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An Artist’s Decades Long Dysautonomia Treated With Thiamine

Published on June 12, 2023

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Here is the story of my longstanding thiamine deficiency, which was not recognized by doctors. I am 54 years old and have had health issues most of my life.

Early and Prominent Orthostatic Hypotension Missed for Decades

Around the age of 10 or so, I began blacking out upon standing. It never led to syncope — just a brief dizziness and loss of vision. A particular church practice at school caused me to black out often. Lots of kneeling and rising — a great challenge for what would be later diagnosed as orthostatic hypotension. I sometimes had to be led out of church by a fellow student and taken to the school nurse. A friend reported to me that on those occasions, as I was being led out, even my lips were white.

In my teenage years, another challenge was orthostatic intolerance. I would get dizzy and feel light-headed if made to stand a long time. Hot, crowded buses were a particular nemesis: I would black out and feel on the brink of fainting. It was mortifying to be an 18 year old who had to request someone older give up their seat to me because I felt faint. I used to pray before I got on a bus.

During these years, heart palpitations were also a constant issue. It was a way of life for me — my “normal.” I didn’t find out until years later that not everyone experienced violent heart pounding upon climbing a set of stairs. Abnormal sweating was a problem, too — I sweated profusely from the underarms, but nowhere else. Exercise would make my face red and hot — I would get terribly overheated and feel unwell, because my body wasn’t able to sweat and cool itself.

All of these things point to a malfunction of the autonomic nervous system, but I didn’t know that then, and no doctor seemed to put it together, either.

The lower part of the brain, the brainstem, controls the autonomic nervous system.

The autonomic nervous system regulates the most basic aspects of living: heart rate, breathing, blood pressure, sweating, hunger and thirst, fight or flight response, etc. It requires thiamine to function properly.

I was also a good deal underweight and never had as much energy as others. I was terrible at sports and was weakly but did well academically and with art.

Mitral Valve Prolapse, Tachycardia and Heart Palpitations: Signs of Dysautonomia

During art school and afterwards, I waited tables to support myself, as well as worked at school to help pay my tuition. The output of energy this required would prove too much for someone deficient in thiamine. Thiamine plays a fundamental role in energy metabolism, so a deficiency is consequential. My schedule overwhelmed me — I dropped out after my second year. (I eventually went back three years later to complete my degree — this is just one example of how chronic fatigue affected the trajectory of my life.)

Somewhere in those years, I was diagnosed with mitral valve prolapse. I remember being astonished that the diagnosis had been missed all these years. I was told it was something I had been born with, so it was surprising that no one had noticed it until I was 22. I now know that mitral valve prolapse is associated with defective functioning of the autonomic nervous system, that I likely had *not* been born with it, and that this instead was yet another sign of my malfunctioning autonomic nervous system. Mitral valve prolapse is also associated with magnesium deficiency. The pieces of the puzzle were all there — they just needed someone who understood how they fit together.

It was a relief to be out of school and to be able to rest, but my undiagnosed thiamine deficiency continued to affect me. Palpitations and tachycardia were an exhausting way of life. I became good at avoiding things that would exacerbate that, but things I couldn’t avoid — like oral presentations in a literature class I was taking — would so exhaust me as to render me incapacitated the next day. The intellectual rigor of it thrilled me, however. Life continued like that — avoiding many things that a healthy person would be capable of, in order to preserve energy, while making exceptions for certain things I loved — but paying for that with crushing fatigue.

A busy night of waiting tables was now capable of doing me in so much that I couldn’t get out of bed for hours the next day. My description of how I felt at the time was like a broken stick. I later learned that severe thiamine deficiency is called beriberi, which translates to “I can’t, I can’t.” My heart symptoms also became more complex: palpitations and tachycardia, as always, but now chest pain and an occasional flutter, too. I saw a doctor, who recommended I get an echocardiogram. I didn’t have health insurance, so that wasn’t possible.

Decades Later: Debilitating Fatigue and Arrhythmia

I went many years without medical care. At age 44 my symptoms worsened — the fatigue was debilitating and I was now experiencing an arrhythmia. I was able to teach one day a week in an art school, but the energy it required made me incapacitated the next day.

I was also told by a doctor that I should be evaluated for Marfan syndrome, a connective tissue disorder. I twice landed in the ER due to chest pain and a new arrhythmia while waiting for my appointments with genetics and cardiology. When I finally saw the geneticist, I got great news: I did not have Marfan syndrome. I was clinically diagnosed with a related but less serious connective tissue disorder: MASS phenotype, an acronym for Mitral valve prolapse, Aortic enlargement, Skeletal and Skin findings. Though I was relieved by the news, I was also perplexed: why did I feel so awful and fatigued all the time?

My cardiologist had me wear a 30-day Holter monitor, which resulted in him diagnosing me with dysautonomia. Orthostatic hypotension, and also sinus tachycardia, premature ventricular contractions (PVCs), and paroxysmal atrial tachycardia. His first intervention helped me more than any other — he recommended at least 32 ounces of an electrolyte drink daily, along with 500 mg of magnesium. I felt elated — the particular elation of someone long sick who finally feels better. After a while, however, it wasn’t enough, and he prescribed fludrocortisone (florinef). That made my feet swell so awfully that I developed blisters and couldn’t walk.

The cardiologist referred me to an electrophysiologist for my arrhythmia. That cardiologist put me on a beta-blocker. That also caused some milder foot and ankle swelling, but the relief it provided from decades-long tachycardia, palpitations, and an awful constant awareness of my heart was so welcome. It also reduced my PVCs. Again I felt hopeful and thought this might be the solution. It wasn’t. It temporarily and mercifully relieved some symptoms, but it did nothing to determine and address the true cause of my dysautonomia — which was thiamine deficiency. The beta-blocker eventually caused diarrhea. Because it didn’t happen at first, I didn’t associate it with the beta-blocker and neither did my doctors. The bout of diarrhea lasted 5 months. When I finally decided to quit the beta-blocker, the diarrhea ceased.

In the meantime, I was also dealing with a whole array of other issues: GI distress; food intolerances; peripheral vascular insufficiency (which led me to an unsuccessful and unnecessary surgery); chilblains; costochondritis; debilitating menstrual pain; and ever-looming, crushing fatigue.

Hypovolemia and Undiagnosed Thiamine Deficiency Almost Killed Me

At my lowest health point, my undiagnosed thiamine deficiency nearly killed me (via low BP and hypovolemia). I was at a lab getting a slew of blood tests ordered by my immunologist. I had requested that I be permitted to lie down for the blood draw, because I sometimes passed out otherwise. There was no room available for me, so the technician asked if I thought I could manage sitting up. I should have said no: big mistake on my part. I was sitting up in a chair with a kind of shelf clamped across me. I closed my eyes for the blood draw, and after just a short time felt the unmistakable onset of blacking out. I started to lose my vision and asked the technician to unclamp me from that chair so I could put my head between my knees. She seemed to have no grasp of basic medical knowledge, because she refused, saying she didn’t want my head down and to instead try to “stay with her”. I was unable to free myself because I could no longer see. Then I lost my hearing, and that’s all I remember. I fainted. Thank goodness my husband was there in the waiting room. They called an ambulance and then called my husband back to see me. He said I looked terrifying. Completely white, with white lips, and two techs trying to call me to. He told them they needed to put me flat on the floor. Inexplicably, they wouldn’t let him. He acted quickly and dragged a big box across the room and put my feet up on it. That made me come to. For a long time, I had cuts missing from my vision. I later asked my cardiologist if I would have had a stroke if my husband hadn’t intervened. The cardiologist was angry at what had happened and told me not only would I have had a stroke, I would have died.

Putting the Pieces Together: It Was Thiamine All Along

Like all chronically-ill patients, I had to rely on my own research to try to figure out how to improve my health. I first managed to help myself with some orthomolecular interventions. High-dose vitamin c was life-changing. After starting that and taking steps to support methylation, I was finally able to put on weight and muscle. By the age of 51, I was no longer underweight for the first time since early childhood. And I managed to raise my chronically low BP a bit. Fatigue was still overwhelming but then, gratefully, I came upon the research of Dr. Derrick Lonsdale and Dr. Chandler Marrs. I learned about beriberi, thiamine deficiency, and its relation to dysautonomia. I recognized myself immediately.

I read everything I could on the subject before starting to supplement thiamine. Because I had been so long deficient, I knew to expect a paradoxical response. I also knew, per Dr. Lonsdale, that a paradoxical response was a good indication that thiamine might help me. And it has. It has helped me immensely.

I started with thiamine HCL, 10 mg. Even that tiny dose gave me a paradoxical response. My fatigue became even worse, as did my heart issues — terrible palpitations and much more frequent arrhythmia. My ankles were more swollen than they had ever been. I felt shaky, tired, horribly fatigued. It was difficult and lasted about 2 months. Initiating thiamine supplementation in a patient long deficient causes a kind of refeeding syndrome. I continued titrating up my dose, very slowly, while taking supporting co-factors like magnesium and potassium and a b-complex.

Gains Made With Thiamine

Increased energy in general
Increased exercise tolerance
Raised BP by over 20 systolic points: huge gain for me. I am now regularly around 110/70. If I get exhausted by physical activity and/or stress, it drops again. (For years, my BP was around 79/56)
Heart rate normalized
Arrhythmia almost non-existent
No more heart palpitations after eating
Got rid of the constant awareness of my heart
Now able to walk rapidly
My ankles are rarely swollen now. They used to be swollen every day, particularly if I was active that day.
After 8 years, I no longer need to keep my feet elevated when sitting (cardiologist’s recommendation to counteract swollen ankles).
I am able to maintain mental clarity even after active or stressful events. Until very recently, I could not think clearly after a day of teaching — used to have to ask my husband to speak slowly and break down complex ideas into simple ones after I taught, because my fatigue affected my cognition. That’s gone now.
I very rarely get headaches at base of head (used to be almost daily)
No more costochondritis. This used to be a regular, painful complaint of mine. I was astonished to learn that costochondritis is caused by thiamine deficiency, especially since costochondritis is a common complaint in those who suffer connective tissue disorders.
I sleep through the night now, even if I was active that day. Until recently, if I was active — and in my limited-energy world, active might mean as little as attending a party — I would have great trouble falling asleep, and then I would awaken in the night after 4 hours of sleep and be awake at least 1 to 2 hours. That’s gone, and good riddance.
No more debilitating menstrual periods. I suffered enormous pain with my period for over 35 years. Thiamine treats primary dysmenorrhea.
Joint pain relief
No more stuffy nose at night when I’m exhausted
I wake up singing. I report this not as an indication of mood so much as an indication of energy — I simply never possessed the energy required to sing, at least not in the morning.
I wake up early now. Completely new.
I’m remembering my dreams again! (Couldn’t recall them for at least the past 5 years).
I rarely experience the dreaded “jelly legs”.
I am no longer cold all the time.
I now am able to sweat more normally.
Increased my left ventricular ejection fraction (EF) from 55 to 65 percent. Thiamine has been shown to improve EF in heart failure patients, and though I was never in heart failure, this is the first ever increase of my EF in 10 years, and it appeared after I began thiamine, so I suspect it’s related.

One thing that hasn’t gotten better yet is abdominal bloating. Hoping that improves eventually. I have low stomach acid and am working on that. And I still tire much easier than a normal person, but I’m so much better than I was, and I hope to continue improving.

