thiamine deficiency Archives

Recovering From Medically Induced Chronic Illness

Published on August 5, 2026

19.1K views

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.

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This article was published originally on February 6, 2020.

SIDS and Vaccination

by Derrick Lonsdale MD, FACN, CNS

Published on July 30, 2026

14.3K views

Posted on Child Health and Safety on January 13, 2015 was an announcement that vaccines had been proven to cause sudden death in children (SIDS). The announcement indicated that death in 67 cases was only explicable as caused by vaccines. Drug safety regulators were said to have had the information for over two years. In this post, I am going to contest vaccination as the sole cause and try to explain why I think it is a much more complex problem.

In 2001, I published a paper that hypothesized the requirement of three variables: Sudden infant death syndrome requires genetic predisposition, some form of stress and marginal malnutrition. I have just published another paper on the same subject: Thiamin and Magnesium Deficiencies: Keys to Disease.

What History Tells Us about SIDS

Back in the seventies, I was working at Cleveland Clinic in Cleveland Ohio in the Department of Pediatrics. At that time there was a great deal of professional interest in SIDS. In the course of my research, I had found a paper written in a prestigious medical journal in 1944 by a British Medical Officer of Health by the name of Lydia Fehily. Readers will remember that Hong Kong was then a British protectorate and Fehily was sent out from England in order to investigate a common form of sudden death in breast fed infants of Chinese mothers in the colony.

A little bit of history is important to the final solution. Before World War II, the Japanese had invaded China. The rice ration was cut to starvation levels, thus cutting down the calorie intake. Although the symptoms of starvation prevailed in the mothers and the infants, the sudden infant death had disappeared. After the Japanese were driven out, the pregnant mothers in Hong Kong had as much rice as they wished. The calorie intake had been restored, overwhelming the required concentration of vitamin B1 for adequate oxidation of the calories. The sudden death in the breast fed infants immediately reappeared.

Fehily had discovered that the reemergence of SIDS was due to infantile beriberi because the infants were fed by vitamin B1 deficient breast milk (Human milk intoxication due to B1 avitaminosis). Those affected were almost always regarded by their mothers as the healthiest appearing infants in the family prior to their death. These events were rare under two months and after six months of age. It occurred almost always at night, was often associated with a runny nose interpreted as a mild cold and was more common in winter months. The epidemiology of this is almost exactly like that of modern SIDS. Although the modern interpretation is related to the positioning of the infant in the crib, it is certainly not the whole story. I came across the report of a meeting of beriberi researchers held at that time. A statement in that report had said that:

any sudden otherwise inexplicable infancy death is a guarantee of infantile beriberi. No other disease has a similar outcome.

Predicting SIDS

During the early part of the seventies it was thought that SIDS could not be predicted, that there were no symptoms to provide a warning. Later on in the decade, it was shown that there was such a thing as “threatened SIDS” judged by a few non-specific symptoms. Coincidentally, an alarm system had been invented that an infant could wear in the crib. It indicated when breathing stopped for a given interval or when the heart slowed. If and when such a thing happened, it was very easy to resuscitate the infant by a simple slap on the buttock.

SIDS, Thiamine and Brain Development

I began to admit infants with this kind of history to the hospital and place them on an alarm system. Believe it or not, by giving thiamine by injection to these infants, the alarms ceased to be initiated. I found this to be very exciting and I continued my research. I even went to Australia to do sabbatical research with the late Dr. Read at the University of Sydney who had evidence of implication of thiamine metabolism in SIDS. I found that there were families where SIDS had been occurring in more than one related infant. There was no pattern that indicated a direct genetically determined outcome and I concluded that it was a genetic risk rather than a genetically determined disease.

The overall logical conclusion to this series of facts was as follows:

That genetic risk implied an unusually well developed brain that required a great deal of energy to function. The only means by which this could be acquired was through pristine nutrition for the mother during pregnancy.
That calories from simple carbohydrate with insufficient thiamine was extremely dangerous. (Note that rice rationing had stopped the infancy deaths in Hong Kong). The brain of an infant in the first six months of life grows at a tremendous rate and the oxidation of glucose to provide the required energy is crucial. Vitamin B1 is essential to that oxidation. This had been shown by Dr. Peters in Cambridge, England as early as 1936.
That some form of stress may or may not be necessary, depending on the state of biochemistry in the brain. The infant is already at risk at birth because of the nature of nutrition supplied by the mother during pregnancy. A state of marginal malnutrition in the infant is insufficient to meet the energy demands of adapting to the vaccination as a stress factor.

Readers of this website may or may not be aware of a series of posts on the relationship of post Gardasil postural orthostatic tachycardia syndrome (POTS) with thiamine deficiency. I believe that this post on SIDS bears comparison with the logical reasoning applied in that post. Also, Dr. Marrs has repeatedly pointed out the relationship between drugs and seemingly unrelated disease caused by them.

