thiamine deficiency

Are Thiamine Deficiency Symptoms Too Narrowly Focused?

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thiamine deficiency symptoms too narrowly focused

Much of our understanding regarding thiamine deficiency comes from early reports of illness from far-off lands, case reports that suggest rarity, and from rodent studies. While all of these are useful, none easily translate to the realities of this disease process on the ground, in the clinician’s office, or in the hospital. Do we really know what thiamine deficiency, or more appropriately, thiamine insufficiency looks like in everyday practice? Would we recognize it in the patients who walk through the doors of any medical facility? Probably not. And that is a problem.

We tend to think about nutrient deficiencies as emerging only in populations affected by starvation or absence-based malnutrition. This interpretation evolved from the early descriptions of beriberi, where the individuals most afflicted included Japanese sailors, Pacific Island communities, and regions afflicted by food scarcity. Later, alcoholics were added to the list of potential populations affected by thiamine deficiency. More recently, post gastric bypass patients, hyper-emetic pregnant women, and patients with critical illnesses were identified as at risk for deficiency. With each set of populations though, we are given the impression that thiamine deficiency is rare but easily recognized. It is neither, but the lens through which we view this disease process was focused generations ago on only the most severe examples, and that lens has remained ever since.

The Legacy of Early Scientists

The typical descriptions of thiamine deficiency disease, come from the perspective of the early investigators who described these conditions and have changed very little in decades since. Definitions of beriberi, which in Japanese means I cannot, I cannot, was, and still is, largely focused on the progression to heart failure in later stage deficiency. Here, there are two primary types of beriberi: wet beriberi, which is defined as high output cardiac failure with edema, and dry beriberi described as the central and peripheral nervous system and cardiovascular disturbances without edema. In recent years, gastrointestinal beriberi and neuritic beriberi have been added but they remain poorly recognized.

Likewise, our understanding of Wernicke’s encephalopathy (WE), a disease process that was first described by Carl Wernicke in 1881 and later associated with alcoholism and thiamine deficiency, is still described using Wernicke’s original triad of symptoms: mental confusion, ocular abnormalities, and ataxia. This despite the fact that 1) these symptoms represent a later stage manifestation of the disease process, where the deficiency is sufficient to produce brain damage and 2) these symptoms infrequently present, either alone or in combination, in most cases of WE. In fact, one study found that 80% of cases WE were identified only postmortem, meaning they were missed entirely while the patient was alive. Of those, only 16% had documentation of all three symptoms, 44% had one or two of the classic triad symptoms and 19% had none at all. This suggests that the classic triad, while a brilliant original observation, requires adjustment.

Korsakoff’s syndrome, a later stage and more severe form of thiamine deficient brain damage that includes neuropsychiatric and neurocognitive manifestations like confabulation, psychosis, and significant memory deficits, shares a similar lack of diagnostic clarity and is often mistaken for more traditionally defined psychiatric cases and dementias. Like Wernicke’s syndrome, Korsakoff’s is named after the scientist who first reported it in the late 19th century, a Russian by the name of Sergei Korsakoff. Like Wernicke’s, the lens through which we view this disorder owes largely to the original descriptions. Both syndromes are now combined as Wernicke-Korsakoff syndrome (WKS). For that reason, there are no clear data on the prevalence of Korsakoff’s syndrome or on how many patients progress through the different stages of brain damage associated with thiamine deficiency.

Those Rare Cases of Thiamine Deficiency

Modern case reports reinforce these legacy definitions of thiamine disease and continue to portray thiamine deficiency as a rare manifestation of severe illness. The literature is replete with cases of patients who demonstrate none of the classic symptoms associated with thiamine deficiency and yet are clearly deficient. Likewise, in each of these reports, the development of thiamine deficiency is considered rare. Indeed, the rareness of this condition is almost always explicitly emphasized in the text with statements like:

  • “A severe depletion is not commonly seen, except in cases of inadequate nutrition and/or alcoholism.”
  • “Cardiac beriberi, or heart failure due to thiamine deficiency, is considered rare in the developed world.”
  • Thiamine deficiency is rare in developed countries and is most commonly associated with chronic alcoholism. The other predisposing conditions include chronic dietary deprivation and impaired absorption or intake of dietary nutrients.
  • Nowadays, in the developed world it is relatively rare.

