of the same catastrophic side effects.

Through her own research and contact with Dr. Lonsdale and Dr. Marrs, the founder of the group discovered that metronidazole and other drugs in its class block thiamine in the body. The symptoms of the toxicity mimic those of Wernicke’s encephalopathy.

The solution? Take thiamine.

I thought it was going to be an easy fix. It wasn’t.

Like many posts on Hormones Matter, the topic of paradox frequently comes up, and I am the perfect case study.

In retrospect, I had longstanding symptoms of mild beriberi for a lot of my life. I was constantly dealing with low blood pressure and strange heart symptoms that date back to my teenage years. I grew up eating a typical American diet and started drinking large amounts of coffee in my teens. I loved sugar.

With longstanding thiamine deficiency, the human body changes its chemistry to adapt and survive. When thiamine is reintroduced and things get turned back, your body goes haywire until the chemistry can normalize.

For me, it took three attempts. Every time I would start even the tiniest dose of thiamine HCL, I would erupt in panic, tachycardia, feelings of “seizures” and doom and gloom, chest tightness and head pressure. It was akin to the feeling when somebody knows that they ingested way more marijuana than they should have. Sheer terror. When I took too much one time, I almost landed in the ER because I thought for sure that I was going into cardiac arrest.

My first attempt was in January 2020. I failed miserably and stopped because of the side effects. But I wasn’t getting better and my health continued to spiral. I tried again in March 2020 and made it for 2 weeks before dropping out again. I would crumble pills to get just a little thiamine HCL in my system and I would still feel like a total wreck.

Finally, on my third attempt in May 2020, I made it.

The solution is to start LOW and SLOW. I found a company in the UK that has a liquid form of thiamine HCL that allowed me to do this. I started with 10 mg per day and gradually increased by 10-20 mg over the course of many weeks. I also spread my dose out throughout the day. Dr. Lonsdale predicted the paradox will lift within a month, but for me, it took a bit longer. Within 8 weeks I began to notice that I could safely take a 100mg thiamine HCL pill without experiencing too many symptoms. It continued to get better with time.

Now, almost a year later, I’m taking 300-400mg of thiamine HCL a day and mixing in benfotiamine and allithiamine. In the last 6 months, my health has slowly started to trend upward. I’ve added in a B complex at times and I’m also working on my B12. The heart palpitations are significantly better, I’m less prone to panic attacks than I have been in years, and my brain fog has lifted. What I’m left with is some slight dizziness (though it is significantly better), blurry vision that waxes and wanes, and my blood sugar is still presenting some issues. Still, I feel like I’m trending in the right direction and that things continue to slowly improve.

My advice for those of you encountering paradox symptoms is this: BE PATIENT. It sucks. But the rewards on the other end are so worth it. I would also advise you to dramatically increase your potassium through food. This didn’t eliminate the paradox feelings entirely but it did help reduce them.

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

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This article was publish originally on January 26, 2021.

Longstanding Mitochondrial Malnutrition in a Young Male Athlete

by OC

Published on July 16, 2025

12.3K views

Male athlete with mitochondrial malnutrition

My health issues started rearing their head in ninth grade, and given the vitiligo of my mother and MS (stabilized) of my father, perhaps it should not have been much of a surprise. I had mono in middle school, and then after getting a bad virus at the start of freshman year, my health deteriorated rather quickly.

Over the course of the first few years of high school, I was diagnosed with immunoglobulin deficiencies, gastritis induced anemia that was often recurrent, IBS, elevated blood sugar, insomnia, and hypothyroidism. I also developed hand tremors and was told I had SIBO. I was a student athlete and was often exercising over eight hours a week at the time. My diet in middle school represented the Standard American Diet, but after my health issues started, I ate a diet that loosely resembled the paleo diet without much benefit.

Entering college, doctors convinced me that my issues were due to malnutrition from undereating. I was encouraged to eat more and so I did. Over the next two years, I followed an unrestricted diet with a mix of junk and traditional health food. I went from 130 to 190lbs, a 60 pound weight gain. My stomach issues got better, but everything else remained the same, except I started experiencing anxiety and exhaustion. The doctors were right, but their advice was wrong. I wasn’t malnourished from a lack of food, but from a lack of the micronutrients that allow the mitochondria to convert food into energy. Looking back, it is no wonder I had no energy.