Does Thiamine Deficiency Underlie Post Vaccination SIDS?

The epidemiology (study of cause) of infantile beriberi (vitamin B1 deficiency) is sudden death. The commonest time for this is between three and four months and more commonly in male infants. Although this is almost the exact epidemiology of modern SIDS, this well researched truth is ignored. The classical vitamin deficiency diseases (beriberi, pellagra, scurvy) are considered to be of only historical interest because vitamin enrichment of foods has abolished them. This is simply not true. A high intake of sugar in the form of simple carbohydrate, empty calories is widespread in America and other Westernized countries, automatically overwhelming the insufficient concentration of vitamin B1, the equivalent of a choked engine in a car. “Soft” drinks are all too well advertised and encouraged in opposition to the consumption of “hard” alcohol that is regarded as more dangerous. Although the dangers of alcohol are well known, the danger of “soft” and “Diet” drinks, particularly during pregnancy, is almost totally unknown to consumers who erroneously believe they are preventing weight gain and contributing to personal health. The advertising is misleading.

Looking again at history, we also know that the very first symptoms of beriberi could occur in a group of patients when exposed to sunlight. We now know that ultra violet light is very stressful to the human body, demanding an adaptive “stress” response that is automatically initiated by the lower part of the brain, the limbic system and brainstem. The word “stress” must be used in its proper connotation. It must be defined as a mental or physical force to which we have to adapt. For an infant, stress would include weather changes, infection, trauma, vaccination, partial suffocation from being placed in the prone position, inhalation of chemicals in the crib mattress and other possible variables. This part of the brain is particularly sensitive to thiamine deficiency, diminishing the supply of energy required by the cells in order to perform this complicated adaptive process.

We live in a hostile environment to which we have to adapt automatically 24 hours a day by brain/body mechanisms initiated by the lower brain. Damaging the brainstem affects the nervous control of automatic breathing and control of heart rhythm. Thus, breathing or heart beat may cease in an infant during sleep when thiamine deficiency prevails. During the first six months of life brain growth is tremendously fast, requiring an enormous amount of energy. I am proposing that the infant with the highest, genetically determined brain energy requirement is more at risk. If this is true, the tragedy of SIDS may be removing the most superior future citizens. Obviously, the mother’s diet must provide a proper balance between the calories that provide the fuel and the capacity of the cell to burn the calories by means of the appropriate vitamins. Because we now know that sufficient thiamine or vitamin B1 is critical to prevent beriberi and I have published evidence for deficiency of this vitamin in threatened SIDS, it makes sense to consider the interplay of three variables in SIDS. The three variables are as follows:

Genetic risk, “e.g. a high brain energy requirement”
A non specific stress factor, “e.g. vaccination”
Marginal high carbohydrate calorie malnutrition

It also makes sense to consider the possibility that the stress of vaccinations is too great a risk for infants who are genetically and/or environmentally predisposed to oxidative damage in the brainstem.

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

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This article was published originally on Hormones Matter on January 21, 2015.

Rest in peace Derrick Lonsdale, May 2024.

Diet Induced Pseudo-Hypoxia and Hypertension

by Derrick Lonsdale MD, FACN, CNS

Published on July 1, 2026

14.7K views

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

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

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

Understanding the Autonomic Nervous System

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

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

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

Chronic Activation of the Sympathetic Nervous System

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

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

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

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

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

Hypothesis: High Calorie Malnutrition Induces Chronic Sympathetic Overdrive

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

Spontaneously Hypertensive Rats

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

Conclusion: Diet Matters

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

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

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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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Panic Attacks or Thiamine Deficiency?

by Madalin Ispas

Published on June 18, 2026

2.1K views

As far back as 2022, I would get tingling and numbness in my arms. After eating I would get so tired that I couldn’t think or do anything. I would just stay in my seat like a zombie until it was time to go home. When I got home, I would sleep for an hour or two and then recover. This was in addition to the more than 8 hours of sleep a night. Even with all of that sleep, I could barely crawl out of my bed to get to work. I was always so tired.

In 2023, when I worked out, I had to take 10 minutes pauses between sets. I was completely drained. Eventually, it got so bad that I could no longer workout. After about 6 months, my body decided enough was enough and I was hit with 3 days where I couldn’t get up from my bed. My muscles ached painfully and I felt incredibly sick. Eventually, I recovered though.

Fast forward to 2024 and everything took a turn for the worse. After a stomach bug, I developed IBS and SIBO. Out of nowhere, I started waking up in the middle of the night with insane panic attacks. My heart would pound all the time and my nervous system was stuck in fight or flight 24/7. I could only sleep 3-4 hours a night for many months. I had a lot of blood tests done, including all the vitamins, but they were serum, and I know now they were worthless. Everything came back normal except vitamin D which was low, so I started supplementing and staying in the sun. After a couple of months, somehow I recovered again and I thought that was it, the vitamin D was the culprit and I had solved it.