Final Thoughts

My symptoms started at about the age of 10, which is the age I was when a dentist placed 10 large amalgam (mercury) fillings. A few years later, I got 5 more. Mercury causes vitamin and mineral derangement. (I have since gotten most of my amalgam fillings removed by a SMART dentist using a procedure to minimize mercury exposure.) There are indications that a thiamine deficiency heightens susceptibility to mercury toxicity. Many of the symptoms of mercury poisoning are observed in persons with thiamine deficiency. Additionally, there is a metabolic component to connective tissue disorders that most doctors do not recognize. Along with being diagnosed by a geneticist with MASS phenotype, another doctor (rheumatologist) diagnosed me with Ehlers-Danlos syndrome. Being diagnosed with both, even if not correct, has given me access to both cohorts of connective tissue patients, through online support groups. Most suffer from dysautonomia and have accepted this as genetic fate rather than something that can be improved through vitamin therapy. There is a great need to get the word out on thiamine and vitamin therapy to the chronic illness community.

I am deeply indebted to Drs. Lonsdale and Marrs for their research. It is giving me my life back.

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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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Image: Original painting by the author.

This article was published originally on April 19, 2021.

Post Lupron Mitochondrial Collapse: A Case Story

by Derrick Lonsdale MD, FACN, CNS

Published on April 3, 2023

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Dr. Marrs and I became aware of the symptoms and some of the laboratory results in a 38 year old woman. We wish to describe the case because it represents what should be an entirely new approach to medicine in general.

Before Lupron

The patient had been an active 38-year-old woman caring for her home and two children, ages 7 and 9 that were her focus, prior to Lupron. She had walked her dog daily, worked out at the gym twice a week and she had renovated her home in the summer of 2017. She had had her gallbladder removed in 2016, said to be because of a polyp. She had received allergy shots once a month for a couple of years. She took birth-control pills. Her history revealed that she had had a severe reaction to penicillin as a child, resulting in a rash and joint swelling causing inability to walk for a short time. She also had a history of frequent sinus infections and antibiotic treatment. In 2017, she began experiencing heavy menstrual bleeding and hysterectomy was recommended. She refused this and a second doctor recommended Lupron in an attempt to change her hormonal balance before hysterectomy.

After Lupron

She had received an injection of Lupron into her left hip and side effects, beginning within a few days, included:

Fatigue
Skin redness
Severe weakness in the legs, and tingling in the left side of the head and right leg.
A few days later she developed severe headaches and vomiting.

An initial estradiol patch caused no improvement, so another one at double the dose was prescribed with some improvement (presumably in menses). By November 2017 the patches were discontinued. She began to experience

Joint pain
Pain throughout her body
Nervousness
Shaking
Panic attacks
Changes in personality.
In December she experienced cyclic vomiting and weight loss.

The estrogen patches were prescribed again. She saw an endocrinologist and some laboratory tests were abnormal, including what was described as a borderline high blood glucose.

These symptoms continued and in February 2018, three drugs were prescribed (Celexa, Neurontin, Ambien). They were discontinued two weeks later because there was no relief of symptoms.

In March, she experienced severe fatigue and had episodes of difficulty in walking which were intermittent and described as “almost like being paralyzed”.

In April, she saw a geneticist and some lab tests were performed that I will comment on shortly. A diagnosis of fibromyalgia and possible chronic fatigue syndrome were each entertained. The endocrinologist said that test results indicated that she was not producing estrogen or progesterone.

Based upon conversations with us, she began supplements of thiamine, fish oil, alpha lipoic acid, B complex, folinic acid, ferrous sulfate and methyl B12. Estradiol patches were resumed. We suggested the use of intravenous water-soluble vitamins, since Dr. Marrs and I agreed that giving the nutrients by mouth probably could not reach the necessary concentration of vitamin therapy needed. This was not followed through on by her current physician.

Discussion of Symptoms and Side Effects

The patient’s medical history indicated that she had experienced many different symptoms throughout her life. These included a severe reaction from penicillin and multiple sinus infections. The side effects from Lupron were fatigue, leg weakness, headaches, general body pain, panic attacks and cyclic vomiting. In other words, she had been a classic “problem patient” to her physicians. Since the symptoms could not be defined by usual and customary laboratory evidence the general conclusion was repeatedly that this was evidence of psychosomatic disease. Curiously, this common diagnosis in modern medical circles appears to be that the patient is thought of as inventing her symptoms neurotically without ever considering an underlying mechanism. Even worse, polysymptomatic disease of this nature is usually experienced by the brightest and the best. This is because high intelligence is developed within a brain which is more energy consuming than that of a less intelligent person. Such individuals are much more prone to unforeseen stress events, making them more susceptible to side effects from medication and inoculations. A car engine uses more energy to climb a hill. Stresses that we meet in life are like “hills to be climbed” and involve a commensurate supply of energy.

Laboratory Results: Low Amino Acids, Vitamin Deficiency and Defective Energy Metabolism

Many tests were performed on this patient. Two amino acid tests were performed, one measuring the amino acids found in blood plasma, the other measuring those excreted in urine. A word of explanation is necessary. Amino acids are the building blocks of proteins in the body and finding a given amino acid in very low or unusually high concentration can be used to define important aspects of body chemistry. Of 34 amino acids recorded in the plasma of this patient, aspartic acid, serine, ethanolamine, and tyrosine were severely decreased, while glutamine, histidine, alanine, ethanolamine and tyrosine were severely decreased in urine. All the others were in their expected normal concentration.

Amino acids are used in the body to create proteins, and this is an energy consuming mechanism. One of the deficient amino acids was aspartic acid whose metabolism is important in a mechanism known as transamination. The enzyme that carries out this function requires vitamin B6.

Two of them, ethanolamine and serine, play an important part in transmethylation, a mechanism that is dependent on folate and B12.

The fourth one was tyrosine and it is involved in the synthesis of thyroid hormone.

These low levels suggested that their respective vitamin dependent mechanisms were at fault. Since all the vitamins involved are water-soluble, it invited their administration by intravenous infusion. However, because they were energy dependent reactions, it is likely to construe the possibility that the underlying common fault was energy synthesis.

Was there any evidence from these laboratory results for defective energy metabolism? Yes.

Isocitric and citric acids were reported to be low in the urine and they are vital metabolites in the citric acid cycle, the “engine” of the cell. Also, there was a deficiency of pyruvic acid and this is the fuel that enables the citric acid cycle to function. This constituted strong evidence for energy deficiency with its major effect on the brain and nervous system.

Mitochondrial Energy Synthesis

Our bodies consist of 70 to 100 trillion cells that are being broken down and reconstructed throughout life. Relatively simple molecules are acted on by enzymes in a series of chemical reactions known by biochemists as “pathways”. Each enzyme requires a vitamin and/or essential mineral that assists the action of the enzyme and are known as cofactors to the enzyme. Several pathways reflect the synthesis of energy that is stored in the cell as ATP (adenosine triphosphate). ATP is a little like a battery that is being continuously charged and discharged and most of this occurs in the mitochondria. All the other pathways consume energy, either in enabling function or rebuilding cells. They might be compared loosely to the transmission in an automobile. In other words, the healthy body functions because energy synthesis meets energy demand. The abnormally low amino acids each could be used to suggest a defect in the energy consuming pathways and possibly a reflection of missing cofactors, making the “transmission” defective.

Vitamin Cofactors, Energy Deficiency, and Symptomology

The symptoms expressed by this unfortunate patient pointed strongly to cofactor deficiencies derived from diet that could easily be tested by their administration and clinical effect. The net effect is produced by a gap between energy synthesis and its utilization to meet the stresses of life in general. The administration of cofactors does not necessarily answer the underlying question because of the possibility of unknown genetically determined factors. However, it is safe, non-toxic, may have an epigenetic effect and is relatively cheap. It therefore should be the first approach. The greater the urgency or the severity of symptoms, the stronger the indication for intravenous administration of all the water-soluble vitamins. I have successfully treated many polysymptomatic patients this way, suggesting that mitochondrial function is as much an acquired disease as well as being genetically determined.

A Note About Oxidants and Antioxidants

Think of the body as a machine that consumes fuel by uniting it with oxygen to produce energy. This combination is called oxidation. Like a fire or any form of burning, it can be slow or fast and cellular oxidation seeks an intermediate level. If the oxidation is too slow, energy production is imperiled. If it is too fast or too vigorous, oxygen atoms are “thrown out” of the oxidation process like sparks are thrown out of a vigorously burning fire. These are referred to as “free oxygen radicals”. Like sparks from a fire, they can do damage. Some vitamins act to assist or accelerate oxidation, an example being B complex. They are known as oxidants. Others quench the free oxygen radicals (sparks) and are known as antioxidants. Vitamins C and E are examples.

Without going into the highly technical details, thiamine acts as an oxidant and an antioxidant, thus increasing its importance in metabolism. From this it is easy to see the essential importance of these substances that are obtained from naturally occurring foods and why their deficiency causes disease. Of course, we have known this for a long time, but current medical belief is fixed in the concept that “vitamin deficiency disease has been conquered and the resultant diseases are only of historical interest”. For example, this patient had “borderline high glucose”, something that would occur in the thiamine deficiency disease beriberi. She also had frequent “infections”, now known to be related to free oxygen radical production, indicating that her regulation of metabolism was extremely inefficient. The amino acids that were extremely low in the plasma and urine could be used to interpret the possibility of missing cofactors, reflecting a chaotic state of metabolism. I must end this by saying that the use of vitamins and minerals in this manner is not (repeat not) simple vitamin replacement. We believe that the vitamin/mineral combination used in high-doses is resuscitating the activity of the corresponding enzyme and it is therefore acting as a drug. Identifying the underlying biochemical lesion is the essential nature of future diagnosis.

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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 July 25, 2018.

Elimination Dieting and Progressive Thiamine Deficiency

by M. Ross

Published on March 7, 2023

4228 views

My issues began after the birth of my second child 21 years ago. I would get extreme indigestion for a couple days each month and my skin broke out. This continued for years until I ended up having several rounds of antibiotics. Months later, I developed severe and never ending acid reflux. After struggling for a year, my local health food store owner mentioned the blood type diet and recommended I avoid dairy. The result was magic. Unfortunately, this started a cascade of elimination diets that would set the tone for the next fifteen years.

After eliminating dairy and seeing a resolution of symptoms, at least temporarily, I decided to eliminate gluten too. As with the dairy, the indigestion disappeared temporarily when I eliminated gluten, but other symptoms eventually crept in, including hypothyroidism and bile reflux. I read about a vegetarian diet and decided to give it a try. Again amazing results from removing meat. The bile reflux disappeared. I thought things were going pretty well, but in these years I started to have other issues: ataxia, fatigue, heat intolerance, numbness and tingling, gait and bladder issues. In addition, I was always starving. I ate a tremendous amount of food each day, but at the same time I was losing weight.

My naturopath had mentioned possible problems with my gallbladder, but I didn’t think too much about it until I had constant pain. It was eventually discovered that I had a non-functioning gallbladder and I reluctantly had it removed, hoping it would solve my problems. I had tried changing my diet to the autoimmune paleo several times, but would always crash after a couple weeks. After surgery, I could eat meat without major issues, but nothing seemed to digest well. I felt like I never really recovered and other issues started to creep in.