Just recently, I discovered the articles about thiamine on this website. It all began to make sense. Thiamine is a required mitochondrial nutrient, one that I was likely missing. I began thiamine and magnesium. I had previously tried magnesium, but I was intolerant to it. Since taking the duo for two weeks, I have started to notice a bit more energy, much better warmth in my extremities, and more stable blood sugar. However, that was preceded by major nausea, freezing low body temps, and worse blood sugar instability than ever suggesting a thiamine paradox at work. Here’s to hoping that this treatment works wonders going forward.

Health History

Current Age: 20
Height: 6ft
Gender: Male
Weight and body fat: 190lbs 15% Body fat

Family History

Mom with vitiligo
Dad with stabilized MS

Middle School

Had mono at one point, always generally had minor fatigue
Junk food diet

Ninth Grade

Got terrible stomach virus at start of year
Developed hand tremor
Found out I was anemic with collagenous gastritis. (I suspect it was actually iron overload aka Morley Robbins theory.)
Treated with Prilosec and iron supplements
Ate relatively low carb
Lots of tennis

Tenth Grade

Developed IBS
Discovered IGG and IGA deficiency and low vitamin D
Got SIBO diagnosis
Restricted diet even more by eliminating gluten and dairy
Lots of tennis and track

Eleventh Grade

Diagnosed hypothyroid
Took synthroid without success
Lots of tennis and track

Twelfth Grade

Unrestricted diet as doctors convinced me that undereating was the cause of my issues. I went from 130lbs to 160lbs.
Lots of tennis, track, and weightlifting

Freshman Year of College

Ate paleo style to drop weight, dropped to 150lbs.
Main issues were insomnia, chronic dry mouth, cold hands and feet, GERD, bloating, anxiety

Summer Before Sophomore Year Through End of Sophomore Year

Started eating a lot again, unrestricted, and went up to 175lbs over the course of a year with lots of heavy lifting
Fasting blood sugar of 99 and then 104
Same symptoms as freshman year
Tried things like megadosing zinc, megadosing vitamin D without success

Junior Year Through March 2021

Same symptoms as freshman year, but slightly improved due to nutrient density
Got shingles and recovered
Ate lots of eggs, whole milk, liver, oysters, ground beef, chocolate, liver, potatoes, rice, bagels, butter — Ray Peat style
Felt a bit better and warmer, but exhaustion became a symptom
Had negative reactions to magnesium supplements despite low RBC
I was trying to implement root cause protocol (Morley Robbins) after discovering my ceruloplasmin was low
Donated blood per Morley Robbins advice. Of all the stuff I have done, this provided the most benefit to me in terms of improved thyroid function and general sense of wellbeing, but still had tons of issues

Present

Discovered thiamine and this website and began thiamine supplementation. First with thiamine mononitrate March 20, 21. Suddenly, I had energy.
Switched to 250 mg Benfotiamine with 120 mg magnesium on March 24^th.
Switched again to 100 mg Thiamax with 125 mg magnesium on March 25th.

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

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This story was published originally on April 5, 2021.

Virginia Woolf and Me – Moments of Being Misunderstood

by Jo Dixon

Published on July 14, 2025

2.3K views

Did Virginia Woolf Suffer from Thiamine Deficiency

Virginia Woolf, an English writer who pioneered the use of stream of consciousness narration, was a tremendous diarist. Her diaries and her collection of autobiographical essays, ‘Moments of Being’¹, reveal her longstanding struggle with health issues that today might be classified as Myalgic Encephalitis/Chronic Fatigue Syndrome (ME/CFS). Reading her work for a creative writing class, I realized that her unrelenting fatigue, brain fog, and memory issues might have been due to unrecognized thiamine deficiency; an issue that I have struggled with, and published articles here and here and written two books about: The Missing Link in Dementia and Swimming in Circles.

‘My Brain Is Like a Scale’ – A Familiar Symptom of Thiamine Deficiency

Virginia’s diaries logged, in vivid detail, the symptoms she experienced – a condition which, like many today, had no clear diagnosis or treatment. She suffered with severe fatigue, ‘such an exaggerated tiredness’²(p.121), which fluctuated, ‘My brain is like a scale: one grain pulls it down. Yesterday it balanced: today it dips’²(p.260). The fatigue was noticeably worse after physical exertion, ‘But I am too tired this morning: too much strain and racing yesterday’²(p.263), but also deteriorated after socializing, ‘I’m too tired to go on with [reading]. Why? Talking too much I daresay. I thought, though, I wanted “society”’² (p.230). Her symptoms recovered with rest – ‘A day off today’²(p.230).