Surprisingly, for most of 2025 I was fine, in the sense that I didn’t have critical symptoms like before, except, there were times I would get so tired that I couldn’t think or do anything but sleep and my body felt incredibly heavy. Since I would recover quickly, I thought nothing of it. Also, during this time, I would wake up in the middle of the night, feeling extremely hot, and being irritable in a way that it not like myself. After about 20-30 minutes I would get really cold and instantly fall asleep again. This happened every night for many months. I would also be either extremely anxious or extremely tired during the day, alternating.

Persistent Tachycardia Considered Panic Attack

In 2026, I decided to start working out again. I managed to do so for 3 months before an array of symptoms, the likes that I never thought I could experience, began. They began with me being so tired that I almost fell asleep at the wheel. Then I would get home and instantly fall asleep from early in the day, until the next day. This lasted for about two weeks. After this, the panic attacks started. One night I woke up around 1 am in a full blown panic attack thinking I was going to die. I knew how to deal even with the worst panic attacks previous experience. I would just go out for a walk, and so I did that this time too. I walked for two hours but this panic attack was like nothing I experienced before. It didn’t stop. Eventually I ended up in the ER. I stayed there for 9h, during which time my resting heart rate did not come under 100bpm, and with the slightest movement it would jump to 140-150, even while laying down.

By morning this worried the ER doctor but the cardiologist that checked on me, and couldn’t find anything wrong after a whole bunch of tests. Even so, they kept me in the hospital for a few days for monitoring. Having similar experiences in 2024, where I was told by everyone that it was just anxiety and all in my head, I accepted it.

They gave me some pills to slow my heart rate down and I was discharged. That day, after more than 14 hours of non-stop tachycardia, my heart eventually slowed down. This was just the beginning of my declining health though. My sleep became restless and my heart felt like it was beating out of my chest for hours on end, again.

Since I went through something like this in 2024, I brushed it off to anxiety. I just tried to live my life and not think about it too much, but the symptoms persisted and diversified. I experienced frequent panic attacks that would wake me up from sleep. Sometimes, I would lay there in bed feeling a huge weight on my chest, unable to breathe properly. Other times, I would wake up and feel my muscles aching, heart pounding, and be so utterly tired that I just couldn’t move, no matter how much I wanted to. During that period, even minimal exertion would tire me very quickly.

Relentless Heart Palpitations, Insomnia, and Breathing Difficulties

On top of that, the insomnia and the feeling that my heart was pounding out of my chest was relentless, every night and day just non-stop. At one point, I was hit with a wave of tiredness like I had never felt before. I just couldn’t move. I couldn’t think and my heart was beating out of my chest and extremely fast. I was taking shallow and slow breaths and it felt like I was running out of oxygen. I thought I was dying and yet I was so tired that I couldn’t even call the ambulance. I couldn’t move at all. After about an hour, the episode resolved by itself, with me being completely normal.

In the same time period, I had two weeks in which my heart rate wouldn’t come down from 100, along with hours and hours of adrenaline surges, heat flashes, arrhythmias, and one episode in which my heart beat so fast that I was sure it was a medical emergency. My parents convinced me it was all in my head and so I just waited it out. Eventually it stopped, and I was so utterly tired that I simply passed out. I couldn’t stay awake anymore. This happened more times than I can remember: the utter tiredness, where I couldn’t think, move or do anything, but just lay there and watch it. It happened around friends, family, by myself, at random times.

Another time when I ended up in the ER because I felt my heart beating out of my chest, and my BP reader kept throwing errors when I tried to take my blood pressure, the doctor that listened to my heart was visibly worried, gave me a beta blocker which didn’t do much, and moved me from minor emergencies to major ones. Unfortunately, the doctor in charge of the major emergencies wasn’t so caring. He asked what I was doing there and said that I was wasting his time and released me. I went home with my heart beating out of my chest constantly, even while trying to sleep. I had many such episodes when I would wake up from dead sleep with my heart beating out of my chest, sometimes in a panic attack, sometimes not. Honestly, these episodes made me want to go to the ER each time, but I just tried to tell myself it was anxiety, because everyone was telling me that.

Of course all these symptoms made me seek many doctors and do a bunch of tests. As of now, I have been checked by four cardiologists, all of whom cleared me. I have had two thyroid panels, with autoimmunity and everything else, and they came back normal. I had a pheochromocytoma metanephrines test, all normal. During these episodes, my hands would tingle and so I checked Hb1ac. It was normal too. I only have slight insulin resistance because my glucose came at 99 fasting one time and 84 another. My insulin was 15 I think. Considering that I have been in a constant state of fight or fight for more than 3 months now, I think those results are pretty good. Really, the only thing besides the insulin resistance that came slightly elevated was my RBC which was 17.3.