Next time you are reading a case study, or really, any report on thiamine deficiency, note the remarks of rarity. What if thiamine deficiency is not rare, but simply under-recognized? If we rarely consider it based on the lack of matching symptoms, how do we know what the real prevalence is?

Of Rodents and Men

The rodent research, although more adept at addressing the progression of deficiency symptoms across time, is still problematic. Aside from the obvious differences between rodents and humans, the highly controlled and contrived experimental conditions under which this research occurs in no way reflects the messiness of life. Rarely are we exposed to an absolute deprivation of a single nutrient, unless under some sort of duress or a medical error. More frequently, the progression to thiamine deficiency is an extended process of months to decades, where exposure to thiamine or anti-thiamine factors varies across time, and as a result, so too does the expression of illness.

From the rodent research, we do know, however, that there is a clear progression of symptoms across the period of deprivation. Here, among the first manifestations of thiamine deficiency are hair loss, apathy, and anorexia. These symptoms emerge within two weeks of thiamine deprivation. At about 4 weeks, neurological symptoms emerge, and death by cardiac arrest occurs at about 6 weeks.

Whatever the problems there are translating patterns gathered from animal research to those of human studies, and there are many, at least with these studies we can see the early indicators of problems. If a patient were to complain of new-onset hair loss, apathy, or anorexia, or even newly emerging neurological symptoms, more often than not, the symptoms would be dismissed as stress-related and relegated to the category of psychosomatically induced. An antidepressant or anxiolytic would be prescribed and that would be the end of it. Thiamine or other nutrient deficiencies would not be considered until a much later stage, if at all.

The Progression of Symptoms in Human Females

From some highly unethical studies conducted on female psychiatric patients in the late 1930s and early 1940s, we know that the human progression of thiamine deficiency does indeed mirror what is illustrated by animal research somewhat. The early symptoms are so benign that most would miss them. Similarly, as the symptoms build over time, although they worsen considerably, they remain more general than specific and might easily be ascribed to other conditions if one were not trained to consider thiamine.

A few notes about the studies. There were three in total, two with four women each and one with 11 women maintained on a diet of .15mg of thiamine per day for 147 days, .45mg of thiamine for 88 days, and 11 women at ~.15 – .2mg thiamine per day plus 1mg of thiamine given intermittently for up to 196 days, respectively. In the third study, where additional thiamine was provided, when averaged, the total thiamine consumed was ~.175mg per 1000 calories of food or .35mg for a 2000 calorie per day diet. Also, in this study, 5 of the 11 women were maintained on the diet for an undisclosed period before resuming a normal diet, while the remaining 6 were kept on the diet for as long as 196 days. This is approximately 30% of the recommended daily allowance needed to stave off deficiency symptoms and syndromes.

Before each study period, the women were provided a normal ‘healthy’ diet for up to 52 days. It is not clear what that constituted. Upon beginning the study, the diets became quite unhealthy, consisting of food products using white flour, sugar, tapioca, corn starch, polished rice, raisins, egg white, cottage cheese, American cream cheese, butter, hydrogenated fat, tea, and cocoa. Additional B vitamins, as well as some fat-soluble vitamins, were provided via supplement, even though thiamine was all but eliminated.

Below is a compilation of the observed symptoms in two of the case descriptions provided.

  • First few weeks: emotional instability, irritability, moodiness, anxiety, agitation, depression, reduced activity, and numerous, often vague, somatic complaints. Weakness and anorexia begin to present.
  • 30 days: anorexia, weight loss, epigastric distress, increasing weakness, periodic vomiting
  • 50 days: nausea and vomiting after meals, progressive weakness from low energy to bedridden, sometimes constipation
  • 70 days: constant nausea, severe weakness, apathy, confusion, numbness, and tingling in extremities
  • 90 days: inability to read or focus, aberrant to absent sensory recognition, tender calves, inability to stand from squatting position, hypoactive Achilles tendon reflex, nausea continues progressing to regular vomiting after meals
  • 110 days: appetite fails, apathy, vagueness and confusion, low blood pressure and heart rate at rest, rapid increase upon ordinary exertion, aberrant and absent sensory perceptions, aberrant and reduced reflexes, reduced flexion of ankles and knees, ataxia, inability to stand on toes.
  • 120 days: impaired pain perception on legs, loss of patellar and Achilles reflex, weakness in abduction, adduction, and flexion of thighs, weakness in the legs with limited ability to extend legs with quadriceps, inability to stand or walk without support, ankle and knee clonus absent, Babinski response absent.