My calf muscles would spasm upon standing and I was so weak I was having difficulty walking a block. A year after surgery, I was diagnosed with primary progressive multiple sclerosis, as it matched my symptoms and lesions were seen on my cerebellum and down my spine. The hallmark of PPMS is neurodegeneration without inflammation. The next three and a half years were a quick decline. I quickly became unable to walk unaided, mainly because I was too fatigued and my muscles too weak. PPMS used to be called creeping paralysis and that is exactly what was happening; I was unable to move my arms or legs, my equilibrium was so off that I couldn’t stand without tipping over and I couldn’t look down to even zip up my jacket.

I had really bad edema in my lower legs and feet and they were a nice shade of purple. My brain was easily overwhelmed and not committing things to memory, which left me going in circles. I lost my appetite, but blamed it on my ever changing diet and my fear of eating the wrong food. I would alternate between diets, cutting various food groups with very limited success.

I visited multiple naturopaths, a functional medical doctor, a NUCCA chiropractor and a MS specialist. I have researched endlessly and have a cupboard full of supplements. I had tried B vitamins before but had not noticed a difference. I joined a Facebook group called Understanding Mitochondrial Nutrients and did not think much about the vitamin I needed most, thiamine, until a post by a desperate husband came up in my feed. I began to research thiamine and found I was able to piece together a timeline of my life based on a progressing thiamine deficiency. I am only three weeks into dosing with thiamine (I take 200mg thiamine HCL and 240mg benfotiamine) and a B complex, but it has made such a difference in my balance, fatigue, edema and mental energy. My appetite is back and I can zip up my coat! I am cautiously optimistic, only because I have suffered so much disappointment in the past. I am hopeful that I can make a recovery.

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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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Understanding Mitochondrial Energy, Health and Nutrition

by Derrick Lonsdale MD, FACN, CNS

Published on March 2, 2023

12455 views

I live in a retirement community. In my everyday discussions with fellow residents, I find that the idea of energy metabolism as the “bottom line” of health is almost completely incomprehensible. Since my friends are all well-educated professional people, I came to the conclusion that few people really have an idea about energy. For example, we talk about people who indulge in physical sports being energetic, while people sitting behind a desk are classed as sedentary. What we fail to realize is that mental processes require even more energy than physical processes. Both physically and mentally active people consume energy, so it is obvious that some kind of attempt must be made to talk about energy as it applies to the human body.

Hans Selye and the Stress Response

I will begin by giving an outline of the work that was performed many years ago by a Canadian scientist by the name of Hans Selye. Originally he was a Hungarian medical student. Some of the teaching was done by presenting individual patients to the class of students. The professor would describe the details of the disease for each person. What interested Selye was that the facial expression of each patient appeared to him to be identical. He came to the conclusion that this was the facial expression of suffering, irrespective of the nature of the disease. He referred to this as the patient’s response to what he called “stress”. He decided to study the whole concept of stress. He immigrated to Canada and in Montréal he set up a research unit that came to be called “The Research Institute of Stress”.

Of course, Selye could not study human beings and his experiments were performed on literally thousands of rats. He subjected them to many forms of physical stress and detailed the laboratory and histological results. He found that each animal would begin by mustering the well-researched fight-or-flight reflex. If the stress was continued indefinitely, the metabolic resistance of the animal gradually decayed. He called this ability of the animal to resist stress the “General Adaptation Syndrome” and came to the conclusion that it was driven by some form of energy. If and when the supply of energy was exhausted, he found laboratory changes in blood and tissues that were listed carefully. Although extrapolating this information from animal studies, he ended up by saying that humans were suffering from “diseases of adaptation” and that they were the result of a failure to adapt to the effects of life stresses.

My addition to this is that it would have been better to describe them as “the diseases of maladaptation”, meaning that humans have to have some form of energy to meet life. If there is energy failure, disease will follow. The remarkable thing is that energy production in the human body was virtually unknown in Selye’s time, so his conclusion was a touch of genius. The mechanism by which energy is produced in the cells of the body is now well-known. We know that energy consumption is greatest in the lower part of the brain and the heart, organs that work 24 hours a day throughout life. The lower part of the brain that organizes and controls our adaptive capabilities is particularly energy consuming. So before we begin to think about energy as a driving force, let us consider what we mean by stress and how we adapt to it.

Human Stress: Surviving a Hostile Environment

We all live in an environment that is essentially hostile. We have to adapt to natural changes such as cold, hot, wet and dry. We are surrounded by enemies in the form of microorganisms and when they attack us, we have to set up a complex mechanism of defense. Add to this the possibility of trauma and the complexity of modern civilization, involving business and life decisions. We possess the machinery that enables us to meet these individual stresses, meaning that we are adapting. Health means that we adapt successfully and that is why “diseases of maladaptation” makes a lot of sense. Obviously, the key is that the machinery requires energy.

Energy Metabolism, Physics, and Chemistry

First of all, let us begin by trying to define energy. The dictionary describes it as “a force” and the only way in which we can appreciate its nature is by its effects. It is not a substance that we can see but the effects of light energy enable us to have vision. The old riddle might be mentioned; “Is there a sound in the forest when a tree falls?” The answer is of course that the only way that the resultant energy can be perceived is when it is felt by the human ear. Even that is not the end of the story, because the ear mechanism has to send a message to the brain where the sound is perceived. Thus, there is no sound in the forest when a tree falls. It is the perception of a form of energy, a force that impacts on the ear of any animal endowed with the ability to hear. Energy can be stored electrically in a battery or as heat energy in a hot water bottle, but the inevitable process is that the energy drains away. A hot cup of coffee cools. A battery gives up its stored energy and becomes just “another lump of matter”.

For example, if a stone is rolled up a hill, its natural tendency would be to roll down the hill again. Whatever force is being used to roll the stone up the hill is known as “potential energy”. In other words, there has to be a constant supply of energy as long as the stone is moving up a gradient against gravity. When it reaches the top, we say that the potential energy is being stored in the stone. It is the equivalent of electricity being stored in a battery. The “potential energy”, however, requires an electrical force to “electrify” the battery. The potential energy in the stone can be released by allowing it to roll down the hill and Newton called this kind of energy “kinetic” (the use of a force to produce movement). The force that is being used is of course the effect of gravity and the stone becomes stationary when it gets to the bottom of the hill. The use of gravity as the source of energy is simply wasted, but note that gravity has not changed. It is still available for use. Let us take a simple example of this energy being used for a purpose. Suppose that there is a wall at the bottom of the hill and a farmer wishes to create a gate. In a fanciful way he could use the stone to create a gap in the wall. The gap in the wall is the observable mark of the effect produced by consumption of kinetic energy.

The body consists of between 70 and 100 trillion cells, each of which has a special function. Each is a one-celled organism in its own right and in order to perform their function they need a constant supply of energy. This is developed by complex body chemistry. The “engines” in each cell are called mitochondria and one of their many different functions is to synthesize energy. The energy that is developed is stored in a chemical substance known as adenosine triphosphate (ATP) and in order to understand this a little more, perhaps we should think of the Newtonian analogy for comparison. The Newtonian hill is replaced by an electronic gradient and the stone by the chemical ATP

Of Mitochondria and ATP

Cellular energy is produced in the mitochondria by oxidative metabolism. This simply means that a fuel (glucose) combines with oxygen but, like any fuel, it has to be ignited. The best way to analogize that is to say that thiamine can be compared with a spark plug that ignites gasoline in a car. It “ignites” glucose. The resultant energy is used to add a phosphate molecule to adenosine three times to make ATP (the electronic gradient). We have “rolled an electronic stone up an electronic hill”. As the adenosine donates phosphate molecules, it becomes adenosine monophosphate (AMP) that must be “rolled uphill again”. As it is “rolling down the electronic hill”, it is transferring energy. Therefore, ATP can be thought of as an energy currency. Note that there must be a continuous supply of fuel (food) that must contain the equivalent of a spark plug (thiamine) in order to maintain an energy supply with maximum efficiency.

The loss of any one of a huge number of components in food that work in a team relationship with thiamine, lowers the energy maximum. That is why thiamine deficiency has been earmarked as the major cause of a disease called beriberi that has haunted mankind for thousands of years. Its deficiency particularly affects the lower part of the brain and the heart because of their huge energy demand. Since the lower brain contains the control mechanisms that enable us to adapt to the environment, as depicted above, it is easy to see that we would be maladapted if there is energy deficiency, just as Selye predicted. In fact, one of his students was able to produce a failure of the General Adaptation Syndrome by making his experimental animals thiamine deficient. It also suggests that a lot of heart and brain disease is really nothing more than energy deficiency that could be easily treated in its early stages. If the energy deficiency is allowed to continue indefinitely because of our failure to recognize the implications, it would not be surprising that changes in structure would develop and produce organic disease.

Health and Disease in the Context of Energy

With this concept in view, the present disease model looks antiquated. There are only three factors to be considered. The first one is obviously our genetic inheritance. If it is perfect, all it requires is energy to drive it. However, DNA is probably never perfect in its formation. It may not be imperfect enough to cause disease in its own right, but a slight imperfection would constitute what I call “genetic risk”, causing disease in association with a stressor such as an otherwise mild infection or trauma.

Suppose that a given patient died from an infection (think of the 2018 flu).The present medical model would place the blame on the pathogenic virulence of the virus without considering whether malnutrition played a part by failing to produce sufficient energy for the complex immune response. Therefore, the second factor to be considered is the perfection of the fuel supply and that obviously comes from the quality of nutrition. Stress (the viral attack or non-lethal trauma) becomes the third consideration, since we have shown that an adequate energy supply is required for adapting on a day-to-day basis. There is even a new science called epigenetics in which it has been shown that nutrient components can be used to upgrade genetic mistakes in DNA. A fanciful interpretation of these three factors, genetics, nutrition and stress can be portrayed by the use of Boolean algebra. This is a mathematical representation as interlocking circles. The area of each circle can be easily assessed, marking their relative importance. The interlocking area between any two of the three circles and that of the three circles together completes the picture. It becomes easy to perceive how a prolonged period of stress can impact health. The present flu epidemic may be an example of the Three Circles of Health in operation, explaining why some people have only a mild illness while others die. Could the appalling nutrition in America play a part?

Why Thiamine

The pain produced by a heart attack has always been a mystery in explaining why and how it occurs. The answer of course is that pain is always felt by sensory apparatus in the brain. The brain is able to identify the source of the signal as coming from the heart but cannot interpret the reason. I am suggesting that in some cases, the heart is having difficulties from energy deficiency and notifying the brain. A coronary thrombosis would introduce local energy deficiency, but other methods of producing energy deficiency would apply. It is logical to assume also that brain disease is a manifestation of cellular energy deficiency. That is why I had found that so many children referred to me for various mental conditions responded to megadoses of thiamine. It is also why I had found that so much emotional disease was related to diet and not to poor parenthood.

I recently came across a patient that I had seen many years ago when he was a child. He had a diagnosis of Tourette’s syndrome, made elsewhere. I treated him with megadoses of thiamine and his symptoms resolved completely. Medical skepticism would answer this by calling it a placebo effect, but since this effect is well-known, it must have a mechanism. For many years I have believed that therapeutic nutrition “turns on” this effect by enhancing cellular energy. A small group of physicians known as “Alternative Medicine Practitioners” use water-soluble vitamins, given intravenously, irrespective of the acceptable clinical diagnosis. For example, I remember a young woman who came to see me with a diagnosis of “Thrombocytopenic Purpura”. This disease is a loss of cellular elements known as platelets and it had resisted orthodox treatment for years. I gave her a series of intravenous injections of water soluble vitamins with complete resolution of the problem. I must end by stating that healing is a function of the body. The only way that a healer can be justifiably recognized is by supplying the body with the ingredients that it requires to carry out the healing process. Perhaps spontaneous healing, as for example initiated by religious belief, is an ability to muster those ingredients that are present, but hitherto unused.