In my memoir, ‘The Missing Link in Dementia’, I describe an illness characterized by extreme fatigue, insomnia, post-exertional malaise and significant memory problems. My condition progressively deteriorated, and I became extremely tired all the time. Severe insomnia left me restless most nights, and I would awake each day feeling unrefreshed and permanently exhausted. Any physical exertion, even walking, worsened the fatigue, my legs would feel heavy like dead weights, powerless and clumsy.

The most frightening symptom was short-term memory loss. I would spend hours reminiscing; spectacularly clear distant memories were more easily retrieved than any recent event. I experienced brain fog, reminding me of my pregnancy-induced woolly brain. I was forgetting things – outcomes of discussions or meetings at work, names, and then faces. I struggled to concentrate. I feared I was developing early dementia, and that my brain was becoming encased in amyloid plaques. In my memoir I described how I imagined these smothering my brain like a fleece in winter. Over time I steadily deteriorated with frightening moments of being unable to recognize my surroundings.

I wrote my memoir before reading the description of Virginia’s vivid memories of a happy childhood that were, ‘more real than the present moment.’¹(p67). She tried to rationalize this experience – the strength of simple childhood memories compared with the weak later memories, describing ‘non-being’ as everyday activities that did not assimilate into our memory banks. She wrote, ‘I’m brain fagged’²(p.309), ‘I have already forgotten what we talked about at lunch; and at tea;’¹(p70) but she knew that ‘although it was good day the goodness was embedded in a kind of nondescript cotton wool.’¹(p70). Shortly before the end of her life she wrote: ‘I can’t concentrate’, ‘I can’t read’³. She had cognitive decline with short term memory loss.

The Emotional Component of Inadequate Thiamine

In contrast to my numbed senses, my emotions were far from muted, I was overly excitable or would burst into tears or become inappropriately angry at minimal provocation. I suffered with palpitations which were disconcerting, and at times, disturbing. Virginia wrote that she, ‘felt such rage’¹(p125) and that her, ‘heart leapt: and stopped: and leapt again…and the pulse leapt into [her] head and beat and beat, more savagely, more quickly.’²(p.179)

I was scared, not knowing where to turn to for help. My quality of life was extremely poor. I had always been an optimist, but I could see no future living like this. I even contemplated suicide, because I did not wish to become a burden. I thought I was going to die anyway, and I was extremely sad that I wouldn’t see my children grow-up, but I thought that they would be better off without me. It seems terrible now – selfish even, but I was unable to control how I felt.

Virginia had suffered with an illness that had features of depression, she felt ‘such anguishes and despairs’²(p.94).She wrote that she was spoiling Leonard’s life. Tragically, she committed suicide in 1941 shortly after completing the manuscript of her last novel. She was 59. In her suicide note she wrote that: ‘Everything has gone from me’³(p.481).

Anorexia: A Cause and Consequence of Inadequate Thiamine

As a young adult Virginia had a stressful seven years with multiple deaths in the family¹(p.117), sexual abuse during adolescence¹(p.69), and probably had anorexia according to her great niece, Emma Woolf. Virginia was almost 6 foot and weighed 7st 6lb (104lbs) when she was institutionalized for rest and feeding, her body mass index (BMI) was 14.5, a marker that she was significantly underweight.

I found out in my forties that I had a congenitally malrotated gut, presenting unusually as an adult. I had developed marked slowing of my guts, so that it was becoming impossible to eat. The slowing of my guts meant that I no longer felt hungry. I had to remember to eat, to force myself to eat. I lost weight, dropping from size 12 to 6. I lost muscle mass; where previously I had muscles there were now gutters. The muscles were constantly twitching – fasciculation’s, tics, tremblings or flutterings.

Neurasthenia: The ME/CFS of the Time

It is likely that Virginia was influenced by Jane Austen. Virginia’s first novel has many links to Austen’s novels, including the names of characters. Famous quotes from Austen’s Pride and Prejudice hint at Mrs. Bennet’s underlying condition: ‘Mr. Bennet…You have no compassion on my poor nerves.’⁴(p.7), ‘…I am frightened out of my wits; and have such tremblings, such flutterings, all over me, such spasms in my side, and pains in my head, and such beatings at heart, that I can get no rest by night nor day’⁴(pp.273-4).