One of these two subjects developed severe neurological defects at 120 days and so the experiment was stopped. The researchers noted that appetite had completely failed and remarked that ‘inanition seemed imminent. They also remarked that with 60-80mg of thiamine given orally and parenterally many, but not all, of the deficits. Appetite returned and strength was regained within the first week, and within 30 days, the less severely ill of the two women was mostly recovered. At 60 days, she was fully recovered. For the other women, recovery was incomplete, even after 120 days of treatment.  Of note, it was the younger and more active woman who suffered the most serious neurological deficits and who was unable to fully recover.

In the 88-day study, the most common and debilitating symptoms included vomiting and subsequent anorexia. The authors note:

We nevertheless are impressed by the degree of debility induced by the isolated withdrawal of thiamine. Fatigue, lassitude, and loss of interest in food developed early and increased progressively as the period of deficiency extended, to the point of intolerance for food. So great was this intolerance that uncontrollable vomiting, even after tube feeding and parenteral injection of solutions of sodium chloride and dextrose, automatically brought the observations to a close.

Also observed in this study, was an association between pre-deficiency energy levels and severity of illness propagated by the deficiency.

The time of development of symptoms and the time of development of severe symptoms differed among the subjects and seemed to be related to physical activity. The subjects who were more active showed symptoms earlier and were more seriously affected later than others who from the beginning were less energetic.

A few additional observations:

  • When thiamine was added intermittently, even though the total levels were still considerably below normal, symptoms improved for a period of a few days to a week. This happened repeatedly. The improvement was so noticeable that some of the women begged to remain on the higher levels of thiamine.
  • Pyruvate and lactic acid levels were higher throughout the period of thiamine deprivation but peaked differentially by individual, by duration of thiamine deficit, and across time, relative to when dextrose was given.
  • Pyruvate and lactic acid levels increased variably after meals and when dextrose was given but returned to the pre-meal/pre-dextrose basal rate within 120 minutes.

Finally, the most notable symptoms in each of the studies involved gastric distress, with vomiting, severe constipation, severe food intolerance, and anorexia. This, of course, was in addition to a decline in energy, polyneuropathy, changes in blood pressure, heart rate, and rhythm, and a decline in cognitive capacity.

So What Does Thiamine Deficiency Look Like?

Everything. And nothing. It is non-specific. It is the sickness behaviors of which Selye writes that underlie all illnesses. Thiamine deficiency looks like every other non-specific illness until it becomes severe enough to approximate some of the more well-recognized aspects of beriberi or WKS. Even in its most severe stages, however, the symptoms could easily be ascribed to other types of illness. Making matters more difficult, unlike the research presented above where thiamine is restricted consistently across time, in modern, developed countries, thiamine is rarely restricted so consistently. Thiamine consumption waxes and wanes across time, as does the demand. It is that mismatch between consumption or availability and needs that initiates the molecular events, deep in the mitochondria where thiamine is critical, that is responsible for the bevy of symptoms attributable to thiamine deficiency. This means that if we rely on the conventional diagnostic parameters, defined generations ago, we are all but guaranteed to miss it. Instead, we ought to be considering thiamine and other nutrient deficiencies in all cases of illness, whatever their manifestation, but that demands an entirely new lens through which to view health and disease; a lens that is quite at odds with the current model of medicine.

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This article was published originally on April 29, 2021. 

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Depression, Anxiety, and the Chronically Hypoxic Brain

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I couldn’t help noticing the Wall Street Journal of Thursday, June 7, in which a column reported a completely unexpected suicide. The title of the column was “Kate Spade’s Family Recounts Her Battle With Depression”. It was reported that “Ms. Spade had suffered from depression and anxiety, and was being treated with medication and therapy. Depression and anxiety disorders occur simultaneously in about 25% of general practice patients. In the abstract, the author says “about 85% of patients with depression have anxiety and 90% of patients with anxiety have depression. Benzodiazepines may help alleviate insomnia and anxiety but not depression”. It must be obvious that the general impression is that these are two different expressions of psychological disarray that require different drugs to treat them. Evidently, Ms. Spade had left a suicide note indicating that she had been under mental stress from her marriage. There were other stresses reported. She had been living separately from her husband for 10 months and had been seeking help for the past five years.