All the doctors tell me that my symptoms are ‘all in my head’ and send me to psychiatry. I’m now tapering off the paroxetine that was prescribed, since it’s not helping at all. I never liked psychiatric medication. I only accepted to take it now because I was desperate.

A Horrible Diet

As a kid I used to eat a lot of candy and pizza. I lived off of breakfast cereals, pizza, and bread with ketchup; anything except natural foods. Honestly, I’m surprised I did not have health issues sooner. I am 29 years old now, and although I cleaned up my diet a bit over the years, maturing over the years, I still ate a lot of fast food.

What really tipped the scales was the SIBO. In the last 6 months leading up to all this, I craved carbs, and I ate a lot of them. Even if I wasn’t eating fast food all the time, white rice and potatoes were staples. I ate very little protein because it didn’t appeal to me anymore. With working out, I thought it was even more important to eat more carbs for energy. I did not understand why I would get so tired, to the point of not being able to continue, after 20-30 minutes, while my friends could do hours-long workouts. I couldn’t understand how they could have that much energy. I figured that was just the way I was built. I never considered diet.

Discovering Thiamine and Other Nutrients

More recently, I have learned about vitamin deficiencies, especially vitamins B1 and B12. Given my diet, I think these may be at the root of all of my symptoms. There may be additional deficiencies, but these two seem to fit. A few weeks ago, I began supplementing with vitamins B12 and B1 (100 mg thiamine HCL), a multivitamin, and 200mg magnesium daily.

Surprisingly, ever since starting the thiamine, I have noticed that my heart recovers much faster. Where I used to wake up before with it pounding for hours on end, now it only pounds a few seconds then stops. I am still in an almost constant fight or flight state but it doesn’t go crazy like before. My heart used to fluctuate wildly. It could 80 one moment, 97 the next and so on. This could go on for hours. Now, even if I have the surges, they are somewhat milder and don’t last as long.

Also, over these past two weeks, I have had days where I slowly recovered to feeling almost normal, in the sense that I wasn’t in constant fight or flight anymore, but then I would crash back to being exactly like before. It gives me hope that I might be on the right track, but the crashes are discouraging. Also, supplementing B1 seems to have fixed my IBS and SIBO. This is something I have been suffering with for more than two years and had tried everything to heal.

I have only been taking the thiamine for few weeks and I know that it is very little in the grand scheme of things but things seem to be improving slowly. I haven’t seen this pattern of recovery in the cases I have read. A lot of people seem to get a paradox reaction initially. I did not have that experience. I seem to get better and then backtrack again. Has anyone else experienced this pattern?

Also, I haven’t read any case stories where the person experienced adrenaline attacks that lasted hours and hours on end like I have. This is what made me think of pheochromocytoma initially. Maybe it was thiamine though. Does anyone have any insight on this?

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Eosinophilic Esophagitis May Be a Sugar Sensitive Disease

by Derrick Lonsdale MD, FACN, CNS

Published on June 16, 2026

67.2K views

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

Eosinophilic Esophagitis: Inflammation of the Esophagus

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

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

A Complex Medical History Misdiagnosed As Psychosomatic

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

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

A Family History of Alcoholism and Thiamine Metabolism

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

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

Dysautonomia

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

Conclusion: Inflammation Is a Defensive Response

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

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

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

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This article was published originally on February 8, 2016.

Rest in peace Derrick Lonsdale, May 2024.

Lab Mice Get More Thiamine Than We Do

by Chandler Marrs, PhD

Published on June 9, 2026

1.8K views

How much of our understanding of molecular mechanisms related to mitochondrial energy metabolism is wrong because the chow fed to the mice and rats used for this research is heavily supplemented with vitamins and minerals at quantities exceeding that of an equivalent human diet? I have been pondering this question for a few years now, but this morning the magnitude of the problem became clear when the pathway I had been studying was viewed positively when (hyper) activated in rodent research, but one that was clearly not so in humans. This is a pathway for which drugs had been designed to activate based upon the patterns identified in said research; research where the animals are fed a steady diet containing markedly higher concentrations of vitamins and minerals than humans will ever get, unless supplementing, and where the animals are sheltered from the bevy chemical stressors that deplete those same nutrients. So, on top of all of the other challenges associated with extrapolating data from animal research to humans, deriving data about the ‘normal’ behavior of molecular pathways that are incredibly sensitive to nutrient status and chemical exposures from well fed and environmentally isolated animals is extraordinarily problematic.