Virginia Woolf and Jane Austen’s Mrs. Bennet were both thought to have suffered with neurasthenia, literally weak nerves, a term originally used in the nineteenth century United States, when it was associated with busy society women and overworked businessmen. The first description of neurasthenia was published by American neurologist Beard in 1869. Virginia wrote that she was ‘extremely social…for ever lunching and dining out…or going to concerts…and coming home to find the drawing room full…of people.’¹(p.163) She was obliged to participate because the ‘pressure of society was now very strong.’¹(p.128) She repeatedly spoke of a ‘world of dances and dinners’¹(pp.170, 172).

Low Thiamine Causes Low Energy Levels

One of the problems in ME/CFS/neurasthenia is that there are no tests. A clue is that the predominant symptom is fatigue. After excluding other causes of fatigue, a prime suspect must be faulty energy production. Another problem in ME/CFS/neurasthenia is that there is a lack of understanding about the basic energy producing processes or the fact that thiamine, or vitamin B1, is crucial.

ATP (adenosine with three phosphates) is the main energy currency. Energy is released each time a phosphate group is removed from adenosine, becoming ADP (adenosine with two phosphates). This is the human equivalent of a rechargeable battery.

Respiration is the breakdown of food-fuel to release energy. The predominant fuel, glucose, is broken down to produce pyruvate via glycolysis – literally glucose breakdown. This pathway doesn’t require thiamine (or oxygen). It produces two ATP. This is just small change in comparison with the energy produced in the battery factory – mitochondria.

Entry into the battery factory is through the gatekeeper enzyme – pyruvate dehydrogenase. This enzyme breaks down pyruvate, and importantly, requires thiamine as a co-factor – it malfunctions without thiamine.

Once inside the factory there are two production lines: one continuously uses recycled components (tricyclic acid cycle) and the other is a chain of reactions (electron transfer chain). These processes make significantly more ATP, producing more charge, more efficiently – like ultra-rapid charging for EVs. Obviously, this is a simplified version to hammer home the message that thiamine matters. A more accurate, detailed and scientific (less creative) description can be found here.

A shortage of thiamine (or oxygen) results in the excess pyruvate being converted to lactic acid. A familiar sensation to anyone who has sprinted 100m, when the demand for energy is higher than production, is the build-up lactic acidosis in the muscles, causing cramping, burning or weakness. This diversion of metabolism to an anaerobic (without oxygen or thiamine) pathway is inefficient, because another chemical reaction, requiring yet more energy, is required for the muscles to remove the lactic acid and recover. This results in an energy debt as it costs more energy to return the lactic acid to the usable pyruvate – akin to buying back the family silver from the pawn shop.

During exertion thiamine is required to ensure the higher power charge is readily available. Excess lactic acid results when energy requirements outstrip production, whether from a lack of oxygen or thiamine. In patients with ME/CFS, lactic acid accumulates more readily during exercise and before oxygen supplies are exhausted, and an elevated lactic acid level is found in the fluid surrounding the brain. Malfunctioning pyruvate dehydrogenase has been identified as key in ME/CFS. These patients feel like they are doing a 100m sprint whenever they try to walk. The (now debunked) treatment of patients with ME/CFS with exercise therapy, shows that their condition was misunderstood.

For those with a more sedentary existence, falling asleep with an arm above your head gives the same sensation. When the blood starts to circulate the arm temporarily feels like a dead weight. The arm is incredibly weak and lacks coordination. This is because the nerves no longer respond to the instructions from the brain.

Weak Nerves? Think Thiamine.

Nerves are highly susceptible to thiamine deficiency. The poorly insulated nerves – the autonomic nerves – are particularly vulnerable to thiamine deficiency. These autonomic nerves control the fight and flight response and regulate gut movement, sweating and heart rate – the ‘housekeeping’ functions which are outside voluntary control. After prolonged thiamine deficiency, eventually all nerves are affected, including the larger, better-insulated sensory and motor nerves. Arguably, the term neurasthenia is more appropriate than ME, it indicates the underlying problem – reduced nerve function.