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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 14, 2018.

Severe Gut Dysmotility, Dysautonomia, and Malnutrition

by Charlotte

Published on February 23, 2023

18151 views

History of Gut Pain and Epigenetic Malnutrition

I am 32 years old and have suffered from ill health all of my life. From as long as I can remember, I’ve experienced gut pain, fatigue, and hyper-sensitivity. If there was something to catch, I would catch it. I react to everything and suffer chronic gut and nerve pain.

As a young child, I had chronic abdominal pain in the lower right quadrant and would often be buckled over in pain. Doctors thought it was appendicitis so removed my appendix but the pain continued. I was chronically tired and sensitive to the cold. I would struggle to get up in the morning to go to school and would stand in the shower dousing myself in hot water for as long as I could to warm up my body. Cold hands and feet has continued into adulthood.

I was born into a family that struggled with spine, neck, head, and gut issues. I was raised on cow’s milk and barley formula as my mother was unable to breastfeed. My mother and aunt had Ehlers Danlos Syndrome. I was diagnosed with it 8 years ago. My mother has Arnold Chiari malformation, my aunt scoliosis. They were post-war children. My grandmother had spinal issues and likely was very deficient in the B Vitamins. My grandfather, aunt and mother all suffered from gut issues, my grandfather eventually dying from bowel cancer. He was sensitive to many foods, particularly FODMAP rich ones.

I had many allergies – dust mite, grass, cow’s milk etc. I suffered an adverse reaction to the MMR vaccine when I was eight – with an intense full body rash. I was bedridden with intense fatigue for two weeks. Around the same time, tests found huge numbers of the parasite dientamoeba fragilis (D fragilis) in my stool. Dientamoeba fragilis together with Blasto hominis, another intestinal parasite, have been found in large numbers in my stool ever since. Despite trying many things, I’ve never been able to get rid of them.

Increasing Food Sensitivities, Weight Loss, Amenorrhea, and Osteoporosis

By the age of ten, I was struggling with depression and increasing sensitivities to many foods – particularly gluten and dairy. The only thing that seemed to help was exercise. I played competitive soccer, did cross-country and athletics and rode my bicycle everywhere. At this time, I started becoming vegetarian, in response to my growing concern about the state of the world, animal cruelty and the environment. This meant consuming a lot of gluten and dairy based foods. As I entered puberty, my body couldn’t keep up with the energy demands of this stage of development and I began losing weight rapidly, despite eating a ton of carbs.

I was working hard at school, and have always pushed myself to succeed, but as my body became more and more unwell, I struggled with focus and concentration. My depression became worse and the world felt very bleak. Everything I ate caused pain, bloating, and fatigue. I was eating lots of pasta and cheese to try to fuel my sports but I continued to lose more and more weight. Throughout my parents had been doing everything to investigate and treat the cause of the illness, but I just kept getting more and more unwell. My weight dropped dangerously low, I developed bradycardia and I struggled to think clearly.

The years passed through adolescence and into early adulthood. Through sheer willpower and making myself eat, despite the intense pain it caused, including severe abdominal cramping, sulfur gas, burning, over-heating, swelling, headaches and more, I could get some extra weight on for a while, but it would quickly fall off again. My growth and development suffered. My bones froze in time – a bone age at 19 showed the bones thought they were 13. I had amenorrhea. I developed osteoporosis. An endoscopy showed an inflamed caecum and inflammatory spots in my sigmoid colon.

Through my teenage years and twenties, I had to follow extremely restrictive diets. I had to quit being vegetarian, as it didn’t leave anything to eat and my body clearly needed nutrients from animal foods to survive. I reacted to FODMAPs, histamines, too much fat, too many carbs – there was so little I could eat without feeling extremely unwell.

I would often experience intense nausea attacks, severe bouts of sudden pelvic pain, stomach bugs, and caught giardia several times. I got shingles at the age of 21, a strange fever induced by tick bites at 22, and viral meningitis at the age of 26.

Gut Dysmotility, Progressive Neuropathy, and Migraine

My gut was becoming lazier and lazier. At the age of 23, I wound up in emergency in extreme abdominal pain after it stopped moving altogether and my intestines became fully impacted. The pain was excruciating. Eight sachets of heavy duty laxatives did nothing to the situation. I was started on prucalopride (an enterokinetic drug) to help get it moving again. I cannot function without this drug now. When I stop taking it, my gut ceases to move altogether.

Through my twenties, I also started suffering from tingling in my arms and legs and increasing peripheral neuropathy. By the age of 27, I would experience episodes where an entire arm or leg was completely numb. Blood work showed my B12 had dropped very low. I went on B12 injections and increased food sources of B12. Things improved for a while but then the neuropathy returned. I subsequently developed Reynaud’s syndrome.

Around the same time, I started developing worsening headaches and a few years later migraines. The migraines were so bad I couldn’t move without intense vertigo and extreme nausea. I had to lie in a pitch dark room and wait it out. Some migraines were preceded by a confusional aura where I couldn’t tell what anyone was saying to me. I could understand the individual words but not when they were strung together in sentences. The vertigo continued for about 6 months.

Exercise became more painful too. Despite being fit, I would suffer from intense DOMS, headaches and nausea after running. Muscles started becoming more and more sore and painful despite taking electrolytes, being careful about my nutrition and warming up and down.

I woke up every morning feeling exhausted and sleep studies revealed I had developed sleep apnea – something I had thought wasn’t so common in women of my age and build.

Stress Fractures, Worsening Neuropathy, and Hypoxia

Earlier this year, I wound up with a bad stress injury in my hip – several stress fractures in my femoral neck despite no blow to the area and no fall – which doctors thought quite unusual for someone of my age who was running low mileage recreationally. The injury brought with it chronic nerve pain along my right side on top of worsening neuropathy.

I would wake up in the middle of the night with numb limbs. Nerves would fire spontaneously in my legs and arms. Nerves in my jaw felt constantly stimulated and my tongue would swirl uncontrollably around in my mouth. My gut stopped moving more and more frequently and I would have to take laxatives regularly to clear it out.

I had severe GI burning and was unable to eat anything other than clear broth and coconut water without pain. An endoscopy found bleeding in my sigmoid colon. My hemoglobin dropped 17 points and I struggled with breathlessness, unable to get up a flight of stairs or even walk a few hundred meters without feeling deeply exhausted.

To date, I have been diagnosed with POTS, Ehlers Danlos Syndrome, dysautonomia, gastroparesis, severe osteoporosis of the lumbar spine, and peripheral neuropathy. This comes against the backdrop of the gut problems experienced since childhood. These other health issues were, to no small degree if not caused, then significantly worsened by my gut issues. I have had long periods of time where I couldn’t absorb food or eat very much due to my gut problems, so I have been underweight for most of my life. As a result, I am likely deficient in many nutrients.

Current Diet, Activity, and Recent Testing

Diet

Breakfast: steamed greens (e.g. some combo of broccoli, beans, spinach, asparagus, etc.), 1-1.5 scrambled organic egg, 1 cup bone broth with 1 desert spoon collagen peptides + 1 desert spoon seaweed.
Lunch: 1 cup bone broth with 1 desert spoon collagen peptides + 1 desert spoon seaweed with 1 egg yolk stirred through OR some homemade chicken liver pate on carrot sticks instead of the egg yolk; 1 raw carrot and/or raw cucumber sticks; sometimes 1 packet of roasted nori.
Snacks: 1 glass homemade carrot, celery and ginger juice; some blueberries and/or a kiwi fruit.
Dinner: some protein (e.g. half a single piece of salmon, 8 prawns, small amount of red meat), green veggies (e.g. steamed beans, asparagus, spinach, broccoli), a starchy veggie (e.g. pumpkin, sweet potato, beetroot), sometimes some green salad.
After dinner: a few blueberries and/or pieces of mandarin, 30-40g vegan carob (cocoa butter, carob powder, no sugar), a cup of herbal tea.

Activity and Exercise

Daily: walking – approx. 12-13km over the course of a day including daily activities, as measured on Fitbit.
Running: 3x per week – currently at 9km total over the week; very slow 6’20” pace.
Yoga: 2x per week 1hr classes – beginner.
Physio: 3x 20-25min per week – core exercises for lower back, hips, shoulders etc as set by exercise physiologist.

Recent Testing

These tests were conducted by RN Labs and Great Plains Laboratory before I began thiamine.

Stool – GI-360

Klebsiella pneumoniae – very high
Proteobacteria – very high
Akkermansia muciniphila – very high
Escherichia spp. – very high
Bacteroides spp. – very high
Endolimax nana – very high
Eubacterium siraeum – very high
Enterobacter cloacae – high
Elastase – low
Butyrate – low
Clostridia – very low
Faecalibacterium prausnitzii – very low
Veillonella spp. – very low
Secretory IgA – very low

Urine – Organic Acid Test

Yeast and fungal markers:

3-Oxoglutaric – 0.69 (<0.33) – Elevated levels of 2-Oxoglutaric suggest dietary vitamin deficiencies or supplementation with 2-ketoglutaric acid. Coenzyme A (derived from pantothenic acid), flavin adenine dinucleotide (FAD) (derived from riboflavin), and thiamine are required for conversion of 2-oxoglutaric acid to succinyl-CoA.
Arabinose – 70 (<29) – Urinary levels higher than the reference range may simply reflect a high dietary intake of these fruits. However, arabinitol (which converts to arabinose) is also documented to be produced by the Candida genus of yeast. When elevated in body tissues, it can link with lysine and arginine. In theory, this may block some binding sites for coenzyme pyridoxal phosphate, biotin or lipoic acid at the lysyl residue in apoenzyme proteins. This would impair enzymatic processes, such as transamination of amino acids (in spite of “normal” intake of vitamin B6). A finding of high arabinose, without dietary intake of the above-mentioned fruits, suggests a stool analysis or other tests/examinations for Candida overgrowth.
Tricarballylic – 2.3 (<0.44) – Tricarballylic acid is a chemical by-product released from fumonisins during passage through the GI tract. Fumonisins are fungal toxins produced primarily by F. verticillioides. Tricarballylic acid is an inhibitor of the enzyme aconitase and therefore interferes with the Krebs cycle.

Bacterial markers:

4-Hydroxybenzoic – 1.9 (<1.3) – A marker for intestinal dysbiosis.

Oxalate metabolites:

Glyceric – 16 (0.77-7) – High glyceric levels on an organic acids test usually relates to primary hyperoxaluria type 2.
Oxalic – 389 (range = 6.8-101) – High oxalic with or without elevated glyceric or glycolic acids may be associated with the genetic hyperoxalurias, autism, women with vulvar pain, fibromyalgia, and may also be due to high vitamin C intake.

Glycolytic Cycle Metabolites:

Lactic – 51 (<48) – Elevated by a number of nonspecific influences, such as vigorous exercise, bacterial overgrowth of the GI tract, shock, poor perfusion, B-vitamin defciency, mitochondrial dysfunction or damage, and anemia, among others.