An Eye Opening Experience

As someone not trained in animal research, I never considered chow composition as influencing variable on all research. Sure, if the research question involved diet or nutrients specifically, the composition of the chow would obviously affect outcomes, but that there were would such stark differences in relative micronutrient content compared to humans is something I had not contemplated. A few years ago, however, I worked briefly with a foundation sponsoring some research into the various effects of thiamine supplementation on health. One series of investigations looked into genetic and metabolomic changes, along with variety of cognitive and behavioral measures, relative to a diet high in soybean oil, with and without thiamine supplementation. Since the foundation disbanded and the funding was cut, except for a few posters and abstracts, the results were never published. It was disappointing, because the results were remarkably enlightening – despite the issues with the chow.

That said, what struck me early on was the high intake of thiamine even in the control mice. In this particular set of experiments, the control mice were getting ~2.5mg/kg of bodyweight, while the mice in the two experimental ‘high thiamine’ groups were getting 51 and 102 mg/kg of bodyweight. This is an insane amount thiamine, even in the control group. By comparison, the average human eating a lot of processed and fortified foods, which is never a good idea, may get up to 4mg per day total and a large majority Americans get less than recommended daily allowance (RDA) of 1.1-1.2 mg/d. If he/she weighs 70kg that works out to between .02mg/kg and .06mg/kg daily – a minute fraction of what a lab mouse is given.

Why such a high intake of thiamine? It was explained to me that mice need more thiamine because they have a higher metabolism than humans.

Okay. Sure. But…

This never sat right with me, but not having the experience lab animals, I let drop and moved on. And then I began studying some molecular pathways that just happened to be influenced by thiamine and it occurred to me that conclusions drawn may not accurately reflect the true behavior of those pathways because of the chow fed to these animals. I began digging, and oh, what a mess this is. Not only do most of the published studies not list the vitamin concentrations in the particular chow used and make the assumption that all them contain equivalent amounts, they do not, but some may misinterpret the metrics. Most chow labels report nutrient doses in mg/kg of diet consumed by the animal. I suspect, in some studies they are using, or at least reporting, mg/kg of the animal’s body weight. Is the animal really consuming 5mg/kg of body weight or 5mg/kg of food? It is not always clear. Alternatively, other studies, including the one I reviewed for the foundation, scale the doses between the species using a multiple of 12. Apparently, this is to account for differences in body surface area. It is based upon the presumed rate of which organisms convert food into energy (heat dissipation) and it relies heavily on measures of body mass relative to caloric intake such that while larger animals consume more calories, their ‘metabolism’ by unit of mass is lower. This is a linear metric developed to estimate drug toxicity and may not accord with nutrient needs. Importantly, kcal burn and body mass are poor indicators of metabolic energy (here, here, here).

Reviewing methods sections from random studies that I have reported on in the past, there is no way to tell how much thiamine or other nutrients the animals actually consumed, unless the study was specifically designed to assess something related to thiamine. Even then, however, most studies assessing thiamine deficiency experimentally either use diets that include no thiamine and/or induce deficiency by administering anti-thiamine molecules like oxythiamine or pyrithiamine. That said, whatever the actual amount, even at the lowest possible intakes to prevent deficiency, the animals were consuming far more than a human would consume, and this is what troubles me most. Do lab rodents really require more thiamine than humans or have we simply underestimated human requirements? I believe it is the latter, but let us explore the basis for this argument before drawing conclusions.

Thiamine Requirements For Mice

According to the literature, the daily thiamine requirement for mice used experimentally ranges from ~2ug of thiamine per day up to 6ug per day. This does not sound like much unless we consider that mice weigh only about 25g. This means that a lab mouse gets at least somewhere between .08 -.48 mg/kg. In a 70kg human, this equals 5.6 – 33 mg daily. The human RDA or DRI (daily reference intake) is only 1.1-1.2 for women and men respectively, per day, and accumulating research shows that many people do not even get that much. Nevertheless, by these metrics, the lab mouse is getting 5 -~30x the amount of what is considered necessary for the average human, and as was illustrated previously, if other metrics are used, these animals get even more thiamine.

This begs the question, how are we calculating the metabolic needs of these animals such that they require more nutrients than we do? It turns out that, like anything, the answer depends upon what assumptions we make and how we factor those assumptions into the math we create to estimate those values. As I mentioned previously, the research I reviewed was using a drug toxicity metric that included surface area differences to calculate dosages between humans and mice. This, apparently, is a common metric. Others include different allometric variables like bodyweight and/or caloric intake to calculate metabolism. All of these are linear calculations where the change in one variable is assumed to perfectly and linearly correspond to the other. Biology is not linear, and at some point researchers recognized this and began multiplying the exponents of the body surface area. Needless to say, multiplying by different exponents changes the result dramatically. Whether it changed its accuracy, however, is questionable.

Just How Much Does Nutrient Intake Vary?