According to the hypothesis that I describe in my memoir, excess thiamine-destroying bacteria, in the part of the gut responsible for absorbing nutrients, reduce thiamine availability. Vitamin D deficiency is common in bacterial overgrowth; it makes sense that it is a surrogate marker for thiamine deficiency. Vitamin D deficiency often occurs in patients with ME/CFS.

Rest, Recover, and Recharge

Back then, the best treatment for neurasthenia was the ‘rest cure’. Beard, a sufferer himself, astutely remarked that it was due to the body being drained of nervous energy due to an overtaxed supply of energy. Virginia was treated with rest and recognised that her nerves required respect: ‘Only nerve vigour wanted’²(p230). She was also treated with a high protein diet. Similar approaches have been popularised today. Diets such as paleo, South Beach and Mediterranean support a higher protein consumption. I ate a low carbohydrate diet for years and still avoid sugar now. I also took thiamine supplements, had corrective gut surgery and antibiotics. Popular techniques for resting the mind and body include meditation, yoga, relaxation and mindfulness. Resting helped me. It wasn’t easy, because I felt agitated and compelled to move. I spent hours doing jigsaws, aware that I was recharging my batteries – a term I’ve used but not reflected on. Strangely, this is the underlying problem: low charge, faulty charging, poor battery capacity. We have a far better understanding of modern technology that has been around for a few decades than the human system in existence for millennia which is reliant on thiamine.

Thiamine Deficiency, Modern Lifestyle, and Sugar Cravings

Humans have some design glitches predating our modern lifestyles. The first anomaly is that ATP is not stored, and the ATP generated is used 1000 times over each day – the body must constantly produce and recycle ATP. The second design fault is that thiamine, despite being essential, is not stored and is only poorly absorbed through the gut. Low thiamine levels are prevalent in society, leading to faulty recharging of our internal batteries.

Beard, who wrote about his neurasthenia in 1869, thought it was due to American modernization. He was right; we have made poor lifestyle choices. In the United States, sugar became readily available after 1864, following the civil war, with the construction of the biggest sugar refinery in the world on Long Island and a reduction in taxes. In the UK, sugar consumption escalated a century earlier, Britain was described as the ‘sweetshop of Europe’, thought to be in part due to our tea-drinking habit. By the time Jane Austen was writing, sugar was Britain’s most valuable import. Originally a condition affecting the upper classes, neurasthenia spread to the lower classes, as sugar became more affordable, although this may reflect access to medical care.

I had been craving sugar for years to gain short bursts of energy as I flagged, adding sugar to tea, one teaspoon became two, then three. Like topping up a meter constantly with small change, the sweet tea momentarily cleared the brain fog, allowing me to see another patient or simply make it to the end of the day. I experienced the same sensation in my colleague’s office after a dose of intravenous thiamine – the cotton wool vaporized.

The brain only uses glucose for energy production, whereas muscles can use protein as a fuel. I now understand that by drinking sugar-charged tea I had been supplying my glucose-dependent brain with glucose for the glycolysis pathway but because I was deficient in thiamine, the products of glycolysis could not enter the TCA cycle and progress to the electron transport chain where most of the ATP is made. The sugar craving was a sign that my brain was starving – desperate for energy – for titbits of ATP.

Factors Affecting Women

ME predominantly affects women. In many cases there is a deterioration during the peri-menarche or perimenopause, times of marked growth and/or hormonal changes. Progesterone slows gut motility. Estrogen improves nerve connections in the hippocampus – the part of the brain responsible for working or short-term memory, it also increases glucose uptake into the brain.

Being perimenopausal, my falling estrogen levels meant that the brain uptake of glucose was less efficient. Glucose offered short-term relief but exacerbated the bacterial overgrowth and malabsorption. It was clear that I had been breaking down muscle and using it as a protein source to produce energy outside my brain, contributing to the muscle wasting I experienced.

Thiamine is depleted during pregnancy, breast feeding, growth, infections and exercise. Having had four children, all breast fed, I had started exercising to get fit, and lost weight, initially intentionally. Other familial factors, immune deficiency causing recurrent infections or defective thiamine uptake genes, might have contributed. I had multiple factors, any one of which would deplete thiamine.

Was Virginia Woolf Deficient in Thiamine?