The incongruity requires explanation. Here was a 55-year-old woman who was highly successful in the eyes of the world and her suicide appears to be completely incongruous, as indeed most suicides are. There should be a logical explanation for such an anachronism. The instinct for life is incredibly strong for us and indeed for all creatures in the animal kingdom. I offer my explanation here, based on the contention that the human brain is an electrochemical machine and that its functions are highly dependent on an adequate supply of energy. This does not take into account the concept of a soul that must remain one of the great mysteries of life.

Revisiting Freud: The Ego and the Id

According to Sigmund Freud, the id is the subconscious mind supervised by the ego and what he called the super-ego. All are built upon the presupposed existence of conscious and unconscious thoughts. Modern research has failed to find individual areas in the human brain dealing with the control of specific action. Its function is now regarded as an integrated organ, all parts of which share that action. However, much of this activity is entirely automatic and below conscious level. All brains in higher members of the animal kingdom are built on the same anatomical principle, presumably reflecting a “oneness” in design. If we are to accept evolution as the driving force, the brain of each animal has been developed to service that animal in its natural niche. The niche of Homo sapiens appears to be that of the dominant species and it has evolved from a more primitive state to a more sophisticated one, gradually introducing increased complexity. Brain action would be expected to become more and more sophisticated over time, perhaps making us more cooperative.

We have no idea what is in store for us with continued evolution, but it has long seemed to me that we are still relatively primitive at the philosophical level. Under stressful conditions, the actions of the human brain are much less predictable. However we consider the distribution of brain function, it is an electrochemical machine and a great deal of its activity is unconscious and purely automatic. Body organs signal the brain that then gives instructions to them via the autonomic and endocrine systems. It is therefore convenient to accept the ego and the id, each with its separate functions, however, they are controlled, by the conscious and unconscious mind. Some of the net behavior might be perceived as actions of the automatic component, governed and permitted by the conscious component. It has been suggested that human beings are built as “mean fighting machines equipped for self-interest”.

The Nervous System

Many posts on this website describe the difference between the so-called voluntary and the autonomic nervous systems. The term “voluntary” indicates that we can think and move at will and its actions are dictated by the conscious mind. The autonomic nervous system is almost completely automatic and governs many purely reflex actions, the fight-or-flight reflex being the best known. Hunger and thirst are self-preservatives. The sex drive preserves the continued existence of the species. Yes, these reflexes give us a sense of pleasure, which is the driving incentive and the brain provides us with sensory mechanisms that provide that pleasure. Everything is tied together by a complex code known as DNA, whose individual characteristics describe the physical profile and personality of each animal including humans. From a purely philosophical point of view, it calls into question whether we truly have free will or whether we are programmed by the environment in which we find ourselves. If all components fit together as designed, we can say that the “blueprint” for each person dictates the nature of the personality and reflects his/her mental and physical health. Our training to meet life starts in infancy and is in the hands of parents.

Of Stress and Stressors

Stress is a physical or mental event to which each of us has to adapt. As I have mentioned in other posts on this website, a Canadian researcher by the name of Hans Selye studied the effect of physical stress in animals for many years. He came to the conclusion that virtually any form of stress demanded an increase in the supply of cellular energy, much like the engine of a car climbing a hill. A stressed animal had to adapt to the injuries applied by Selye. He called it the “General Adaptation Syndrome”. He used many different methods to induce stress because he wondered whether there were different responses, depending on the nature of the stressor. He found that the stress response was uniformly identical across species and was able to divide the General Adaptation Syndrome into several predictable phases, each of which was repeatable in each experiment. Not surprisingly, his studies included an array of sequential biochemical changes in the body fluids. I found these changes to be similar to the laboratory changes seen in chronically sick patients. One of his students was able to produce the syndrome by first making the animal deficient in the vitamin thiamine, thus supporting the role of energy deficiency as the causative factor. Selye suggested that human health broke down as a result of energy failure, particularly in the brain, leading to what he called “the diseases of adaptation”. It is probably true that some form of life stress is absolutely necessary for a person to contemplate suicide. Therefore, it seems necessary to discuss the mechanisms by which the brain responds to stress.