Per a review of such things, rodents get between .2 -.26ug of thiamine daily with three different chow formulas. The human equivalent dose (HED) for these values ranges anywhere from 2.8 mg/d to 69 mg/d depending upon which variables are included in the calculations.

For example, if the calculation considers kcal required per day to maintain function (a 25g mouse requires 15kcal daily, while a 70 kg human requires 2000 kcal per day), the human equivalent for daily thiamine intake would be from 2.8-3.3 mg – double and triple the current RDA/DRI. In contrast, if the calculation uses body weight as the key variable, the human equivalent would be 56-69mg per day, or more, as bodyweight increases. This is ~50x more than current RDA/DRI values.

Conversely, if we run the math backwards, the 1.2 mg per day thought to be acceptable male humans weighing 70kg equals only .017mg/kg or .0004mg per day total – clearly below the intake of the chow fed lab mouse (likely below that of the wild mouse), but also, well below what is required prevent deficiency in the mouse. Although I am focusing on thiamine, because that is what I know best, the issues with scaling dosages between mice and humans carries the same problems for each of the micronutrients.

…extrapolations of nutrients from mice to humans overestimate the nutrient intake for a human, while scaling for humans to mice would underestimate nutrient intakes for a mouse and theoretically result in nutrient deficiencies.

I will ask the question again: are we really overestimating nutrient doses when scaling from mice to humans or have we fundamentally underestimated the nutrient requirements of humans all along?

The Development of Human Nutrient Requirements

The nutrient estimates of humans to which all animal research is compared is equally flawed but for entirely different reasons than those of animal estimates. Not only was metabolism not considered as variable in human dosing, and is thus not scalable in either men or women of difference sizes or from humans to mice or any other species, but our assumptions regarding the accuracy allometric models of metabolism are likely incorrect as well.

Nutrient requirements for humans were developed using food surveys of different populations. From the average caloric intake of an average man (70kg), thiamine and micronutrient consumption more generally, were estimated. Adequacy was determined purely upon the absences of observable symptoms of deficiency. A number just above the point at which deficiency symptoms were observable became the recommended daily dose. Doses for women and for pregnancy were largely guestimates based upon presumed differences between male and female size, activity levels, and calorie consumption.

There was never a mg/kg dosing strategy developed for micronutrients for humans, so there is no ability to scale relative to bodyweight, caloric intake, or surface area, as there is with lab animals. Neither were there ever any attempts to calculate the actual metabolic rates relative to micronutrient needs, then or since. The human micronutrient standards were developed based entirely on observational data and the absence of deficiency symptoms. Like many accepted medical truths, there was no math, just observation, some contention, but ultimately, consensus, and eventually, entrenchment – even when data suggested otherwise. Notably, there have been no changes to the RDA/DRI for thiamine for over 80 years.

That said, how do we really know if the thiamine requirements for humans are less than that of rodents? Could the recommended dose in humans, which causes deficiency in mice, also be causing deficiency in humans but the complexity of our biology and variability of our environment, paired with the longevity differences between the species, mask that deficiency – sometimes indefinitely? Possibly.

A Question of Metabolism

And then there is this: how do we really now that mice have a higher metabolic rate than humans? We don’t, and that is the other problem with scaling micronutrient needs between rodents and humans. We simply have no logical basis upon which to make these calculations. Certainly bodyweight, surface area and caloric intake differences are important, but those variables do not, in any way, address the fundamental question about metabolism, which is energy used. Energy is the basis for metabolism. Energy usage should be in the calculations we use to estimate nutrient requirements and it is not.

In study published in 2024, researchers did something almost heretical – they added energy variables to metabolic calculations and standardized for body mass, fat free mass, and environmental temperature to more appropriately estimate the energetic needs of rodents, versus other animals, versus humans. In doing so, they were able to calculate expenditures with a common metric that could compared across species: megajoules per day (MJ/d). From there, they calculated total energetic expenditure (TEE), resting energetic expenditure (REE) and active energetic expenditure (AEE).

By these estimates, humans have higher metabolic demands than rodents (and many other animals including apes). Per their research, the TEE of humans globally was ~27% greater than that of rodents. In the US, where the population is largely sedentary and overweight, TEE for humans was still 18% higher than that of rodents. While the AEE are largely the same between rodents and humans (~1% difference), the differences in resting metabolic needs are huge. Humans require 40-45% more energy at rest (US and global, respectively) than rodents.

Per the authors of the study, humans evolved to be an ‘energetically extravagant species’ due in part to our larger brains, which consume an awful lot of energy, even when we do not use them. None of the previous studies considered this variable (or several others) when calculating the presumed metabolic differences between the species.

If humans do indeed have higher metabolic needs than rodents, then shouldn’t we also need comparably higher micronutrient intakes to sustain optimal energetic capacity?