We will never know. What we do know though is that thiamine deficiency leads to poorly functioning housekeeping nerves and slow guts, predisposing to small intestinal bacterial overgrowth. This causes reduced appetite, trouble eating, reducing thiamine intake further. It is a physical problem caused by vitamin deficiency, poor nerve function initially, and eventually, nerve damage. Thiamine deficiency is treatable. It is not a psychiatric illness – the mental symptoms I experienced were caused by thiamine deficiency. Virginia Woolf was probably thiamine deficient too, having suffered with anorexia nervosa. She had a diagnosis of neurasthenia, now known as ME/CFS. Millions of people suffer with ME/CFS. Perhaps it is time we look into thiamine.

References

Woolf V. Moments of being unpublished autobiographical writings. Schulkind J (ed). New York and London: Harcourt Brace, Jovanovich; 1976.
Woolf V. A writer’s diary: being extracts from the diary of Virginia Woolf. Woolf L (ed). New York: Harcourt inc.; 1953.
Woolf V. The Letters of Virginia Woolf. Vol. 6, 1936-1941. Nicolson N, Trautmann J (ed). London: The Hogarth Press; 1980.
Austen J. Pride and prejudice. Vivien Jones (ed). London: Penguin Classics; 2003.

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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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Are You Attractive? Connections Between Low Thiamine and Mosquito Bites

by Mahmood Bilal PhD, DABCC, FADLM, TS(ABB)

Published on July 10, 2025

14K views

A new study shows that you can be “highly attractive” if you have enough carboxylic acid on your skin. Highly attractive to mosquitos, that is.

Mosquitoes are an ideal vector for pathogen contraction and transmission between hosts. These pathogens include viruses such as Dengue, Yellow Fever, Zika, West Nile Virus, and Chikungunya. Parasites that cause malaria in tropical and subtropical countries are also transmitted by mosquito bites. It is therefore logical that increased exposure, or attractiveness, to mosquitos will increase the probability of contracting such pathogens. Why then do some individuals seem to be targeted by mosquitoes more than others?

A new study attempted to shed light on this age-old question of why some people are greater mosquito magnets than others. Indeed, some are victims of relentless mosquito bites and could in fact function as a “mosquito adsorbent” – a courtesy for those around them on a humid day at the park. It turns out that mosquitoes utilize their sense of smell to find food, as expected, but that those with higher levels of certain metabolites get bit more frequently than others. What is interesting is that some genes in mosquitoes allow this sensing to occur. To determine how all of this worked, researchers induced olfactory deficits by knocking out genes in mosquitoes. This caused less odor sensing to occur, but surprisingly mosquitoes were still able to distinguish between highly and weakly attractive individuals. This all indicates that attractiveness to mosquitoes is likely an amalgamation of mechanisms involving genetics and metabolomics.

The specific metabolites analyzed in this study are pentadecanoic, heptadecanoic, and nonadecanoic acids – all grouped as carboxylic acids. These are considered odd number fatty acids (ONFA), a minor group of the fatty acid repertoire in humans. Pentadecanoic and heptadecanoic acids are the most abundant ONFA, composed of 15 and 17 carbon chains, respectively. In contrast to other fatty acids, ONFA are thought to predominantly accumulate in the body from foods (e.g., dairy, meats). However, they can be synthesized in the body from straight chain fatty acids, through the mechanisms of alpha-oxidation.

The Thiamine Connection

It has long been rumored that thiamine could prevent, or at least reduce, mosquito bites. Is there research supporting this claim?

The literature is not clear, but does seem to indicate an indirect connection between thiamine (Vitamin B1) deficiency, or inadequacy, and attractiveness to mosquitos. For example, a research group studying yellow fever mosquitoes, showed that mixed with lactic acid, the carboxylic acid strongly synergizes to elicit mosquito attraction. The authors state:

Addition of lactic acid markedly increased the degree of attractiveness of formerly less attractive human odour samples and they were preferred over those which were originally the most attractive.

Indeed, lactic acid alone, acts as a sufficient mosquito attractant, but is relatively weak compared to the synergism with carboxylic acids. Another older study utilized a bioassay to identify attractants from human skin extracts. Here the mosquitoes were allowed to fly upwind toward odor sources (human skin wash extracts). They found that lactic acid was a major constituent of skin extract and that it was a necessary component for mosquito attraction.