The Biological Brain

Whether we like to recognize it or not, the brain is an electrochemical machine whose functions, like any machine, require energy. The fact that the brain requires 20% of the total oxygen inhaled is an absolute indication of its energy requirement. There is much evidence that even a mild reduction influences brain activity and this will be reflected in some kind of change in thought processes and the consequent behavior resulting from it. Nutrition affects mood. A deficiency of many vitamins is associated with psychological symptoms. In some elderly patients, folate deficiency is associated with depression. Iron deficiency is associated with apathy, depression, and rapid fatigue when exercising. In several studies, an improvement in thiamine status was associated with improved mood. One of the major manifestations of obstructive sleep apnea is profound and repeated (episodic) hypoxia (insufficient oxygen) during sleep. This increase in activity in the sympathetic nervous system affects blood pressure. Thiamine deficiency induces gene expression similar to that observed in hypoxia and has been referred to as causing pseudo-hypoxia. Magnesium and thiamine deficiency have both been implicated in depression.

Hypoxia and Pseudohypoxia in Depression and Anxiety

During many years of medical practice, I found that a mild degree of thiamine deficiency was responsible for symptoms that are often regarded as psychological. Chronic anxiety and depression were regularly alleviated by getting people to understand the importance of an appropriate diet, together with the administration of supplementary vitamins, the most important of which were thiamine and magnesium. I could never understand how a patient could be actually blamed for producing symptoms beyond the comprehension of the physician. Abnormal thoughts, emotions, and all forms of mental activity are produced by electrochemical reactions that are exaggerated by a mild degree of hypoxia or pseudo-hypoxia.

Anxiety and depression are perfectly normal emotional reactions but when they are sustained for absolutely no reason, it is because of this biochemically initiated exaggeration. In particular, the sympathetic branch of the autonomic nervous system is easily activated because any degree of oxygen lack is obviously dangerous to the organism and a fight-or-flight reflex reaction would be initiated by the perception of danger. This reflex, because of its nature, might give rise to aggressive behavior when a nursed a grievance explodes into violence. The widespread intake of empty calories, particularly in the form of sugary and fatty substances, is responsible for polysymptomatic disease in millions. Such individuals cannot handle the normal stresses of life and are much more easily imbued with a sense of hopelessness. Suicide seems to be the only option. The idea that dietary excesses might be responsible for depression and suicidal ideation is not a presently acceptable concept, but the biochemical results of alcohol and sugar ingestion are identical in the part of the brain that has to deal with these inbuilt vital reflexes.

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

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This article was published originally on June 20, 2018. 

Rest in peace Derrick Lonsdale, May 2024. 

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Recovering From Medically Induced Chronic Illness

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Recovering from chronic illness

Unexplained or Medically Induced Chronic Illness?

Unexplained. That’s what doctors call chronic illness. Conventional medicine says, ‘learn to live with it.’ Rather than offer a true treatment or cure for these debilitating conditions, they suppress the immune system and offer more drugs for depression and anxiety – none of which are effective. I’m here to tell you that common wisdom is wrong. I know, because my own lucky story proves we can heal from chronic illness. Pharmaceutical insults created my disabling illnesses  – Chronic Fatigue, Fibromyalgia, estrogen dominance, adrenal fatigue, POTS, Graves’ Disease, Hashimoto’s, Bell’s Palsy, infertility and more. I share my journey to offer hope. The doctors were wrong. I have recovered and am once again, healthy.

Early Clues and Pharmaceutical Insults

My childhood had some clues – things I now know predict chronic illness. My lymph glands swelled when I was otherwise healthy. Mosquito bites turned into angry 3” welts. Childhood bunions and hyper-mobile joints suggested leaky gut. All these issues correlate with chronic illness and, seen in hindsight, hint at the difficulties that awaited me in adulthood.

My immune system may have been awry from the start, but pharmaceuticals tipped the scale toward chronic illness. As a teen, I took birth control pills for heavy periods and cramps. When vague symptoms appeared in my early twenties, I asked about pill side effects. The gynecologist laughed at the idea, but I trusted my gut and finally stopped the pill. I felt better in some ways but developed new symptoms.  Sleep became difficult. I was hypersensitive to noise and light and struggled with unquenchable thirst.  The doctor suggested my extreme thirst stemmed from hot weather and salty foods. This explanation didn’t add up to me, but I was young and so was the internet. I had no resources to connect the dots. Today, I recognize that 10 years of hormonal birth control created nutrient deficiencies (folic acid, vitamins B2, B6, B12, C, and E, along with magnesium, selenium and zinc) while also raising my risk for future autoimmune disease.