Comparing Well Nourished Mice to Malnourished Humans

To the original question that sent me down this rabbit hole, how do we know what we think we know about the activity of different nutrient- sensitive and nutrient – dependent proteins, either in isolation or within a pathway, when we study those proteins in animals that are very well nourished and the species to which we are extrapolating those findings is most decidedly not? And a question that I did not address, how do we know what we think we know when the study animals are never exposed to the bevy of nutrient depleting chemicals that the human is exposed to? We do not, and that is the problem.

This means that all of the conclusions I (and others) have drawn based upon animal research, where the animals receive far and above the nutrients that a human might, are likely skewed, if not entirely incorrect. That is a sobering realization, particularly when one considers all of the other problems associated with extrapolating data from lab animals to humans. Moreover, this is yet another reason why humans need more thiamine and other nutrients than are currently recommended by governmental entities.

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Beriberi is Alive and Well in America

by Derrick Lonsdale MD, FACN, CNS

Published on May 28, 2026

24.8K views

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

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

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

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

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

Additional Cases of Thiamine Deficiency

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

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

Ondine’s Curse

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

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

The Complexity of Treating Vitamin Deficiencies

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

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

Common Presentations of Thiamine Deficiency: The Walking Sick

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

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

We Need Your Help

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

Yes, I would like to support Hormones Matter.

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

This article was published originally on April 11, 2019.

Rest in peace Derrick Lonsdale, May 2024.

An Over Medicated and Chronically Ill Millennial

by Jeff Mitchell

Published on May 19, 2026

12K views

over medicated millennials benzodiazepine

Frequent Infections, Antibiotics, and Asthma

As I’ve reflected on my current health challenges, I’ve come to the realization that I need to head back in time to my earliest years. Like many kids born in the early 90s, I was the first to receive a slew of vaccinations that were previously never given to children. I suffered from frequent “earaches” that led to multiple courses of antibiotics before kindergarten, and by the time I reached middle school, I was taking yearly courses of antibiotics for all sorts of things: colds, sinus infections, acne. It was around this time that I was also diagnosed with exercise induced asthma. I remember almost passing out in a lacrosse practice in 7th grade, and before I knew it, I was put on Advair (daily inhaled steroid) and was hitting the albuterol 2 or 3 times before a workout. My allergies also raged during this time.

Anxiety and Doctor Prescribed Benzodiazepine

I started getting increasingly anxious in early high school. I remember getting what I now know are symptoms of a panic attack in late middle school. Though part of this was due to the fact that I was hiding my sexuality (and hiding it well), I also realize that I had been slamming my adolescent body with drugs, vaccinations and the standard high sugar American diet for 14 years at that point.

My anxiety caused sleeping issues and I was placed on Ambien when I was 16. When I was withdrawn from that, the anxiety got worse (I know now it was Ambien withdrawal), and I was finally sent over to a psychiatrist. After listening to my description of panic attacks, she placed me on Klonopin, one of the most potent benzodiazepines on the market that should never be used for more than a few weeks. She told me to take up to four a day (an insane dose) and that like a diabetic, I needed GABA enhancement, and I would have to take these for the rest of my life.

At 17, I was buzzing on a benzodiazepine every day. I remember that it actually felt quite good and erased all worry. But then I began to experience one of the most terrifying side effects of long-term benzodiazepine dependence: I was getting dementia! I couldn’t remember things for tests or quizzes no matter how hard I studied. When I brought this up to the psychiatrist, she assured me that a little amnesia was a common benzodiazepine side effect, but that the benefits outweighed this. Essentially, giving a teenager dementia outweighed him having anxiety.

Benzodiazepine Withdrawal and Repeat Concussions

When I decided I needed to come off the benzodiazepine after taking it for a year, her instructions were to taper over one week and then jump. Now, this was 2010, and the internet was alive and well at that point. Upon doing just a little bit of research, I knew this woman was insane. All recommendations were that benzodiazepines needed to be tapered over the course of many weeks if not many months. I found a benzo support group online that became my lifeline for the next 4 months as I gradually weaned myself off the drug with the support of my parents and a new primary care doctor. Throughout this time, the one drug that I actually credit with saving me is marijuana. Without it, I’m not sure I would have done as well as I did getting off the drugs and then staying off of them.

I went right off to college that fall, which in retrospect was a miracle. I struggled a lot that first year. I was experiencing post acute withdrawal syndrome (PAWS) from the benzodiazepine and almost flunked out. I gradually improved but was still dependent on nightly marijuana to go to bed. In 2014, I finally stopped smoking weed and was 100% drug free.

That summer, I ended up getting my first concussion, though I suspect I had many others growing up as I played soccer and lacrosse. As if one wasn’t bad enough, I somehow ended up getting another the next summer in 2015 when I was at the beach and hit my head on a car door. I was later told by a neurologist that once you have a concussion, it becomes significantly easier to get a second, and then a third, and so on.