Mitochondrial Markers – Krebs Cycle Metabolites:

Succinic – 24 (<9.3) – The most common cause of elevated succinic acid is exposure to toxic chemicals which impairs mitochondria function.
Malic – 2.7 (0.06-1.8) – Higher levels of malic acid in urine indicates inefficiencies in energy production. Elevated malic acid values suggest increased need for niacin and CoQ10. When malic acid is simultaneously elevated with citric, fumaric, and alpha-ketoglutaric acids, it strongly suggests cytochrome C oxidase deficiency, indicating dysfunction in the mitochondrial energy pathways.
Aconitic – 6.6 (6.8-28) – Elevated in mitochondrial disorders. Aconitase metabolizes citric and aconitic acids, and is dependent on glutathione. Increased levels may indicate additional requirement for reduced glutathione.

Neurotransmitter Metabolites:

HVA / VMA Ratio – 2.3 (0.16-1.8) – An elevated ratio is often the result of decreased conversion of dopamine to norepinephrine by the enzyme, dopamine beta-hydroxylase. This inhibition is commonly caused by Clostridia by-products, including HPHPA, 4-cresol, and 4-hydroxyphenylacetic acid, which are also measured in the OAT.
Dihydroxyphenylacetic (DOPAC) – 3.9 (0.08-3.5) – DOPAC levels may be elevated due to inhibition of dopamine beta hydroxylase (DBH) from Clostridia metabolites, the mold metabolite fusaric acid, pharmaceuticals such as disulfiram, food additives like aspartame, or to deficiencies of the DBH enzyme due to copper deficiency, vitamin C deficiency, or malic acid deficiency.
Quinolinic – 0.58 (0.85-3.9)

Ketone and Fatty Acid Oxidation:

3-Hydroxybutyric – 5.7 (<3.1) – A moderate urinary increase in 4-hydroxybutyric acid may be due to intake of dietary supplements containing 4-hydroxybutyric acid, also known as gamma-hydroxybutyric acid. Very high levels may indicate the genetic disorder 3-methylglutaconic aciduria involving succinic semialdehyde dehydrogenase deficiency.
Acetoacetic – 32 (<10) – High levels of acetoacetate in blood may result from decreased availability of carbohydrates (eg, starvation, alcoholism) and/or abnormal use of carbohydrates storage (eg, uncontrolled diabetes, glycogen storage diseases).
Methylsuccinic – 5.7 (0.1-2.2) – Very elevated values may indicate a genetic disorder. Fatty acid oxidation defects are associated with hypoglycemia, and lethargy. Regardless of cause, intake of dietary supplements containing L- carnitine, or acetyl-L-carnitine may improve clinical symptoms.
Sebacic – 0.39 (<0.24) – Sebacic acid is a breakdown product of fatty acids. Higher levels can be seen when the breakdown of fats is impaired or blocked. May be associated with Vitamin B2 (aka Riboflavin) deficiency. Riboflavin is needed for fatty acid breakdown.

Nutritional Markers:

Vitamin B2 – 0.38 (0.04-0.36)
Vitamin C – 598 (10-200)

Discovering Thiamine

During this time, I was fortunate enough to learn about the work of Dr. Lonsdale and Dr. Marrs and have started talking high dose Lipothiamine. After several months, the chronic nerve pain is reducing and my gut has improved somewhat however I still struggle with pain and am very sensitive to a lot of foods.

I also have been learning more about the role of genetics and epigenetics in my condition. I am compound heterozygous for the MTHFR mutations and also have SNPs of the PEMT, NOS3, COMT, MOAB, GST genes alongside a number of other SNPs (including CYP, PONI, GAD, GGH, HTR2A, MMAB, NAT2, SLC, SULT, ALD, CBS, DHFR, MTR, TCN1, CBS, DDC, DRD and more).

I am currently taking 1000mg of Lipothiamine orally per day. If IV was possible, I would do that given my gut problems, but we have not been able to find anyone able to administer that here in Australia. In addition to the Lipothiamine, I take magnesium (800mg), liposomal Vitamin C (6000mg), glutathione (450mg), probiotics, a multivitamin, cod liver oil, B-complex, Alpha Lipoic Acid, zeolite, zinc and methylated b12 (shots occasionally and drops in between).

I follow the Auto-immune Protocol diet (including all fresh, unprocessed food, no sugar, lots of veggies and fruits, organic fish, meat, eggs, etc.), walk daily, practice yoga, meditation, daily stretching and gentle jogging a few times a week.

Improvement with Thiamine and Outstanding Questions

In recent weeks, I’ve been finding the nerve pain has significantly improved on this high dose (1000mg) of Lipothiamine however my gut symptoms are quite bad – with a lot of GI burning. I experienced this when I first started taking the Lipothiamine but it subsequently subsided so I am unsure if this is something I need to just push through or if I am on too high a dose.

I would love to hear others experience and hope that sharing mine is of use to others. I am deeply grateful to Dr. Lonsdale and Dr. Marrs for their groundbreaking work in this area and hope to do whatever I can to spread the word about this vital information so that more people can experience full health and happiness in their lives.

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 December 14, 2020.

Narcolepsy, Basal Ganglia, Mitochondrial Fitness, and Kickboxing

by Chandler Marrs, PhD

Published on February 7, 2023

9337 views

Several years ago, when I just beginning to understand the role of nutrient co-factors in mitochondrial health, I was working with a young woman who had been injured by Gardasil. She was my first ‘case’, contacting me online after a post I wrote about the thyroid damage done by this vaccine. Thyroid damage is among the more common disease processes initiated by many drugs and vaccines. It is one of the easiest problems to rule in or out, but more often than not, it is missed by most practitioners. Inasmuch as thyroid and mitochondrial function are reciprocally connected, where there is damage in one, there is damage in the other, and inasmuch as thiamine is requisite for healthy mitochondria, correcting thiamine deficiency can, in many cases, improve thyroid function. When I first met this woman, I did not yet fully appreciate that connection. Eventually, I would be introduced to Dr. Lonsdale and his work on thiamine deficiency, and so began my education. Together, we wrote a book about the role of thiamine deficiency in mitochondrial illness: Thiamine Deficiency Disease, Dysautonomia and High Calorie Malnutrition.

Exercise and Mitochondrial Healing

Her case is unique for a number of reasons, but mainly because, in addition to the thiamine and other nutrients required to heal, she used, and continues to use, exercise to manage her health. That is what I would like to talk about today: the role of exercise in mitochondrial health. Before we do that, below is a synopsis of her case, as reported in our book on pages 286-87. Her full story was provided on our website here.

In 2008, 26-year-old G.C., a previously healthy, athletic young woman, finishing a Master’s program in finance, received the three injections of the Gardasil vaccine. It bears mentioning that 2 years prior she received several travel-related vaccines including diphtheria, typhoid, yellow fever, hepatitis A and B, the flu vaccine, and a tetanus boost and suffered no apparent ill effects.
After the second injection of Gardasil she experienced a flu-like episode with high fever lasting over a week. Full-blown hypersomnia manifested shortly thereafter and worsened to the point where she was able to sustain wakefulness for only 45 min to a maximum of 3 h per day. She experienced fatigue, muscle weakness, and dizziness. Over the next several months she developed tachycardia, intense salt cravings, with concurrent dizziness and thirst. The salt cravings led to blackouts and as she described “waves of extreme somnolence” that included slurred speech, lack of coordination, and imbalance. She learned to keep salt with her at all times. Both physical (e.g., walking, standing up, cooking) and mental exertion were profoundly draining. She reported that if she became angry or experienced any emotional event, she would immediately fall asleep. Multiple doctors had been seen and tests completed. By 2010, only low levels of vitamin D had been recognized.
Narcolepsy, Hypersomnia and Exercise
In late 2010, the fifth physician seen, it was diagnosed as narcolepsy without cataplexy–hypersomnia. She was prescribed 300 mg per day of Modiodal (Modafinil, Australia; Provigil, United States). Wakefulness increased, but she was still dizzy and required multiple hour naps after any exertion. She returned to working out. By the end of 2010 she began a PhD program and was determined to “power through.” She found that exercise, though difficult, allowed her to avoid blackouts. Of note, cardio-type workouts provided respite from the dizziness for 4–6 h, whereas weightlifting netted 24 h without dizziness. Similarly, she observed that if she ate simple sugars or carbohydrates the dizziness and blackouts would return.
Six months after beginning Modiodal her health continued to decline despite experiencing greater wakefulness. She developed severe noise and light sensitivity, continued to experience dizziness, and required excessive amounts of sleep, sea salt, and water. She developed a thick, dry, painful scale on her scalp. Another series of doctors could offer nothing and suggested the illness was in her head, inferring that she “needed to pull herself together.” Despite her health issues she defended her PhD in July 2013.
By October 2013 she had seen 10 physicians as her health continued to decline. She read our work on post-Gardasil thyroid dysfunction and other adverse reactions and requested additional testing. Hashimoto’s, hypogammaglobulinemia, vitamin B deficiencies, and low potassium levels were identified. On several occasions she attempted to get transketolase testing but was unsuccessful. In Nov. 2013 she decided to treat empirically beginning with 100 mg thiamine tetrahydrofurfuryl disulfide (TTFD). She subsequently developed the paradoxical reactions discussed in Chapter 4, with her symptoms worsening.
The Paradox or Refeeding Syndrome
With the dizziness and increased heart rate she reduced her dose to 50 mg of TTFD. Over the course of the next 5 weeks, the tachycardia landed her in hospital on four occasions. By December 2013 her body adjusted to the dosage of TTFD and the tachycardia and dizziness subsided. This is important to note. Long-term dysfunction of this nature requires new knowledge from the physician. Though not damaging to the patient it is regarded as “side effects” and either the patient or the physician stops the treatment. This effect was known to the ancient Chinese and regarded as examples of yin and yang by acupuncturists.
Over the course of the 5 years of progressively declining health she saw a total of 24 doctors. None of whom was able to identify or treat what was ultimately a metabolic disturbance brought on by thiamine deficiency that was likely triggered by the vaccine. Her final diagnoses included cerebral salt wasting, POTS, beriberi, hypersomnia, and Hashimoto’s. Arguably, the thiamine deficiency and the mitochondrial damage that ensued were at the root of each of these diagnoses.
Maintaining Health Post Gardasil
Since 2013 she has continued to maintain her health with thiamine, magnesium, and a cocktail of other mitochondrial supplements (which included very high doses of coenzyme Q10), along with thyroxine for Hashimoto’s and Modiodal to treat the somnolence. As of this writing she is doing well, training in various Asian forms of kickboxing daily and working full time. Without the balance of heavy training, the cocktail of supplements, the Modiodal, and thyroxine, her symptoms reappear.

Her case is remarkable for a number of reasons. First, that she recovered at all is impressive. Many women injured by Gardasil do not recover. She did and continues to thrive all of these years later. Her recovery was not linear though and her continued health requires aggressive attention. I think this process throws many people. We have been trained to expect that recovery from illness proceeds in a logical, linear, and expeditious manner. It does not. There were many setbacks, including several hospitalizations when she first began supplementing with thiamine. Had she not persisted through these setbacks, she might not have recovered her health. Moreover, had she not recognized the fragility of this recovery and continued to actively manage her health all of these years later, she could have easily become seriously ill again. kickboxing, basal ganglia, narcolepsy Indeed, there have been many relapses over the years, where her health declines significantly and requires extended periods of recovery. Nevertheless, she is able to recover and that is remarkable.