Recurrent UTIs, Fluoroquinolones, and New Onset Graves’ Disease

A few years later, recurrent urinary tract infections led to many doses of the fluoroquinolone antibiotic, Cipro. Cipro now carries a black box warning and is known to induce mitochondrial damage. My mid twenties also brought pre and post-menstrual spotting and bleeding for 10 days each month. Doctors did nothing for my hormonal imbalance but diagnosed Graves’ disease (hyperthyroidism). Everything about me sped up. Food went right through my system. I was moody. My mind was manic at times. I was unable to rest and yet physically exhausted from a constantly racing heart.

The doctor said Graves’ disease was easy – just destroy the thyroid and take hormone replacement pills for the rest of my life. I didn’t have a medical degree, but this treatment (RAI, radiation to kill the thyroid) just didn’t make sense. Graves’ disease is not thyroid disease. It is autoimmune dysfunction, where antibodies overstimulate a helpless thyroid.

As I studied my options, I learned that RAI could exacerbate autoimmune illness and many patients feel worse after treatment. It was surprising to find that the US was the only Western country to recommend RAI for women of childbearing age. Armed with this knowledge, I declined RAI and opted for medication. The endocrinologist mocked my decision. I was in my 20s and standing up to him was hard, but it marked a turning point and spurred me to take responsibility for my own health, rather than blindly trusting doctors. Recent reports suggest RAI treatment increases future cancer risks. My Graves’ disease eventually stabilized on medication, although I never felt really well. I pushed for answers for my continued illness, but doctors refused to test my sex or adrenal hormones.

IVF and More Damage to My Health

Things turned south again when I was unable to conceive. The supposed best fertility clinic in Washington, DC could not find a cause for my infertility. I’ll save that story for another day, but the short version involved a few years of torment and four failed IVF attempts. The fertility drugs and the stress worsened my overall health considerably.

Our last try at pregnancy was with a specialist who practiced functional medicine. Labs and charting uncovered a clear progesterone imbalance, and also explained my spotting. This simple diagnosis was completely missed by the conventional fertility clinic. A brief trial of progesterone cream resulted in two naturally conceived, healthy pregnancies. Isn’t it remarkable that several years and over $100,000 failed to produce a baby with IVF and $20 of progesterone cream on my wrist did the trick? This could be a cautionary tale about profit motive in modern medicine, but that, too, is a topic for another day.

Years of Conventional Medicine: Thyroid Damage, Autonomic Dysfunction, and Profound Fatigue

I weaned off thyroid medications and felt fairly well after my babies, but my system took a big hit when life brought an international relocation. The move was intensely stressful and my health sunk after we landed half a world away. I had no energy, gained weight, and lived in a fog. The tropical heat and humidity of Southeast Asia felt like a personalized form of torture.

Perhaps the stress of our move left me vulnerable to the reappearance of autoimmune and adrenal dysfunction, as my next diagnosis was Hashimoto’s Disease and adrenal fatigue. Doctors ordered functional medicine tests (hair, organic acids, stool, saliva cortisol and hormones) that identified nutrient imbalances, but their treatment ideas fell short. Despite replacement hormones and supplements by the handful, I remained very sick, with profound exhaustion, brain fog, sleep disruption, pain, and terribly imbalanced sex hormones.

Taking Matters Into My Own Hands

If setbacks have a bright side, it is in the drive to get better. I started studying when my doctors ran out of ideas to treat my illness. Fibromyalgia was the best description of my pain, but I knew conventional medicine offered no help for this condition. I dug into the topic and found the work of Dr. John C. Lowe, who used T3 thyroid hormone for fibromyalgia, and Paul Robinson, creator of CT3M, the circadian method for using T3. CT3M and high daily dose of progesterone cream improved my quality of life in the short term. Near daily bleeding eventually regulated back into a normal cycle and my adrenal function improved greatly.

Postural Orthostatic Tachycardia Syndrome (POTS) was the next bump, bringing a very high heart rate, very low blood pressure, heat intolerance, and extreme sweating on the lightest activity. By this time, I didn’t even ask the doctor for help. My research pointed to salt and potassium, and so I drank the adrenal cocktail and salt water daily. POTS symptoms vanished quickly with this easy strategy, as did the nocturnal polyuria that plagued me for many years.