I had long suffered minor symptoms from benzodiazepine withdrawal that never went away, like tinnitus in my ears, an inability to take GABA drugs without reactivating withdrawal symptoms, and other neurologic symptoms that always made me feel “different.” The concussions added to this complex situation and I would have what I can only describe as seizures during times of stress or intense workout. It felt like my brain had electric current running through it.

Around this time, I also received the first injection for the Gardasil vaccine. I never followed up with the rest of them because of how off I felt that the first few days after getting it. Only recently have I learned about the severe damage that Gardasil can cause.

By 2016, I had been doing a paleo/plant-based diet and felt generally well, but the symptoms from both benzo withdrawal and my concussions persisted. In 2017, I started using CBD oil, and I found that it relieved a lot of the symptoms. It calmed my brain down significantly. I also began using Truvada (HIV medication) during this time as PreP. The one issue that never went away throughout all of this was my anxiety and panic. I was prone to situational panic attacks that felt like my fight/flight system was in total chaos.

A Complete Crash with Tinidazole

Despite feeling okay in 2018 and most of 2019, my whole world was turned upside down again in the fall of 2019. I contracted some sort of stomach bug that wasn’t going away, and my doctor placed me on a drug called Tinidazole, the sister drug of Metronidazole (Flagyl). I haven’t felt the same since that day.

The symptoms came on almost immediately. Dizziness, depression, increased anxiety, neuropathy in my hands and arms. I became convinced that I had ALS because my hands weren’t working right. It was also unlike me to ever assume something as terrible as a fatal diagnosis, but my brain was in total disarray.

Two weeks after taking the Tinidazole, I had to go back on antibiotics for wisdom teeth removal. Immediately after the surgery, I went into one of the most horrendous panic attacks of my life, in part because I had been injected with novocaine about 20 times. I had to be wheeled out of the doctor’s office because the panic had been so bad. Looking back now, there is a similar case study in Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition.

Things only got worse. By the end of the penicillin, my body was in a total spiral. I began having daily panic attacks that I can’t even describe. My body temperature was low, my fight/flight system was in disarray, I was depressed, I couldn’t think clearly. There were nights when I wouldn’t sleep at all and be in total fight or flight mode. I now know that I was going through Tinidazole toxicity that had gradually gotten worse over a few weeks. Combined with the penicillin, it was a recipe for disaster.

The strangest symptom that has come out of this experience is hypoglycemia. My blood sugar is tanking to dangerously low levels during the day unless I am extremely diligent about eating. There have been a few times that I have almost blacked out. This isn’t a common symptom of Metronidazole/Tinidazole toxicity, but I don’t know where else it could have come from.

Where I Am Now

I’ve improved a bit, but I’m still having symptoms like dizziness, hypoglycemia, altered mental state, neuropathy and a total dysfunction of my fight/flight system.

Looking back at my long and complicated history, I’ve discovered a few things in my research:

Early and frequent antibiotic use is linked to anxiety and depression
I ate A LOT of sugar throughout my life and my thiamine stores were probably always being hit hard and my mitochondria have probably been fighting this battle my life
The benzodiazepine and Ambien have caused deep alterations to my nervous system/GABA receptors that became less noticeable with time but will never fully heal
Concussions cause a cascade of effects that damage mitochondria function and lead to other semi-permanent neurological issues
Truvada (PreP) also harms mitochondria
Tinidazole plummets your thiamine

Thiamine Deficiency and Problems With Paradox

I’d like to start Dr. Lonsdale’s protocol for high-dose thiamine, but I encounter painfully difficult paradox symptoms. I have tried to start with a low dose (less than 10 mg) twice now, and always end up having to stop because it gets so bad. The “heart attack” and “seizure” symptoms are simply too frightening and I’m not sure what’s actually going on in both my brain and heart. I’d like to find a functional doctor that could possibly work with me to measure what’s going on when I take thiamine.

I’m also in the process of working with doctors to run tests on my hypoglycemia issues.

The only other thing I’ve considered is a fecal transplant. Since I’ve been on so many antibiotics, I’m convinced that some of my issues may stem from altered gut microbiota.

Lots of people see improvement from Metronidazole/Tinidazole toxicity over the course of 6-12 months. But unless I can take action, I suspect my thiamine issue will remain.

We Need Your Help

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

Yes, I would like to support Hormones Matter.

This story was published originally on March 11, 2020.

thiamine deficiency

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Recurrent UTIs, Fluoroquinolones, and New Onset Graves’ Disease

IVF and More Damage to My Health

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

Taking Matters Into My Own Hands

The Next Step: Addressing Nutrient Deficiencies

Recovery From Conventional Medicine’s Ills Came Down to Thiamine

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