Secondly, and what I think is particularly unique about her case, is the role that exercise has played in her ability to recover and maintain her health. It is not something that conventional or even functional medicine gives much credence too. Sure, we all recognize the role of exercise in health generally, but mostly, we ignore it. I think this is a mistake. In her case, exercise was and remains critical to maintaining her mitochondrial health and as I have come to understand recently, the type of exercise that she gravitated towards naturally, kickboxing, may be exactly what her brain needs to function.

The Role of Exercise in Recovery

From the beginning of her illness, she forced herself to exercise, even though it was an immense struggle. On her own, she learned that certain types of exercise would prevent her dizziness and blackouts. Specifically, if she did cardio-type exercise, she could prevent a blackout for 6 hours or so, but if she added some weightlifting, the effects would last for up to 24 hours. I attributed this to exercise-induced mitochondrial biogenesis. That is, exercise was forcing the birth of new mitochondria, and somehow, shifting her balance of unhealthy to healthy mitochondria more favorably. It was also likely improving the respiratory capacity of her existing mitochondria. Although it is still not clear to me why one modality yielded better results than another, as the research in this area seems to suggest that the opposite is true, that cardio yields more mitochondrial benefits than weightlifting, the research is clear that exercise induces both mitochondrial biogenesis while improving their functionality.

Her seemingly innate realization of this was and remains one of the more noteworthy aspects of her case. Remember, for several years after Gardasil vaccine, she was seriously ill. When she first contacted me, she weighed less than 100 lbs, was severely fatigued, and could not maintain wakefulness for more than a few hours at a time without blacking out; and yet, somehow, she managed to drag herself to a gym to exercise (and maintain her graduate work in finance). Not only that, she observed a pattern of response to exercise (and salt and other dietary components) and used what she learned to help herself function better. Indeed, throughout her recovery, she would actively observe the patterns and optimize those that appeared beneficial and eliminate those that did not; something that we all should be doing as a matter of course, and yet, very few of us do.

To exercise throughout an illness where intractable fatigue, excessive somnolence and blackouts dominate is very difficult to do, and more often than not, would be discouraged. When I first wrote about her using exercise to heal, the backlash was immediate and intense. For her though, the exercise became an integral component of maintaining her health just as surely as the nutrient elements. Even now, 12 years from initial vaccine-induced illness and with 7 years of recovery under her belt, she indicates that when she misses training because of work or travel, her health declines rapidly and does so in a fairly specific manner. She becomes dizzy, loses balance, and her cognitive capacity diminishes significantly. Her ability to maintain wakefulness declines while fatigue increases. Additionally, when the stress of normal everyday illnesses come into play, a viral infection for example, and her exercise program naturally takes a hit, in order to fully recover she has to double-down on the training for a period of time once the illness passes.

Is this need to exercise unique to her case specifically or could we learn something about how we approach recovery from illness? I would argue that given the mitochondrial fitness attributable to exercise and the noted mitochondrial decline in its absence, some form of movement or exercise should be approached with any recovery plan. If this is the case, the questions become, at what point in the illness or recovery should exercise be considered, how much, and in what form? While the answers to these questions are far too individual to explore fully here, what we learn from her case is that exercise, when implemented early, improves recovery. That brings us to a more complicated question; why kickboxing, boxing, or other dynamically challenging programs might be useful for narcolepsy specifically. From what I have learned, it may be related to activating and training neural connections in a region of the brain called the basal ganglia. And of course, the mitochondria are still involved.

Enter Kickboxing and the Basal Ganglia

I believe there is damage to the basal ganglia for her and other Gardasil injured women. To this point, among the more common symptoms associated with Gardasil injury are tremors, ataxia, and gait issues. While those symptoms can easily be attributed to cerebellar and thyroid damage as well, and both of which are affected by the vaccine and thiamine deficiency, it is not without warrant that we look at the basal ganglia for these symptoms, as well as for the sleep and wakefulness issues. Neural tracts between the cerebellum and basal ganglia suggest that if one is damaged, messaging and functioning to the other would be impaired. Indeed, research shows both efferent and afferent disynaptic (from and too, two neuron) connections between the cerebellum and the basal ganglia. Additionally, personal communications with other women affected by Gardasil regarding imaging results confirm damage to the basal ganglia in some women. This is in addition to potential cerebellar damage.

Symptomatically, many post-Gardasil women display an ataxic, drunken sailor like gait, which is indicative of cerebellar involvement while their tremors occur at rest, along with muscle rigidity and dystonia, indicating basal ganglia involvement. All of them suffer from what could be termed hypersomnia and excessive fatigue, but none that I have met thus far were diagnosed with narcolepsy, like this patient. Of course, that does not exclude the possibility that it does not exist. The post vaccination symptoms are diverse as one might expect with mitochondrial damage and autonomic system dysfunction.

Why the Basal Ganglia?

The basal ganglia are set of nuclei buried deep in the brain that are responsible for controlling movement, motor learning, executive function (via connections with the frontal cortex) and emotional regulation and motivation (via connection to the limbic system). See figure 1.

brainstem basal ganglia — Figure 1. Tracts of the basal ganglia.

The basal ganglia act as a breaking system to complex movement patterns and activities.

The most well known disorders of these nuclei include Parkinson’s and Huntington’s diseases. These are dis-inhibition syndromes, where the normal inhibitory control that the basal ganglia hold over motor movements is lost resulting in tremors and chorea respectively. There are also problems with initiating movement. This occurs via connections to the limbic system, particularly a set of nuclei located in what is called the ventral tegmental area (VTA). These nuclei are central to motivating behavior, addictive behavior in many cases, but also, behavior in general. The dopamine released by the VTA neurons provide reward and reward, as we all know, encourages habit and learning. That hit of dopamine gives us the drive to act. As Parkinson’s disease progresses, patients lose these connections and with them that internal, unconscious motivation that initiates behavior. They become stuck and so absent an external cue, patients will become unable initiate a movement internally on their own. This stuckness might sometimes also manifests as a sort of depression; one where there is no motivation to act at all.

One of the latest alternative treatment modalities for Parkinson’s disease, aside from thiamine, involves boxing. Yes, boxing. Boxing, because of the balance requirements, the bilateral, stop/go and cognitively active nature of the exercise seems to activate tracts in the basal ganglia that increase inhibitory control, reduce tremors, and allow for a smoother initiation of movement patterns. It also improves gait speed and balance, conditioning, cognitive ability, and overall quality of life.

What does all of this have to do with the ability to maintain wakefulness, and as our patient indicated, cognitive clarity? This, as far as I can tell, has not been studied, but I suspect it has to do with enhancing motivation. Not motivation in the psychobabble sense, but motivation as a fundamentally physiological, survival-based behavior; motivation that is controlled by the basal ganglia via connections to the limbic system and the frontal cortex, respectively. That hit of dopamine that engenders motivation is key for not only movement but arousal. When there is damage to that system, wakefulness is near impossible. Rodent studies have born this out. Without ‘motivation’ we cannot remain awake and we cannot sustain the arousal necessary for mental acuity.

Consider for a moment, the key aspect among all of the behaviors controlled by basal ganglia is that they necessitate wakefulness. Given that, it makes sense from a purely logical perspective that the basal ganglia might be involved in maintaining the arousal necessary to perform these activities. Similarly, it makes sense that damage to certain tracts within these nuclei could impair not only one’s ability to maintain wakefulness, but also, one’s ability to manage motor movement with altered sleep/wakefulness patterns. Finally, absent sustained and vigilant wakefulness, mental acuity is impossible. The cognitive fogginess, so often reported by these patients, may very well be linked to disruptions in basal ganglia functioning.

But Wait, There is More: The Orexin System and the Basal Ganglia

When narcolepsy and other sleep/wake disorders are researched, the basal ganglia have only recently come into view. This is despite the fact that the most well-known disorders of the basal ganglia, like Parkinson’s, demonstrate clear sleep/wake disturbances. Instead, another set of neurons located in the hypothalamus, called the orexin/hypocretin neurons (same neurons, different name), dominate the research landscape. Damage to these neurons is clearly linked to narcolepsy, cataplexy and other sleep/wake disturbances, and for our purposes, directly attributable vaccine reactions, especially the flu vaccine. The basal ganglia, not so much. How do we reconcile the known connections between orexin system, narcolepsy, and vaccine damage, the paucity of research on the basal ganglia. Well, like everything in the brain and body, we look for communication patterns. And it just so happens, the orexin neurons clearly interact with the basal ganglia to manage arousal, both directly via orexin receptors in various regions of the basal ganglia and indirectly, via vast projections throughout the limbic system, which then project to the basal ganglia.

Backing up just a bit, the release of orexin induces wakefulness. I have written about this system here, here, here, and here. When orexin neurons are turned on and firing appropriately, arousal is maintained. When orexin neurons are turned off, diminished or dysfunctional, melatonin, the sleep promoting hormone, is turned on. The two work in concert to manage wakefulness and sleep. Orexin receptors are located throughout the central nervous system and in the body. For our purposes, the orexin receptors in the amygdala and throughout the limbic system directly activate the release of dopamine from the VTA. Recall, dopamine projections from the VTA to the basal ganglia are critical for motivating and sustaining wakefulness in Parkinson’s patients. Additionally, orexin receptors have been found in different regions of the basal ganglia themselves, suggesting direct regulation of arousal. Perhaps even more importantly, the orexin neurons have been found to be instrumental in integrating motor movement patterns.

“…numerous neuroanatomical and immunohistochemical studies reveal that essential subcortical motor structures, such as the basal ganglia, cerebellum, and vestibular nucleus, receive direct innervation from orexin neurons. Moreover, during movements, orexinergic neurons are particularly active and orexin release increases. The evidence suggests that the orexinergic system directly participates in central motor control.”

So what we have is an integrated system of arousal, movement control, and cognitive behaviors that relies heavily on the health and functioning of the basal ganglia and its connections through out the brain, including with orexin system in the hypothalamus. And the orexin system itself relies heavily on functioning mitochondria, as does everything, but the orexin neurons are particularly sensitive to diminished mitochondrial function as these neurons require as much as 5-6X the amount of intracellular ATP to maintain firing compared to other neurons. The orexin neurons cease firing when ATP stores become low, inducing sleep to allow the reallocation energy towards more basic survival functions like heart rate and respiration. That means that excessive sleep is to be expected with mitochondrial damage.

Putting It All Together

With direct stress to the mitochondria via vaccines and medications we can expect a variety of negative symptoms. In this case, our patient developed thyroid damage, autonomic dysfunction (cerebellar and brainstem involvement), and likely also, some degree of basal ganglia injury. The hypersomnia, so commonly experienced during illness or adverse medication/vaccine reactions, represents diminished orexin activity likely initiated by diminished mitochondrial capacity. Narcolepsy suggests a specific injury to oxexin system. With the diminished orexin capacity, we can anticipate that basal ganglia function would be impacted, and with it, the ability to maintain the requisite ‘motivation’ for arousal and wakefulness and to coordinate movement and maintain cognitive acuity. Nutrients and exercise improve the respiratory capacity of mitochondria, which in turn, provides the requisite energy to manage autonomic function from the brainstem and cerebellum and to sustain wakefulness by maintaining orexin firing in general and to the basal ganglia more specifically. Additionally, exercise that demands dynamic, bilateral, complex movement patterns, such as kickboxing, may serve to retrain or maintain the strength of synaptic connections to, through, and from the basal ganglia, which ultimately, may offset any damage done by the initial insult.