I steadied after this time. I was not well but functional, despite some major life stressors, including another international move and a child’s health crisis. Even though I managed the daily basics, things like house guests, travel, or anything physically taxing required several days to a week of recuperation.

The Next Step: Addressing Nutrient Deficiencies

The next step in my recovery came thanks to a B12 protocol that includes co-factor nutrients, developed by Dr. Gregory Russell-Jones. Addressing the deficiencies connected to B12 helped and things progressed well until I had a disastrous reaction after eating mussels, which I hoped would raise iron levels. I vomited for hours and stayed in bed for days. I kept up the B12 protocol, but just couldn’t recover. Largely bedridden, and napping 4 hours at a stretch, I got up in the evening only to drive to a restaurant dinner, too exhausted to prepare food or deal with dishes.

Debilitating exhaustion lasted for a month, and then two, with no relief. It was an awful time, but hitting rock bottom proved a blessing in disguise, as desperation turned me back to research. Slowly, I pushed through brain fog and started to review studies on chronic fatigue and fibromyalgia. This led me to a promising Italian study using thiamine for these conditions.

Studying thiamine, it seemed plausible that the allergic reaction to mussels drained my B1 reserves, making it impossible to recover. Inspired by the research, I started on plain B1 at very high doses. To my surprise, I felt better right away. The first dose boosted my energy and mental clarity.

I continued to learn about B1’s benefits, thanks to this website and the text by Drs. Marrs and Lonsdale.  Two weeks went by and thiamine HCL seemed less effective, so I switched to lipothiamine and allithiamine, the forms recommended in Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition. WOW. What a difference! Virtually overnight, my gears began to turn, and I felt better with each new day. In a single month, I went from bedridden to functioning well 2 out of every 3 days. I had ideas, I had energy, and I could DO things. The setback days were mild and disappeared entirely after 2 months on thiamine.

At the 2 month mark, I had to travel for a family emergency. My pre-thiamine self would have needed at least a week of rest following this kind of trip, and I expected pain and fatigue as I stepped off the plane. But to my great surprise, I felt well! I remember walking through the airport late that evening and thinking it felt amazing to stretch my legs. Maybe that sounds like an ordinary feeling, but years of chronic fatigue and fibromyalgia conditioned my body to stop, to sit, whenever possible. It was entirely novel to FEEL GOOD while moving! The next day came and I did not collapse, I did not require days to recover and was able to carry on like a normal person. It was a remarkable change in an unbelievably short time.

Recovery From Conventional Medicine’s Ills Came Down to Thiamine

Getting better feels miraculous, but it’s not. The real credit for my recovery goes to experts like Dr. Marrs and Dr. Lonsdale who spread the word about thiamine. Despite years of illness and dead ends, I believed I could heal and I kept trying. Tenacity eventually paid off when posts on this site helped connect the dots between my symptoms and thiamine deficiency. More than anything, my recovery is a story of tremendous luck, as I finally landed upon the single nutrient my body needed most.

The difference between my “before thiamine” and “after thiamine” self is beyond what I can describe.  Birth control, Cipro, and Lupron created nutrient imbalances and damaged my mitochondria, leading to multiple forms of chronic illness in the years between my 20s and 40s. Replacing thiamine made recovery possible by providing the fuel my damaged cells so badly needed. At this writing, I am 7 months into high dose thiamine and continue to improve. I have not experienced any form of setback, regardless the stressors. My energy feels close to normal, the pain is resolving, and brain fog is a thing of the past. My sense of humor, creativity and mental functioning are all on the upswing. I owe thanks to the real scientists who dare to challenge wrong-headed ideas of conventional medicine, and who provide hope for these so-called hopeless conditions. My wish is that this story will do the same for someone else.

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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.

Yes, I would like to support Hormones Matter. 

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This article was published originally on February 6, 2020. 

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Energy Medicine

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Energy medicine

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.

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Threats to Thiamine Sufficiency in the 21st Century

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challenges to thiamine sufficiency

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 21st 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 21st 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.

Other common dietary contributors to insufficient thiamine.

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.

We Need Your Help

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

Yes, I would like to support Hormones Matter. 

Related posts:

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The Perils of Diagnostic Overshadowing

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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.

diagnostic overshadowing thiamine
July 2025. After two months of thiamine, Lev lifts his head.

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

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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. 

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Virginia Woolf and Me – Moments of Being Misunderstood

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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

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

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