What can cause lactic acid to build up (either in blood or tissues)? One mechanism would be the shunting of pyruvate into the lactate pathway. This can be measured in blood when someone has low thiamine. Indeed, in some conditions, the skin has been shown to carry higher amounts of lactic acid compared to blood levels, due to increased anaerobic glycolysis. Here we would expect lactic and carboxylic acids to suffuse below or above the surface of skin where it can be detected by mosquitos. In addition, a surfeit of lactic acid build up, in an overt thiamine deficiency, may not be required. This is because the mosquitos’ high sense of smell can pick small amount of odors, even when major olfactory-related genes are knocked out.

Contrary Research

On the other hand, a potential argument against the effectiveness of thiamine in repelling mosquitoes comes from a 2005 study. The authors gave individuals over the counter B vitamins in two experiments:

Experiment 1: B-complex containing 50 mg of B1(thiamine)/B2/B3/B5/B6, 400 µg Folate, 50 µg B12, 50 µg Biotin, and 500 mg Vitamin C. Vitamin C by itself was used as a control since the B-complex contained Vitamin C. Subjects (14 males, and 9 females) were utilized in a cross over experiments, meaning that they would start either placebo or the treatment for 7 days and then switch over to treatment or placebo, respectively. In this scheme each individual would act as his/her own paired experiment, statistically.

Experiment 2: Used 100 mg B1, with Vitamin C as a control. Subjects (10 males, and 7 females) were studied in the same manner to experiment 1, with 100 mg B1.

The authors did not find statistically significant differences between the groups, and concluded that B vitamins were not helpful in repelling mosquitos.

Possible Problems With the Research

There may be some caveats to the protocol used in this research, that likely masked the true effects of thiamine supplementation. First, the authors may have been limited, but should have used a non-Vitamin C formulation. Although somewhat inconsistent in the scientific literature, Vitamin C supplementation can reduce blood lactate levels in certain settings, “increase in free radical production and lactate levels….were offset by vitamin C supplementation”. This, in theory, would reduce lactate in skin and therefore the strong synergistic effects of lactic with carboxylic acids would be minimized. Second, and more importantly, the method only evaluated volatile components that can be transferred from the skin into the glass bottle used to attract mosquitoes. Lactic acid is a low volatility organic compound. The other positive studies discussed above had instead extracted skin organic compounds, including lactic acid, utilizing ethanol. Overall, the 2005 study was well designed for the questions asked and provided basic preliminary experiments. Unfortunately, the design of the study negated the effects of one key compound, lactic acid, due to volatility-based evaluation. Hence, a follow up study should be performed with these concepts in mind:

Premeasurement on skin extracts using organic acid extraction methods (ethanol or other compounds).
Treatment with higher dose thiamine. An example would be 0.5 – 1 gram of thiamine-HCl, for 1 to 4 weeks.
Mosquito attraction should be performed concomitantly with measurements of thiamine status (ETKA test). Similarly, measurements of lactic acid in skin extracts of treated and non-treated individuals should be performed in order to correlate quantity with phenotype.

The expectation is that individuals who are thiamine deficient would have increased lactic acid in their skin extracts and therefore would serve as a mosquito magnet.

Does Thiamine Status Play a Role in Mosquito Attraction?

The above studies combined elucidate some of the mechanisms in play in individuals who are highly attractive to mosquitos. These include interplay between genetics of mosquitos and organic compounds present in human skin. Individual differences in mosquito attraction may also be attributed in part to temperature, moisture, visual cues, and body odor. Out of these possibilities, body odor plays a major role in mediating these interactions. Specifically, both lactic and carboxylic acids play a synergistic role in attracting mosquitos, and therefore increase the odds of contracting disease. Mechanisms that result in increased lactic acid production such as exercise, and potentially low thiamine metabolism, are likely a risk factor for mosquito bites. Overall, the role for lactic acid in mosquito attraction seems to stir the arrows of mosquito-magnet theory, in-part, towards a mild/subclinical thiamine deficiency, or at least an abnormal metabolic activity. As suggested above, more studies should be performed in order to directly evaluate the effects of thiamine on lactic acid content of human skin in conjunction with effects on attracting mosquitos. In the meant time though, if you are one of those people who seems to attract mosquitos, consider looking into thiamine.

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

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This article was published originally on February 27, 2023.

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‘My Brain Is Like a Scale’ – A Familiar Symptom of Thiamine Deficiency

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Anorexia: A Cause and Consequence of Inadequate Thiamine

Neurasthenia: The ME/CFS of the Time

Low Thiamine Causes Low Energy Levels

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