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This article was published originally on March 12, 2020.

Progressive Deterioration of Health With Severe Nutrient Deficiency

by TJ

Published on February 2, 2023

8828 views

This is the story of my wife’s decline in health following the surgical reconstruction of a torn left hip labrum. I am writing this for my wife because her health has declined so significantly over the past 5 years that she has become medically homebound and bedridden. She is too weak and unbalanced to walk, has become intolerant to light, to foods (she can only eat 10 different foods without having a reaction), to smells, and is in constant and extreme pain. She has also developed severe skin reactions that are destroying her lower extremities. After seeing more than 50 doctors with little to offer, we are posting her story here in the hope that someone will be able to help.

Post-surgical Development of Complex Regional Pain Syndrome

Megan is a 44 year old female who was athletic, very active, and physically fit her whole life. Prior to left hip labral reconstruction on 6/20/2017, Megan did not take a single prescription. She led a very healthy lifestyle, in which she enjoyed playing tennis, doing yoga, swimming, biking, snowboarding, running, hiking, camping, and backpacking regularly. Postoperatively, she developed left foot edema, redness, allodynia, hyperalgesia, diminished proprioception, and balance, and burning pain in her left foot. Despite diligently participating in physical therapy 3 times weekly, she was not able to fade off of her crutches. She continued to have severe lower extremity pain and was diagnosed with Complex Reginal Pain Syndrome (CRPS) on 11/1/2017. In December 2017, Megan participated in an FDA-approved clinical trial of neridronic acid (bisphosphonate) infusions for CRPS without relief. She developed flu-like symptoms, which got progressively worse after each infusion, but eventually resolved.

Skin Manifestations

By January 2018, Megan started to develop lesions on her left foot. Initially, they were pinpoint to large flat lesions. Some of them were extremely itchy. Overtime, the lesions and rash spread up her ankle and shin on her left leg.

Skin and vascular manifestations of nutrient deficiency — Left foot edema and skin lesions May 2018 (left), June 2018 (right)

Over the next several months, while still attending physical therapy, Megan noted a lack of hair growth on her lower left leg, temperature discrepancies, in which the left foot was subjectively hot but objectively cooler than the right foot, blood pooling, and skin discoloration in her feet (dark red/purple) when standing, nail changes, and bilateral lower leg flushing following a warm shower. During this time, food sensitivities were also first observed – initially with beef and shrimp.

More Diagnoses But Little Help

In October 2018, Megan was evaluated by a physician at Brown Medical School, who is an expert with CRPS. He confirmed the diagnosis of CRPS (bilateral lower extremities) and in his provisional assessment of Megan, also diagnosed her with bilateral common peroneal neuralgia and bilateral foot drop. He also suspected Megan has mast cell activation syndrome (MCAS), orthostatic intolerance/dysautonomia (POTS), and hypermobile type Ehlers-Danlos Syndrome (hEDS) and was able to delineate which symptoms were consistent with CRPS and which were not. He did not attribute the blood pooling, the footdrop, flushing, lesions, rash, food intolerances and allergic-like reactions, dermographia, and other skin manifestations to CRPS. He recommended she be evaluated by another physician at the Steadman Clinic to assess for common peroneal nerve entrapment.

In October 2018, the Steadman doctor concluded that Megan did not have a common peroneal nerve entrapment. Instead, he noted irritations in the saphenous and obturator nerve distributions and diagnosed her with “bad luck”. He recommended Megan have an MRI of her lower back to ensure there is no central based pathology contributing to her bilateral symptoms. A lumbar MRI was conducted, which yielded no significant results.

Catastrophic Progression of Symptoms

All symptoms started after an orthopedic surgery on the left hip. Prior to the surgery on June 20^th, 2017, there is no significant medical history. She had a clean bill of health prior to surgery – no prescriptions were taken, no known allergies. In April 2018, we learned the hospital that performed the surgery was not properly sterilizing the surgical instruments and operating rooms between surgeries, which resulted in numerous infections, injuries, and illnesses, per an investigation.

New symptoms, which have appeared in the last 24-36 months include: heavy sweating, bladder incontinence (especially after eating and some while sleeping), sudden urge to urinate, sudden urge to drink water, decreased vision, extremely dizzy, and feeling lightheaded when standing. Brain fog has been getting progressively worse. Food reactions and extreme sensitivity to stimuli have been getting progressively worse and more frequent. Menstrual cycles have been getting progressively worse – worst symptoms and highest pain are observed during the cycle. Food reactivity is more likely and worse while menstruating.

Current treatment approaches have not resulted in any lasting or significant improvement. Despite intervention, symptoms have gotten progressively worse. Megan has been medically homebound since 2019.

Large patches of skin peel, turn white, and flake off ankles, shins, and legs below the knees. Clusters of tiny “pin prick” lesions appear on tops of both feet and on legs, including thighs. There is a lace-like pattern of purple/brownish skin discoloration above the knees (Livedo Reticularis), which continues up the thighs. The lesions, rash, and discoloration have been progressing up both legs. Skin/tissue on feet appear purple, blue, red, pink, orange, discolored, and shiny in places. There is no hair growth on both legs below the knees. Toenails on both feet are thick, crumbly, extremely brittle, and yellowish/brown. There is little to no growth of toenails.

Progression of skin symptoms over time. Left- April 2022; middle and right – December 2022

Feet and legs appear less reddish and flushed when elevated, however, they quickly turn purple upon standing. The purple discoloration fades when feet are elevated. Flushing is also present after showering and with temperature changes. Edema is present in both feet, ankles, shins, calves, and knees. An extremely painful, deep “itch” is felt in both feet and lower legs. Tremors are present throughout both legs. Standing upright elicits dizziness, tachycardia, presyncope/syncope, heart palpitations, and blurry vision (especially after eating).

Bilateral footdrop is present without a known cause. As a result, walking is exceedingly difficult, and assistance is required to move throughout the house. Balance, motor planning, proprioception, coordination, and gait have all been dramatically impacted. A wheelchair/transport chair is currently being utilized for community access.

Excruciating 9/10 pain in feet and lower legs. Hyperalgesia and allodynia observed. Socks, shoes, and any other clothing/materials are no longer tolerated below the knees due to pain. Severe 8/10 “deep bone pain” in lower legs and shins. Severe 8/10 joint pain in shoulders, hips, knees, hands, fingers, ankles, and wrists. Muscle spasms and tremors (lower back/body), stiffness, and weakness in legs and arms. It is now difficult to type and to write due to pain in wrists, hands, and fingers. Lights, sounds, touch, and weather/pressure changes cause significant 7/10 pain.

Diet is currently limited to about 10 foods (has decreased over time) due to allergic-like reactions that occur immediately after and while eating foods. The severe reactions have resulted in 3 trips to the emergency room. Foods frequently cause swelling to the face, eyes, and lips, dizziness, nausea, excessive eye dripping and tearing, excessive post-nasal drip, and an extremely painful deep itch with a rash and “pinpoint” lesions to appear on legs and feet. Eating also evokes sweating, extreme fatigue, and tachycardia. Only fresh food is consumed. Leftovers are frozen immediately. The family has not been able to cook inside for over 3 years due to serious respiratory distress, reactions, and irritations to eyes, ears, and throat caused by smoke, scents, and odors. In addition to scents, there is an extremely heightened sensitivity to light and sound. Socks, shoes, and any other clothing/materials are no longer tolerated below the knees.

Nutrient Deficiencies

Over the last year, we have learned that Megan suffers from several nutrient deficiencies, including thiamine, which was measured at only <6 nmols/L in December. After stumbling upon a case story about thiamine deficiency here, it is difficult not to wonder if low thiamine was responsible for her rapid decline in health following the surgery. Many of the symptoms she developed immediately following the surgery, the muscle weakness, edema, foot drop, proprioceptive difficulties are indicative of low thiamine. Over time, she developed an intolerance to most foods, which, from what I understand, is also common with thiamine deficiency. This then spiraled into other sensitivities (light, sound, and scent, etc.) and other sets of bizarre symptoms. In fact, as I do the research, I am learning that many of her ‘diagnoses’ are not independent diseases but could actually be manifestations of the low thiamine.

Of course, as her health declined and her ability to safely tolerate foods also declined, other deficiencies likely came into play. The skin issues may be related to deficiencies in vitamin A, which we have tested, and vitamins D and K, which we have not yet tested. She is also severely deficient in vitamins B12, C, and has low iron, copper, and zinc. Each of these can contribute to a wide variety of symptoms and compound her already poor health.

Copper Deficiency 2/16/22
Ferritin Deficiency 3/8/22, 8/12/22
Zinc Deficiency 8/12/22
Vitamin C Deficiency 8/12/22
Vitamin A (Retinal) Deficiency 12/9/2022
Vitamin B1 (Thiamine) Deficiency 12/9/2022
Vitamin B12 (Cobalamin) Deficiency 12/9/2022

Current Symptoms

General: heavy fatigue, migraines, low-grade fever, flushing, swollen lymph nodes, night waking, early waking, difficulty falling asleep, and daytime sleepiness
Eyes: droopy eye lids, blurry vision, eye dripping, and excessive tearing
Ears/Nose/Throat: hoarseness, stuffiness, sore throat, postnasal drip, heightened sense of smell, sinus pressure, ear ringing and buzzing, headache, migraines, sensitivity to loud noises, sores/ulcers on the roof of mouth and tongue, swelling of face/lips/throat, and lips/throat feeling “tingly”
Heart: tachycardia, palpitations, swollen ankles/feet, edema, and blood “pooling” in legs
Respiratory: shortness of breath/breathlessness, coughing, and wheezing
Gastrointestinal Tract: bloating, cramping, acid reflux, alternating diarrhea and constipation, excess flatulence/gas, indigestion, nausea, and poor appetite
Urinary Tract: the sudden urge to urinate, and mild bladder leakage/incontinence
Musculoskeletal: muscle spasms, tremors, cramps, joint pain, joint stiffness, and muscle weakness
Skin: rashes, hives/welts, hair loss, itching, swelling, skin peeling and flaking, livedo reticularis, excessive sweating, “pinpoint” lesions, flat-reddish lesions, and dermatographia
Endocrine: cold intolerance, heat intolerance, urge to drink water, abnormally heavy/difficult menstrual periods, chills, and shaking
Neurology: difficulty concentrating, difficulty thinking, difficulty balancing, brain fog, dizziness, light-headedness, tingling, and tremors

Previous Medical History

Infected with Epstein-Barr/mononucleosis: 1993
Pityriasis Rosea in 2011
Infected with antibiotic resistant strep throat in 2012
Left hip labral tear in 2016
Right hip labral tear in 2016
Erythema ab igne (due to heating pad) in 2017
Left hip arthroscopy on 6/20/2017
- Femoral osteoplasty
- Mild acetabular rim trimming
- Minor shaving chondroplasty
- Acetabular labral reconstruction – transplanted labrum made from 11cm graft (cadaver tissue)
- Capsular closure
- Arthroscopic greater trochanteric bursectomy
- Windowing of IT band
- PRP injection
FDA Clinical Trial of Neridronic Acid for CRPS 12/2017

Current Diagnoses

Right hip labral tear, FAI/CAM Impingement, Bursitis, 2016
Complex Regional Pain Syndrome (CRPS) 11/1/2017
Suspected Ehlers-Danlos Hypermobile Type (hEDS) 10/1/2018
Suspected Histamine Intolerance/Mast Cell Activation Syndrome (MCAS) 10/1/2018
Bilateral Footdrop 10/1/2018
Bilateral Common Perineal Neuralgia 10/1/2018
Orthostatic Intolerance/Dysautonomia (POTS) 10/1/2018
Alternaria Alternata allergy 11/13/19
Secondary Polycythemia 1/5/2020
Hashimoto’s Thyroiditis 9/14/2021
Tinea Pedis Onychomycosis 12/2/2021 (misdiagnosed and overlooked for at least 2 years)
Elevated Leukotriene 2/16/22
Dysautonomia/Postural Orthostatic Tachycardia Syndrome (POTS) 9/6/2022

Current Medications

(updated 1/15/23)

Morning (Before breakfast)	Evening (Before dinner)	Late Evening (Before bed)
Naltrexone (LDN) 4.5 mg	Vitamin C 1000 mg	Metoprolol 12.5 mg
Singulair (Montelukast) 10 mg	Zinc (sulfate) 25 mg	Neurontin (Gabapentin) 300 mg
Aspirin (NSAID) 81 mg	Copper 2 mg	Vitamin B1 (Thiamine) 100 mg*
Tagamet (Cimetidine) 200 mg	Iron 50 mg	Topical Terbinafine Cream (PRN)
Zrytec (Cetirizine) 10 mg	Tagamet (Cimetidine) 200 mg
Synthroid (Levothyroxine) 50 mcg	Zrytec (Cetirizine) 10 mg
Quercetin 500 mg	Quercetin 500 mg
Neurontin (Gabapentin) 300 mg	Vitamin B1 (Thiamine) 100 mg*
Vitamin B1 (Thiamine) 100 mg*

*Vitamin B1 (Thiamine) started 12/23/22

Previous Medications

Short-term Prednisone (following ER Trip) provided significant relief of pain, skin rash, lesions, reduced swelling, and allowed more foods to be tolerated. Produced significant improvement of symptoms.

Ketotifen – This medication was introduced and then discontinued due to potential side effects and lack of progress. Megan was taking 1 mg
Cromolyn – This medication caused mouth ulcers (white spots) to occur, and it was discontinued. A nebulized form was prescribed but given without instructions as to how to introduce.
Xifaxan – 10-day antibiotic course completed on 7/18/22 without improvement

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The Red Thread and Thiamine

by Joanna

Published on January 19, 2023

19589 views

There is a saying in China about a Red Thread connecting people who are destined to meet and/or help one another in a profound way no matter how far apart they may be. Our adopted daughter Abby is that red thread. Abby was abandoned and found on the day our oldest daughter, Kayla, turned thirteen. It was at this time Kayla’s health issues were becoming worse. Although we didn’t know exactly what was amiss, we knew that something was wrong. In our efforts to help Abby, our family’s health issues were brought into stark relief. It seems that all of us have suffered from longstanding thiamine insufficiency. Even though my two daughters were born worlds apart, that red thread connects us. We published Abby’s story last week in the hopes that it might help someone else. Here is Kayla’s story.

Unhealthy Beginnings for My Beautiful Daughter: IVF and Induction

Common sayings like ‘you are what you eat’ can be haunting, leading to guilt when we see our children suffer the consequences of our own ill health, especially during pregnancy. My gut was messed up and had been for a very long time before becoming pregnant. I was likely deficient in thiamine and other nutrients and perhaps that is why I struggled to get pregnant in the first place. Sometimes gut dysfunction is obvious, as with constipation or diarrhea, but more often it manifests itself in other ways. That was me. I had/have Ehlers Danlos Syndrome (EDS) and most likely also, Mast Cell Activation Syndrome (MCAS) and Postural Orthostatic Tachycardia syndrome (POTS). I did not know any of this though before pregnancy and have only recently, after hours upon hours of research, come to learn how my health impacted my daughter’s health.

Kayla was our first hard-fought-for child. We were married 10 years and had undergone numerous fertility treatments before we finally achieved a successful IVF. Looking back, I realize that I was not healthy prior to or during my pregnancy, even so it was mostly an uneventful pregnancy with little to no typical unpleasantries. I had low progesterone early on that required progesterone injections and suppositories, but after 13 weeks everything stabilized. I had a high blood pressure reading at only one routine visit in my 39th week. The doctor decided to induce. We didn’t question it at the time, but later did. At the hospital, he administered Pitocin, a synthetic oxytocin, without any nurses in the room and left. The nurses later commented that they were surprised, since my blood pressure was back in the normal range upon admission. Pitocin is just one of my regrets. Why was my body not triggering labor? Gut dysbiosis? Maybe/possibly/probably or maybe she just wasn’t ready to come out.

A Truly Gifted Child

Kayla was an extremely bright child. She wanted to learn chess at four years old. By age 9, I stopped playing with her because she always won. She gave her math brilliant-grandfather a run for his money. She was homeschooled through 9th grade followed by private and then public school. She was a straight ‘A’ student, participated in various athletics (swim, track, dance, horse riding, etc.) and mastered two musical instruments by the end of high school. Kayla ranked in the top 5th percentile nationally and did well in first semester of college, but little did we know how precarious her health had become. Perhaps because of her intelligence and achievements, many of her health issues and difficulties were disregarded by physicians. On the surface, she looks well. She is very high functioning, but she has been plagued with an assortment of complicated and largely unrecognized health and neurological issues since birth. During her first semester of college, a series of stressors brought her health crashing down and she is only now beginning to recover. Part of her recovery has been diet, part involves thiamine, but we are still missing some pieces, which is why we are publishing her story.

Early Childhood Symptoms and Triggers

Her early childhood was marked by early bouts of bronchitis necessitating antibiotics. She suffered croup through age 7 years and seasonal allergies through her teens for which she used Claritin regularly. Nighttime enuresis was a problem until we removed gluten from her diet when she was 12 years old. Similarly, her speech was often and seemingly randomly slurred. She received speech therapy through the school to no avail. In 2018, we removed dairy from her diet and the slurring disappeared. It appears that just as a gluten reaction triggered her nighttime enuresis, the ingestion of dairy was some sort of trigger for her slurred speech. I should note, before learning this, we experimented with probiotics, fish oils, digestive and pancreatic enzymes, and a variety of other supplements off and on for years with no noticeable or lasting changes. Her younger years were marked also by body temperature dysregulation, i.e., hot in the winter, cold in the summer. Finally, most things, not all, came easy to her. She had extreme strengths and weaknesses with her strengths often masking her weaknesses. Noticed by many of her extracurricular teachers hard things seemed easy, and easy things hard. Her brain craved complexity.

Vaccinations, Cyclic Fevers, and Green Drinks

In her preteen years, she received numerous vaccinations (required and strongly recommended) prior to our trip to China to adopt her sister. Shortly after, she began to develop worsening mood swings, anxiety, depression, brain fog and has experienced dizzy spells off and on since then.

When her menses began, she bled heavy for three straight weeks. Her doctor put her on birth control pills to stop it; again, a symptomatic treatment. She was borderline to severely anemic and often had PMS and painful periods.

During her teen years, she had repeat and unexplained fevers. She was sick with high fever/flu-like symptoms for three days every four weeks for three years. She’d get sick like clockwork! She would become weak, sleep a LOT, as if she were in a coma. Her doctor was stumped. I had been reading a lot about the use of systemic enzymes used by German doctors. The book by Karen DeFelice mentioned viruses often have a cyclical pattern. So we used high doses of ViraStop2x according to her protocol for a 3-week “holding spell” and it was gone. No more cyclical episodes.

In trying to get healthier, she began “green drinks” (spinach/fruit) 5-6x week. Six months later she was very sick: anemic again, double ear infection, abnormal EEG with heart palpitations, chest pain, and shortness of breath. The cardiologist had put her on a heart monitor for three days, but the results were normal. Perhaps oxalates? I began learning more about oxalates and we began eating less of these foods overall. I’m grasping at straws…

The Red Thread and Thiamine

In 2018, we learned about TTFD/thiamine and began taking Sulbutiamine. My younger daughter, Abby, has improved immensely. In fact, my entire family now uses thiamine and we all feel much better. Before taking thiamine, we all used to be so tired after spending a day at the beach and everyone would need to nap. Now, after supplementing with thiamine for a while, everyone still has high energy levels after these trips. Except for Kayla. Her results with thiamine have been mixed. There seems to be more at play. Perhaps she requires a higher dosage of thiamine or maybe additional nutrients are needed.

Her recent labs for CBC/CMP, thyroid, A1C, vitamin D are all normal. Manganese is low and prostaglandin F2 is elevated. There is some indication of malabsorption based on her bloodwork. Recently, an Organic Acids Test indicated normal oxalates, low dopamine and serotonin, and extremely high ketones/fatty acids. She has had high folate levels in the past, but at present are normal. Her B12 levels at present are elevated.

In 2019, she began having occasional extremely painful periods where she would be on-the-bathroom floor curled in the fetal position until Ibuprofen kicks in. Her skin is often very pale. Her doctor is not concerned about the increasingly painful menses or the ketones/fatty acid elevations.

My frustration as a parent is that because most of my child’s bloodwork is normal, the doctors write-off her symptoms as stress-related and recommend things like yoga, meditation or saunas or some fluff. Not that these things are bad, but there is something more at work here and no one seems interested in figuring it out. I am bothered that when they do see markers of inflammation or malabsorption they ignore them or really don’t know what to make of it.

Environmental Causes Of Ill-health and Longstanding Thiamine Insufficiency

Over the course of these last years, I have come to realize how important diet and environment are to health. When the pond is poisoned, sadly the tadpoles are hit first, are hit the hardest and display the affects most noticeably. Our youngest child was hit hard. Her circumstances prior to adoption were not conducive to health and she has had many struggles to overcome those early stressors and nutrient deficiencies. Likewise, owing to my ill-health prior to and during my pregnancy and the subsequent western medical treatments, Kayla struggles too. The pond was poisoned for both of them. All lifeforms that drink from a poisoned pond will manifest problems at some point, in some way. Perhaps if we had known about thiamine when they were younger, their problems wouldn’t have manifested the way they did.

Fortunately, Kayla has always eaten healthy, and has been active and athletic throughout her life. As an adult, she experiments with the removal of foods for periods of time to see if things improve, such as grains or cow’s milk and she is cooking creatively. She has been sugar-free for over a year. She takes vitamins and minerals and Sulbutiamine. She recently switched to Lipothiamine and Allithiamine and is now slowly increasing it to see if her dizziness will abate at some point.

I would trade all of her past accolades to have her in better health. We don’t know where her road will lead. Healing is multi-dimensional and someday we hope to look back at today with those oft used words “remember when…”.

Michelangelo was nearing 90 when he said “I am still learning.” I hope to be too.

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This story was published first on August 31, 2020.

thiamine deficiency - Page 7

Early and Prominent Orthostatic Hypotension Missed for Decades

Mitral Valve Prolapse, Tachycardia and Heart Palpitations: Signs of Dysautonomia

Decades Later: Debilitating Fatigue and Arrhythmia

Hypovolemia and Undiagnosed Thiamine Deficiency Almost Killed Me

Putting the Pieces Together: It Was Thiamine All Along

Gains Made With Thiamine

Final Thoughts

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